thalamus

Developmental and evolutionary perspectives on thalamic function

Brain organization and function is a complex topic. We are good at establishing correlates of perception and behavior across forebrain circuits, as well as manipulating activity in these circuits to affect behavior. However, we still lack good models for the large-scale organization and function of the forebrain. What are the contributions of the cortex, basal ganglia, and thalamus to behavior? In addressing these questions, we often ascribe function to each area as if it were an independent processing unit. However, we know from the anatomy that the cortex, basal ganglia, and thalamus, are massively interconnected in a large network. One way to generate insight into these questions is to consider the evolution and development of forebrain systems. In this talk, I will discuss the developmental and evolutionary (comparative anatomy) data on the thalamus, and how it fits within forebrain networks. I will address questions including, when did the thalamus appear in evolution, how is the thalamus organized across the vertebrate lineage, and how can the change in the organization of forebrain networks affect behavioral repertoires.

How do we sleep?

There is no consensus on if sleep is for the brain, body or both. But the difference in how we feel following disrupted sleep or having a good night of continuous sleep is striking. Understanding how and why we sleep will likely give insights into many aspects of health. In this talk I will outline our recent work on how the prefrontal cortex can signal to the hypothalamus to regulate sleep preparatory behaviours and sleep itself, and how other brain regions, including the ventral tegmental area, respond to psychosocial stress to induce beneficial sleep. I will also outline our work on examining the function of the glymphatic system, and whether clearance of molecules from the brain is enhanced during sleep or wakefulness.

Neural mechanisms governing the learning and execution of avoidance behavior

The nervous system orchestrates adaptive behaviors by intricately coordinating responses to internal cues and environmental stimuli. This involves integrating sensory input, managing competing motivational states, and drawing on past experiences to anticipate future outcomes. While traditional models attribute this complexity to interactions between the mesocorticolimbic system and hypothalamic centers, the specific nodes of integration have remained elusive. Recent research, including our own, sheds light on the midline thalamus's overlooked role in this process. We propose that the midline thalamus integrates internal states with memory and emotional signals to guide adaptive behaviors. Our investigations into midline thalamic neuronal circuits have provided crucial insights into the neural mechanisms behind flexibility and adaptability. Understanding these processes is essential for deciphering human behavior and conditions marked by impaired motivation and emotional processing. Our research aims to contribute to this understanding, paving the way for targeted interventions and therapies to address such impairments.

Combined electrophysiological and optical recording of multi-scale neural circuit dynamics

This webinar will showcase new approaches for electrophysiological recordings using our silicon neural probes and surface arrays combined with diverse optical methods such as wide-field or 2-photon imaging, fiber photometry, and optogenetic perturbations in awake, behaving mice. Multi-modal recording of single units and local field potentials across cortex, hippocampus and thalamus alongside calcium activity via GCaMP6F in cortical neurons in triple-transgenic animals or in hippocampal astrocytes via viral transduction are brought to bear to reveal hitherto inaccessible and under-appreciated aspects of coordinated dynamics in the brain.

Seizure control by electrical stimulation: parameters and mechanisms

Seizure suppression by deep brain stimulation (DBS) applies high frequency stimulation (HFS) to grey matter to block seizures. In this presentation, I will present the results of a different method that employs low frequency stimulation (LFS) (1 to 10Hz) of white matter tracts to prevent seizures. The approach has been shown to be effective in the hippocampus by stimulating the ventral and dorsal hippocampal commissure in both animal and human studies respectively for mesial temporal lobe seizures. A similar stimulation paradigm has been shown to be effective at controlling focal cortical seizures in rats with corpus callosum stimulation. This stimulation targets the axons of the corpus callosum innervating the focal zone at low frequencies (5 to 10Hz) and has been shown to significantly reduce both seizure and spike frequency. The mechanisms of this suppression paradigm have been elucidated with in-vitro studies and involve the activation of two long-lasting inhibitory potentials GABAB and sAHP. LFS mechanisms are similar in both hippocampus and cortical brain slices. Additionally, the results show that LFS does not block seizures but rather decreases the excitability of the tissue to prevent seizures. Three methods of seizure suppression, LFS applied to fiber tracts, HFS applied to focal zone and stimulation of the anterior nucleus of the thalamus (ANT) were compared directly in the same animal in an in-vivo epilepsy model. The results indicate that LFS generated a significantly higher level of suppression, indicating LFS of white matter tract could be a useful addition as a stimulation paradigm for the treatment of epilepsy.

Diffuse coupling in the brain - A temperature dial for computation

The neurobiological mechanisms of arousal and anesthesia remain poorly understood. Recent evidence highlights the key role of interactions between the cerebral cortex and the diffusely projecting matrix thalamic nuclei. Here, we interrogate these processes in a whole-brain corticothalamic neural mass model endowed with targeted and diffusely projecting thalamocortical nuclei inferred from empirical data. This model captures key features seen in propofol anesthesia, including diminished network integration, lowered state diversity, impaired susceptibility to perturbation, and decreased corticocortical coherence. Collectively, these signatures reflect a suppression of information transfer across the cerebral cortex. We recover these signatures of conscious arousal by selectively stimulating the matrix thalamus, recapitulating empirical results in macaque, as well as wake-like information processing states that reflect the thalamic modulation of largescale cortical attractor dynamics. Our results highlight the role of matrix thalamocortical projections in shaping many features of complex cortical dynamics to facilitate the unique communication states supporting conscious awareness.

Obesity and Brain – Bidirectional Influences

The regulation of body weight relies on homeostatic mechanisms that use a combination of internal signals and external cues to initiate and terminate food intake. Homeostasis depends on intricate communication between the body and the hypothalamus involving numerous neural and hormonal signals. However, there is growing evidence that higher-level cognitive function may also influence energy balance. For instance, research has shown that BMI is consistently linked to various brain, cognitive, and personality measures, implicating executive, reward, and attentional systems. Moreover, the rise in obesity rates over the past half-century is attributed to the affordability and widespread availability of highly processed foods, a phenomenon that contradicts the idea that food intake is solely regulated by homeostasis. I will suggest that prefrontal systems involved in value computation and motivation act to limit food overconsumption when food is scarce or expensive, but promote over-eating when food is abundant, an optimum strategy from an economic standpoint. I will review the genetic and neuroscience literature on the CNS control of body weight. I will present recent studies supporting a role of prefrontal systems in weight control. I will also present contradictory evidence showing that frontal executive and cognitive findings in obesity may be a consequence not a cause of increased hunger. Finally I will review the effects of obesity on brain anatomy and function. Chronic adiposity leads to cerebrovascular dysfunction, cortical thinning, and cognitive impairment. As the most common preventable risk factor for dementia, obesity poses a significant threat to brain health. I will conclude by reviewing evidence for treatment of obesity in adults to prevent brain disease.

25 years of DBS beyond movement disorders: what challenges are we facing?; Directional DBS targeting of different nuclei in the thalamus for the treatment of pain

On Thursday, 23rd of February, we will host Veerle Visser-Vandewalle and Marie Krüger. Marie Krüger, MD, is is currently leading the stereotactic surgery unit in St. Gallen but is on her move to join the team at UCL / Queensquare London. She will discuss “Directional DBS targeting of different nuclei in the thalamus for the treatment of pain”. Veerle Visser-Vandewalle, MD, PhD, is the Head of the Department of Stereotactic and Functional Neurosurgery at University Hospital of Cologne. Beside his scientific presentation on “25 years of DBS beyond movement disorders: what challenges are we facing?”, she will also give us a glimpse at the “Person behind the science”. The talks will be followed by a shared discussion. You can register via talks.stimulatingbrains.org to receive the (free) Zoom link!

Orientation selectivity in rodent V1: theory vs experiments

Neurons in the primary visual cortex (V1) of rodents are selective to the orientation of the stimulus, as in other mammals such as cats and monkeys. However, in contrast with those species, their neurons display a very different type of spatial organization. Instead of orientation maps they are organized in a “salt and pepper” pattern, where adjacent neurons have completely different preferred orientations. This structure has motivated both experimental and theoretical research with the objective of determining which aspects of the connectivity patterns and intrinsic neuronal responses can explain the observed behavior. These analysis have to take into account also that the neurons of the thalamus that send their outputs to the cortex have more complex responses in rodents than in higher mammals, displaying, for instance, a significant degree of orientation selectivity. In this talk we present work showing that a random feed-forward connectivity pattern, in which the probability of having a connection between a cortical neuron and a thalamic neuron depends only on the relative distance between them is enough explain several aspects of the complex phenomenology found in these systems. Moreover, this approach allows us to evaluate analytically the statistical structure of the thalamic input on the cortex. We find that V1 neurons are orientation selective but the preferred orientation of the stimulus depends on the spatial frequency of the stimulus. We disentangle the effect of the non circular thalamic receptive fields, finding that they control the selectivity of the time-averaged thalamic input, but not the selectivity of the time locked component. We also compare with experiments that use reverse correlation techniques, showing that ON and OFF components of the aggregate thalamic input are spatially segregated in the cortex.

Private oxytocin supply and its receptors in the hypothalamus for social avoidance learning

Many animals live in complex social groups. To survive, it is essential to know who to avoid and who to interact. Although naïve mice are naturally attracted to any adult conspecifics, a single defeat experience could elicit social avoidance towards the aggressor for days. The neural mechanisms underlying the behavior switch from social approach to social avoidance remains incompletely understood. Here, we identify oxytocin neurons in the retrochiasmatic supraoptic nucleus (SOROXT) and oxytocin receptor (OXTR) expressing cells in the anterior subdivision of ventromedial hypothalamus, ventrolateral part (aVMHvlOXTR) as a key circuit motif for defeat-induced social avoidance learning. After defeat, aVMHvlOXTR cells drastically increase their responses to aggressor cues. This response change is functionally important as optogenetic activation of aVMHvlOXTR cells elicits time-locked social avoidance towards a benign social target whereas inactivating the cells suppresses defeat-induced social avoidance. Furthermore, OXTR in the aVMHvl is itself essential for the behavior change. Knocking out OXTR in the aVMHvl or antagonizing the receptor during defeat, but not during post-defeat social interaction, impairs defeat-induced social avoidance. aVMHvlOXTR receives its private supply of oxytocin from SOROXT cells. SOROXT is highly activated by the noxious somatosensory inputs associated with defeat. Oxytocin released from SOROXT depolarizes aVMHvlOXTR cells and facilitates their synaptic potentiation, and hence, increases aVMHvlOXTR cell responses to aggressor cues. Ablating SOROXT cells impairs defeat-induced social avoidance learning whereas activating the cells promotes social avoidance after a subthreshold defeat experience. Altogether, our study reveals an essential role of SOROXT-aVMHvlOXTR circuit in defeat-induced social learning and highlights the importance of hypothalamic oxytocin system in social ranking and its plasticity.

Prefrontal top-down projections control context-dependent strategy selection

The rules governing behavior often vary with behavioral contexts. As a result, an action rewarded in one context may be discouraged in another. Animals and humans are capable of switching between behavioral strategies under different contexts and acting adaptively according to the variable rules, a flexibility that is thought to be mediated by the prefrontal cortex (PFC). However, how the PFC orchestrates the context-dependent switch of strategies remains unclear. Here we show that pathway-specific projection neurons in the medial PFC (mPFC) differentially contribute to context-instructed strategy selection. In mice trained in a decision-making task in which a previously established rule and a newly learned rule are associated with distinct contexts, the activity of mPFC neurons projecting to the dorsomedial striatum (mPFC-DMS) encodes the contexts and further represents decision strategies conforming to the old and new rules. Moreover, mPFC-DMS neuron activity is required for the context-instructed strategy selection. In contrast, the activity of mPFC neurons projecting to the ventral midline thalamus (mPFC-VMT) does not discriminate between the contexts, and represents the old rule even if mice have adopted the new one. Furthermore, these neurons act to prevent the strategy switch under the new rule. Our results suggest that mPFC-DMS neurons promote flexible strategy selection guided by contexts, whereas mPFC-VMT neurons favor fixed strategy selection by preserving old rules.

Hypothalamic episode generators underlying the neural control of fertility

The hypothalamus controls diverse homeostatic functions including fertility. Neural episode generators are required to drive the intermittent pulsatile and surge profiles of reproductive hormone secretion that control gonadal function. Studies in genetic mouse models have been fundamental in defining the neural circuits forming these central pattern generators and the full range of in vitro and in vivo optogenetic and chemogenetic methodologies have enabled investigation into their mechanism of action. The seminar will outline studies defining the hypothalamic “GnRH pulse generator network” and current understanding of its operation to drive pulsatile hormone secretion.

Identifying central mechanisms of glucocorticoid circadian rhythm dysfunction in breast cancer

The circadian release of endogenous glucocorticoids is essential in preparing and synchronizing the body’s daily physiological needs. Disruption in the rhythmic activity of glucocorticoids has been observed in individuals with a variety of cancer types, and blunting of this rhythm has been shown to predict cancer mortality and declines in quality of life. This suggests that a disrupted glucocorticoid rhythm is potentially a shared phenotype across cancers. However, where this phenomenon is driven by the cancer itself, and the causal mechanisms that link glucocorticoid rhythm dysfunction and cancer outcomes remain preliminary at best. The regulation of daily glucocorticoid activity has been well-characterized and is maintained, in part, by the coordinated response of the hypothalamic-pituitary-adrenal (HPA) axis, consisting of the suprachiasmatic nucleus (SCN) and corticotropin-releasing hormone-expressing neurons of the paraventricular nucleus of the hypothalamus (PVNCRH). Consequently, we set out to examine if cancer-induced glucocorticoid dysfunction is regulated by disruptions within these hypothalamic nuclei. In comparison to their tumor-free baseline, mammary tumor-bearing mice exhibited a blunting of glucocorticoid rhythms across multiple timepoints throughout the day, as measured by the overall levels and the slope of fecal corticosterone rhythms, during tumor progression. We further examined how peripheral tumors shape hypothalamic activity within the brain. Serial two-photon tomography for whole-brain cFos imaging suggests a disrupted activation of the PVN in mice with tumors. Additionally, we found GFP labeled CRH+ neurons within the PVN after injection of pseudorabies virus expressing GFP into the tumor, pointing to the PVN as a primary target disrupted by mammary tumors. Preliminary in vivo fiber photometry data show that PVNCRH neurons exhibit enhanced calcium activity during tumor progression, as compared to baseline (no tumor) activity. Taken together, this suggests that there may be an overactive HPA response during tumor progression, which in turn, may result in a subsequent negative feedback on glucocorticoid rhythms. Current studies are examining whether tumor progression modulates SCN calcium activity, how the transcriptional profile of PVNCRH neurons is changed, and test if manipulation of the neurocircuitry surrounding glucocorticoid rhythmicity alters tumor characteristics.

A draft connectome for ganglion cell types of the mouse retina

The visual system of the brain is highly parallel in its architecture. This is clearly evident in the outputs of the retina, which arise from neurons called ganglion cells. Work in our lab has shown that mammalian retinas contain more than a dozen distinct types of ganglion cells. Each type appears to filter the retinal image in a unique way and to relay this processed signal to a specific set of targets in the brain. My students and I are working to understand the meaning of this parallel organization through electrophysiological and anatomical studies. We record from light-responsive ganglion cells in vitro using the whole-cell patch method. This allows us to correlate directly the visual response properties, intrinsic electrical behavior, synaptic pharmacology, dendritic morphology and axonal projections of single neurons. Other methods used in the lab include neuroanatomical tracing techniques, single-unit recording and immunohistochemistry. We seek to specify the total number of ganglion cell types, the distinguishing characteristics of each type, and the intraretinal mechanisms (structural, electrical, and synaptic) that shape their stimulus selectivities. Recent work in the lab has identified a bizarre new ganglion cell type that is also a photoreceptor, capable of responding to light even when it is synaptically uncoupled from conventional (rod and cone) photoreceptors. These ganglion cells appear to play a key role in resetting the biological clock. It is just this sort of link, between a specific cell type and a well-defined behavioral or perceptual function, that we seek to establish for the full range of ganglion cell types. My research concerns the structural and functional organization of retinal ganglion cells, the output cells of the retina whose axons make up the optic nerve. Ganglion cells exhibit great diversity both in their morphology and in their responses to light stimuli. On this basis, they are divisible into a large number of types (>15). Each ganglion-cell type appears to send its outputs to a specific set of central visual nuclei. This suggests that ganglion cell heterogeneity has evolved to provide each visual center in the brain with pre-processed representations of the visual scene tailored to its specific functional requirements. Though the outline of this story has been appreciated for some time, it has received little systematic exploration. My laboratory is addressing in parallel three sets of related questions: 1) How many types of ganglion cells are there in a typical mammalian retina and what are their structural and functional characteristics? 2) What combination of synaptic networks and intrinsic membrane properties are responsible for the characteristic light responses of individual types? 3) What do the functional specializations of individual classes contribute to perceptual function or to visually mediated behavior? To pursue these questions, we label retinal ganglion cells by retrograde transport from the brain; analyze in vitro their light responses, intrinsic membrane properties and synaptic pharmacology using the whole-cell patch clamp method; and reveal their morphology with intracellular dyes. Recently, we have discovered a novel ganglion cell in rat retina that is intrinsically photosensitive. These ganglion cells exhibit robust light responses even when all influences from classical photoreceptors (rods and cones) are blocked, either by applying pharmacological agents or by dissociating the ganglion cell from the retina. These photosensitive ganglion cells seem likely to serve as photoreceptors for the photic synchronization of circadian rhythms, the mechanism that allows us to overcome jet lag. They project to the circadian pacemaker of the brain, the suprachiasmatic nucleus of the hypothalamus. Their temporal kinetics, threshold, dynamic range, and spectral tuning all match known properties of the synchronization or "entrainment" mechanism. These photosensitive ganglion cells innervate various other brain targets, such as the midbrain pupillary control center, and apparently contribute to a host of behavioral responses to ambient lighting conditions. These findings help to explain why circadian and pupillary light responses persist in mammals, including humans, with profound disruption of rod and cone function. Ongoing experiments are designed to elucidate the phototransduction mechanism, including the identity of the photopigment and the nature of downstream signaling pathways. In other studies, we seek to provide a more detailed characterization of the photic responsiveness and both morphological and functional evidence concerning possible interactions with conventional rod- and cone-driven retinal circuits. These studies are of potential value in understanding and designing appropriate therapies for jet lag, the negative consequences of shift work, and seasonal affective disorder.

Neuromodulation of sleep integrity

The arousal construct underlies a spectrum of behaviors that include sleep, exploration, feeding, sexual activity and adaptive stress. Pathological arousal conditions include stress, anxiety disorders, and addiction. The dynamics between arousal state transitions are modulated by norepinephrine neurons in the locus coeruleus, histaminergic neurons in the hypothalamus, dopaminergic neurons in the mesencephalon and cholinergic neurons in the basal forebrain. The hypocretin/orexin system in the lateral hypothalamus I will also present a new mechanism underlying sleep fragmentation during aging. Hcrt neurons are hyperexcitable in aged mice. We identify a potassium conductance known as the M-current, as a critical player in maintaining excitability of Hcrt neurons. Genetic disruption of KCNQ channels in Hcrt neurons of young animals results in sleep fragmentation. In contrast, treatment of aged animals with a KCNQ channel opener restores sleep/wake architecture. These data point to multiple circuits modulating sleep integrity across lifespan.

Why is the suprachiasmatic nucleus such a brilliant circadian time-keeper?

Circadian clocks dominate our lives. By creating and distributing an internal representation of 24-hour solar time, they prepare us, and thereby adapt us, to the daily and seasonal world. Jet-lag is an obvious indicator of what can go wrong when such adaptation is disrupted acutely. More seriously, the growing prevalence of rotational shift-work which runs counter to our circadian life, is a significant chronic challenge to health, presenting as increased incidence of systemic conditions such as metabolic and cardiovascular disease. Added to this, circadian and sleep disturbances are a recognised feature of various neurological and psychiatric conditions, and in some cases may contribute to disease progression. The “head ganglion” of the circadian system is the suprachiasmatic nucleus (SCN) of the hypothalamus. It synchronises the, literally, innumerable cellular clocks across the body, to each other and to solar time. Isolated in organotypic slice culture, it can maintain precise, high-amplitude circadian cycles of neural activity, effectively, indefinitely, just as it does in vivo. How is this achieved: how does this clock in a dish work? This presentation will consider SCN time-keeping at the level of molecular feedback loops, neuropeptidergic networks and neuron-astrocyte interactions.

Synapses, Shadows and Stress Contagion

Survival is predicated on the ability of an organism to respond to stress. The reliability of this response is ensured by a synaptic architecture that is relatively inflexible (i.e. hard-wired). Our work has shown that in naive animals, synapses on CRH neurons in the paraventricular nucleus of the hypothalamus are very reluctant to modification. If animals are stressed, however, these synapses become willing to learn. This seminar will focus on mechanisms linking acute stress to metaplastic changes at glutamate synapses, and also show how stress, and these synaptic changes can be transmitted from one individual to another.

Cortical-subcortical loops in olfaction (thalamus missing)?

Top-down modulation of the retinal code via histaminergic neurons in the hypothalamus

The mammalian retina is considered an autonomous neuronal tissue, yet there is evidence that it receives inputs from the brain in the form of retinopetal axons. A sub-population of these axons was suggested to belong to histaminergic neurons located in the tuberomammillarynucleus (TMN) of the hypothalamus. Using viral injections to the TMN, we identified these retinopetal axons and found that although few in number, they extensively branch to cover a large portion of the retina. Using Ca2+ imaging and electrophysiology, we show that histamine application increases spontaneous firing rates and alters the light responses of a significant portion of retinal ganglion cells (RGCs). Direct activation of the histaminergic axons also induced significant changes in RGCs activity. Since activity in the TMN was shown to correlate with arousal state, our data suggest the retinal code may change with the animal's behavioral state through the release of histamine from TMN histaminergic neurons.

Bidirectionally connected cores in a mouse connectome: Towards extracting the brain subnetworks essential for consciousness

Where in the brain consciousness resides remains unclear. It has been suggested that the subnetworks supporting consciousness should be bidirectionally (recurrently) connected because both feed-forward and feedback processing are necessary for conscious experience. Accordingly, evaluating which subnetworks are bidirectionally connected and the strength of these connections would likely aid the identification of regions essential to consciousness. Here, we propose a method for hierarchically decomposing a network into cores with different strengths of bidirectional connection, as a means of revealing the structure of the complex brain network. We applied the method to a whole-brain mouse connectome. We found that cores with strong bidirectional connections consisted of regions presumably essential to consciousness (e.g., the isocortical and thalamic regions, and claustrum) and did not include regions presumably irrelevant to consciousness (e.g., cerebellum). Contrarily, we could not find such correspondence between cores and consciousness when we applied other simple methods which ignored bidirectionality. These findings suggest that our method provides a novel insight into the relation between bidirectional brain network structures and consciousness. Our recent preprint on this work is here: https://doi.org/10.1101/2021.07.12.452022.

The thalamus that speaks to the cortex: Spontaneous activity in the developing sensory circuits

Estimation of current and future physiological states in insular cortex

Interoception, the sense of internal bodily signals, is essential for physiological homeostasis, cognition, and emotions. While human insular cortex (InsCtx) is implicated in interoception, the cellular and circuit mechanisms remain unclear. I will describe our recent work imaging mouse InsCtx neurons during two physiological deficiency states – hunger and thirst. InsCtx ongoing activity patterns reliably tracked the gradual return to homeostasis, but not changes in behavior. Accordingly, while artificial induction of hunger/thirst in sated mice via activation of specific hypothalamic neurons (AgRP/SFOGLUT) restored cue-evoked food/water-seeking, InsCtx ongoing activity continued to reflect physiological satiety. During natural hunger/thirst, food/water cues rapidly and transiently shifted InsCtx population activity to the future satiety-related pattern. During artificial hunger/thirst, food/water cues further shifted activity beyond the current satiety-related pattern. Together with circuit-mapping experiments, these findings suggest that InsCtx integrates visceral-sensory inputs regarding current physiological state with hypothalamus-gated amygdala inputs signaling upcoming ingestion of food/water, to compute a prediction of future physiological state.

The role of the complement pathway in post-traumatic sleep disruption and epilepsy

While traumatic brain injury (TBI) acutely disrupts the cortex, most TBI-related disabilities reflect secondary injuries that accrue over time. The thalamus is a likely site of secondary damage because of its reciprocal connections with the cortex. Using a mouse model of mild cortical injury that does not directly damage subcortical structures (mTBI), we found a chronic increase in C1q expression specifically in the corticothalamic circuit. Increased C1q expression co-localized with neuron loss and chronic inflammation, and correlated with disruption in sleep spindles and emergence of epileptic activities. Blocking C1q counteracted these outcomes, suggesting that C1q is a disease modifier in mTBI. Single-nucleus RNA sequencing demonstrated that microglia are the source of thalamic C1q. Since the corticothalamic circuit is important for cognition and sleep, which can be impaired by TBI, this circuit could be a new target for treating TBI-related disabilities

Tectal and Pretectal Circuits of the Visual Thalamus

Visual processing of feedforward and feedback signals in mouse thalamus

Traditionally, the dorsolateral geniculate nucleus (dLGN) of the thalamus has been considered a feedforward relay station for retinal signals to reach primary visual cortex. The local and long-range circuits of dLGN, however, suggest that this view is not correct. Indeed, besides the thalamo-cortical relay cells, dLGN contains local inhibitory interneurons, and receives not only feedforward input from the retina, but also massive direct and indirect feedback from primary visual cortex. Furthermore, it is one of the earliest processing stages in the visual system that integrates visual information with neuromodulatory signals.

Territory cells in the mammalian hypothalamus

A fresh look at the bird retina

I am working on the vertebrate retina, with a main focus on the mouse and bird retina. Currently my work is focused on three major topics: Functional and molecular analysis of electrical synapses in the retina Circuitry and functional role of retinal interneurons: horizontal cells Circuitry for light-dependent magnetoreception in the bird retina Electrical synapses Electrical synapses (gap junctions) permit fast transmission of electrical signals and passage of metabolites by means of channels, which directly connect the cytoplasm of adjoining cells. A functional gap junction channel consists of two hemichannels (one provided by each of the cells), each comprised of a set of six protein subunits, termed connexins. These building blocks exist in a variety of different subtypes, and the connexin composition determines permeability and gating properties of a gap junction channel, thereby enabling electrical synapses to meet a diversity of physiological requirements. In the retina, various connexins are expressed in different cell types. We study the cellular distribution of different connexins as well as the modulation induced by transmitter action or change of ambient light levels, which leads to altered electrical coupling properties. We are also interested in exploiting them as therapeutic avenue for retinal degeneration diseases. Horizontal cells Horizontal cells receive excitatory input from photoreceptors and provide feedback inhibition to photoreceptors and feedforward inhibition to bipolar cells. Because of strong electrical coupling horizontal cells integrate the photoreceptor input over a wide area and are thought to contribute to the antagonistic organization of bipolar cell and ganglion cell receptive fields and to tune the photoreceptor–bipolar cell synapse with respect to the ambient light conditions. However, the extent to which this influence shapes retinal output is unclear, and we aim to elucidate the functional importance of horizontal cells for retinal signal processing by studying various transgenic mouse models. Retinal circuitry for light-dependent magnetoreception in the bird We are studying which neuronal cell types and pathways in the bird retina are involved in the processing of magnetic signals. Likely, magnetic information is detected in cryptochrome-expressing photoreceptors and leaves the retina through ganglion cell axons that project via the thalamofugal pathway to Cluster N, a part of the visual wulst essential for the avian magnetic compass. Thus, we aim to elucidate the synaptic connections and retinal signaling pathways from putatively magnetosensitive photoreceptors to thalamus-projecting ganglion cells in migratory birds using neuroanatomical and electrophysiological techniques.

Thalamocortical circuits from neuroanatomy to mental representations

In highly volatile environments, performing actions that address current needs and desires is an ongoing challenge for living organisms. For example, the predictive value of environmental signals needs to be updated when predicted and actual outcomes differ. Furthermore, organisms also need to gain control over the environment through actions that are expected to produce specific outcomes. The data to be presented will show that these processes are highly reliant on thalamocortical circuits wherein thalamic nuclei make a critical contribution to adaptive decision-making, challenging the view that the thalamus only acts as a relay station for the cortical stage. Over the past few years, our work has highlighted the specific contribution of multiple thalamic nuclei in the ability to update the predictive link between events or the causal link between actions and their outcomes via the combination of targeted thalamic interventions (lesion, chemogenetics, disconnections) with behavioral procedures rooted in experimental psychology. We argue that several features of thalamocortical architecture are consistent with a prominent role for thalamic nuclei in shaping mental representations.

Distinct limbic-hypothalamic circuits for the generation of social behaviors

The main pillars of social behaviors involve (1) mating, where males copulate with female partners to reproduce, and (2) aggression, where males fight conspecific male competitors in territory guarding. Decades of study have identified two key regions in the hypothalamus, the medial preoptic nucleus (MPN) and the ventrolateral part of ventromedial hypothalamus (VMHvl) , that are essential for male sexual and aggressive behaviors, respectively. However, it remains ambiguous what area directs excitatory control of the hypothalamic activity and generates the initiation signal for social behaviors. Through neural tracing, in vivo optical recording and functional manipulations, we identified the estrogen receptor alpha (Esr1)-expressing cells in the posterior amygdala (PA) as a main source of excitatory inputs to the MPN and VMHvl, and key hubs in mating and fighting circuits in males. Importantly, two spatially-distinct populations in the PA regulate male sexual and aggressive behaviors, respectively. Moreover, these two subpopulations in the PA display differential molecular phenotypes, projection patterns and in vivo neural responses. Our work also observed the parallels between these social behavior circuits and basal ganglia circuits to control motivated behaviors, which Larry Swanson (2000) originally proposed based on extensive developmental and anatomical evidence.

The suprachiasmatic nucleus: the brain's circadian clock

Sleep and all of the other circadian rhythms that adapt us to the 24 hour world are controlled by the suprachiasmatic nucleus (SCN), the brain's central circadian clock. And yet, the SCN consists of only 20,000 neurons and astrocytes, so what makes it such a powerful clock, able to set the tempo to our lives? Professor Hastings will consider the cell-autonomus and neural circuit-level mechanisms that sustain the SCN clock and how it regulates rest, activity and sleep.

Hypothalamic control of internal states underlying social behaviors in mice

Social interactions such as mating and fighting are driven by internal emotional states. How can we study internal states of an animal when it cannot tell us its subjective feelings? Especially when the meaning of the animal’s behavior is not clear to us, can we understand the underlying internal states of the animal? In this talk, I will introduce our recent work in which we used male mounting behavior in mice as an example to understand the underlying internal state of the animals. In many animal species, males exhibit mounting behavior toward females as part of the mating behavior repertoire. Interestingly, males also frequently show mounting behavior toward other males of the same species. It is not clear what the underlying motivation is - whether it is reproductive in nature or something distinct. Through detailed analysis of video and audio recordings during social interactions, we found that while male-directed and female-directed mounting behaviors are motorically similar, they can be distinguished by both the presence of ultrasonic vocalization during female-directed mounting (reproductive mounting) and the display of aggression following male-directed mounting (aggressive mounting). Using optogenetics, we further identified genetically defined neural populations in the medial preoptic area (MPOA) that mediate reproductive mounting and the ventrolateral ventromedial hypothalamus (VMHvl) that mediate aggressive mounting. In vivo microendocsopic imaging in MPOA and VMHvl revealed distinct neural ensembles that mainly encode either a reproductive or an aggressive state during which male or female directed mounting occurs. Together, these findings demonstrate that internal states are represented in the hypothalamus and that motorically similar behaviors exhibited under different contexts may reflect distinct internal states.

Using human pluripotent stem cells to model obesity in vitro

Obesity and neurodegeneration lead to millions of premature deaths each year and lack broadly effective treatments. Obesity is largely caused by the abnormal function of cell populations in the hypothalamus that regulate appetite. We have developed methods generate human hypothalamic neurons from hPSCs to study how they respond to nutrients and hormones (e.g. leptin) and how disease-associated mutations alter their function. Since human hypothalamic neurons can be produced in large numbers, are functionally responsive, have a human genome that can be readily edited, and are in culture environment that can be readily controlled, there is an unprecedented opportunity to study the genetic and environmental factors underlying obesity. In addition, we are fascinated by the fact that mid-life obesity is a risk factor for dementia later in life, and caloric restriction, exercise, and certain anti-obesity drugs are neuroprotective, suggesting that there are shared mechanisms between obesity and neurodegeneration. Studies of HPSC-derived hypothalamic neurons may help bridge the mechanistic gulf between human genetic data and organismic phenotypes, revealing new therapeutic targets. ​

A thalamus that speaks to the cortex: Spontaneous activity in development and plasticity of sensory circuits”

Nr4a1-mediated morphological adaptations in Ventral Pallidal projections to Mediodorsal Thalamus support cocaine intake and relapse-like behaviors

Growing evidence suggests the ventral pallidum (VP) is critical for drug intake and seeking behaviors. Receiving dense projections from the nucleus accumbens as well as dopamine inputs from the midbrain, the VP plays a central role in the control of motivated behaviors. Repeated exposure to cocaine is known to alter VP neuronal firing and neurotransmission. Surprisingly, there is limited information on the molecular adaptations occurring in VP neurons following cocaine intake.To provide insights into cocaine-induced transcriptional alterations we performed RNA-sequencing on VP of mice following cocaine self-administration. Gene Ontology analysis pointed toward alterations in dendrite- and spinerelated genes. Subsequent transcriptional regulator analysis identified the transcription factor Nr4a1 as a common regulator for these sets of morphology-related genes.Consistent with the central role of the VP in reward, its neurons project to several key regions associated with cocaine-mediated behaviors. We thus assessed Nr4a1 expression levels in various projection populations.Following cocaine self-administration, VP neurons projecting to the mediodorsal thalamus (MDT) showed significantly increased Nr4a1 levels. To further investigate the role of Nr4a1 in cocaine intake and relapse, we bidirectionally manipulated its expression levels selectively in VP neurons projecting to the MDT. Increasing Nr4a1 levels resulted in enhanced relapse-like behaviors accompanied by a blockage of cocaine-induced spinogenesis.However, decreasing Nr4a1expression levels completely abolished cocaine intake and consequential relapse-like behaviors. Together, our preliminary findings suggest that drug-induced neuronal remodeling in pallido-thalamic circuits is critical for cocaine intake and relapse-like behaviors.

The role of orexin/hypocretin in social behaviour

My lab is focused on how brain encodes and modulates social interactions. Intraspecific social interactions are integral for survival and maintenance of society among all mammalian species. Despite the importance of social interactions, we lack a complete understanding of the brain circuitry involved in processing social behaviour. My lab investigates how the hypothalamic orexin (hypocretin) neurons and their downstream circuits participate in social interaction behaviours. These neurons are located exclusively in the hypothalamus that regulates complex and goal-directed behaviours. We recently identified that orexin neurons differentially encode interaction between familiar and novel animals. We are currently investigating how chronic social isolation, a risk factor for the development of social-anxiety like behaviours, affects orexin neuron activity and how we can manipulate the activity of these neurons to mitigate isolation-induced social deficits.

Multiplexed coding in the higher-order thalamus

Long-term effects of diet-induced obesity on gut-brain communication

Rapid communication between the gut and the brain about recently consumed nutrients is critical for regulating food intake and maintaining energy homeostasis. We have shown that the infusion of nutrients directly into the gastrointestinal tract rapidly inhibits hunger-promoting AgRP neurons in the arcuate nucleus of the hypothalamus and suppresses subsequent feeding. The mechanism of this inhibition appears to be dependent upon macronutrient content, and can be recapitulated by a several hormones secreted in the gut in response to nutrient ingestion. In high-fat diet-induced obese mice, the response of AgRP neurons to nutrient-related stimuli are broadly attenuated. This attenuation is largely irreversible following weight loss and may represent a mechanism underlying difficulty with weight loss and propensity for weight regain in obesity.

Cortical estimation of current and future bodily states

Interoception, the sense of internal bodily signals, is essential for physiological homeostasis, cognition, and emotions. Human neuroimaging studies suggest insular cortex plays a central role in interoception, yet the cellular and circuit mechanisms of its involvement remain unclear. We developed a microprism-based cellular imaging approach to monitor insular cortex activity in behaving mice across different physiological need states. We combine this imaging approach with manipulations of peripheral physiology, circuit-mapping, cell type-specific and circuit-specific manipulation approaches to investigate the underlying circuit mechanisms. I will present our recent data investigating insular cortex activity during two physiological need states – hunger and thirst. These wereinduced naturally by caloric/fluid deficiency, or artificially by activation of specific hypothalamic “hunger neurons” and “thirst neurons”. We found that insular cortex ongoing activity faithfully represents current physiological state, independently of behavior or arousal levels. In contrast, transient responses to learned food- or water-predicting cues reflect a population-level “simulation” of future predicted satiety. Together with additional circuit-mapping and manipulation experiments, our findings suggest that insular cortex integrates visceral-sensory inputs regarding current physiological state with hypothalamus-gated amygdala inputs signaling availability of food/water. This way, insular cortex computes a prediction of future physiological state that can be used to guide behavioral choice.

Neurocircuits in control of integrative physiology

This open colloquia session is part of the special workshop entitled "Obesity at the Interface of Neuroscience and Physiology II". Abstract: Proopiomelanocortin (POMC)- and agouti related peptide (AgRP)-expressing neurons in the arcuate nucleus of the hypothalamus (ARH) are critical regulators of food intake and energy homeostasis. They rapidly integrate the energy state of the organism through sensing fuel availability via hormones, nutrient components and even rapidly upon sensory food perception. Importantly, they not only regulate feeding responses, but numerous autonomic responses including glucose and lipid metabolism, inflammation and blood pressure. More recently, we could demonstrate that sensory food cue-dependent regulation of POMC neurons primes the hepatic endoplasmic reticulum (ER) stress response to prime liver metabolism for the postpramndial state. The presentation will focus on the regulation of these neurons in control of integrative physiology, the identification of distinct neuronal circuitries targeted by these cells and finally on the broad range implications resulting from dysregulation of these circuits as a consequence of altered maternal metabolism.

Plasticity in hypothalamic circuits for oxytocin release

Mammalian babies are “sensory traps” for parents. Various sensory cues from the newborn are tremendously efficient in triggering parental responses in caregivers. We recently showed that core aspects of maternal behavior such as pup retrieval in response to infant vocalizations rely on active learning of auditory cues from pups facilitated by the neurohormone oxytocin (OT). Release of OT from the hypothalamus might thus help induce recognition of different infant cues but it is unknown what sensory stimuli can activate OT neurons. I performed unprecedented in vivo whole-cell and cell-attached recordings from optically-identified OT neurons in awake dams. I found that OT neurons, but not other hypothalamic cells, increased their firing rate after playback of pup distress vocalizations. Using anatomical tracing approaches and channelrhodopsin-assisted circuit mapping, I identified the projections and brain areas (including inferior colliculus, auditory cortex, and posterior intralaminar thalamus) relaying auditory information about social sounds to OT neurons. In hypothalamic brain slices, when optogenetically stimulating thalamic afferences to mimic high-frequency thalamic discharge, observed in vivo during pup calls playback, I found that thalamic activity led to long-term depression of synaptic inhibition in OT neurons. This was mediated by postsynaptic NMDARs-induced internalization of GABAARs. Therefore, persistent activation of OT neurons following pup calls in vivo is likely mediated by disinhibition. This gain modulation of OT neurons by infant cries, may be important for sustaining motivation. Using a genetically-encoded OT sensor, I demonstrated that pup calls were efficient in triggering OT release in downstream motivational areas. When thalamus projections to hypothalamus were inhibited with chemogenetics, dams exhibited longer latencies to retrieve crying pups, suggesting that the thalamus-hypothalamus noncanonical auditory pathway may be a specific circuit for the detection of social sounds, important for disinhibiting OT neurons, gating OT release in downstream brain areas, and speeding up maternal behavior.

Top-down modulation of cortical output is gated by the thalamus

Dynamic regulation of information processing in thalamus

Recurrent corticothalamic feedback in the auditory system: perceptual salience and dopaminergic modulation

Delineating Reward/Avoidance Decision Process in the Impulsive-compulsive Spectrum Disorders through a Probabilistic Reversal Learning Task

Impulsivity and compulsivity are behavioural traits that underlie many aspects of decision-making and form the characteristic symptoms of Obsessive Compulsive Disorder (OCD) and Gambling Disorder (GD). The neural underpinnings of aspects of reward and avoidance learning under the expression of these traits and symptoms are only partially understood. " "The present study combined behavioural modelling and neuroimaging technique to examine brain activity associated with critical phases of reward and loss processing in OCD and GD. " "Forty-two healthy controls (HC), forty OCD and twenty-three GD participants were recruited in our study to complete a two-session reinforcement learning (RL) task featuring a “probability switch (PS)” with imaging scanning. Finally, 39 HC (20F/19M, 34 yrs +/- 9.47), 28 OCD (14F/14M, 32.11 yrs ±9.53) and 16 GD (4F/12M, 35.53yrs ± 12.20) were included with both behavioural and imaging data available. The functional imaging was conducted by using 3.0-T SIEMENS MAGNETOM Skyra syngo MR D13C at Monash Biomedical Imaging. Each volume compromised 34 coronal slices of 3 mm thickness with 2000 ms TR and 30 ms TE. A total of 479 volumes were acquired for each participant in each session in an interleaved-ascending manner. " " The standard Q-learning model was fitted to the observed behavioural data and the Bayesian model was used for the parameter estimation. Imaging analysis was conducted using SPM12 (Welcome Department of Imaging Neuroscience, London, United Kingdom) in the Matlab (R2015b) environment. The pre-processing commenced with the slice timing, realignment, normalization to MNI space according to T1-weighted image and smoothing with a 8 mm Gaussian kernel. " " The frontostriatal brain circuit including the putamen and medial orbitofrontal (mOFC) were significantly more active in response to receiving reward and avoiding punishment compared to receiving an aversive outcome and missing reward at 0.001 with FWE correction at cluster level; While the right insula showed greater activation in response to missing rewards and receiving punishment. Compared to healthy participants, GD patients showed significantly lower activation in the left superior frontal and posterior cingulum at 0.001 for the gain omission. " " The reward prediction error (PE) signal was found positively correlated with the activation at several clusters expanding across cortical and subcortical region including the striatum, cingulate, bilateral insula, thalamus and superior frontal at 0.001 with FWE correction at cluster level. The GD patients showed a trend of decreased reward PE response in the right precentral extending to left posterior cingulate compared to controls at 0.05 with FWE correction. " " The aversive PE signal was negatively correlated with brain activity in regions including bilateral thalamus, hippocampus, insula and striatum at 0.001 with FWE correction. Compared with the control group, GD group showed an increased aversive PE activation in the cluster encompassing right thalamus and right hippocampus, and also the right middle frontal extending to the right anterior cingulum at 0.005 with FWE correction. " " Through the reversal learning task, the study provided a further support of the dissociable brain circuits for distinct phases of reward and avoidance learning. Also, the OCD and GD is characterised by aberrant patterns of reward and avoidance processing.

The thalamus that speaks to the cortex: spontaneous activity in the developing brain

Our research team runs several related projects studying the cellular and molecular mechanisms involved in the development of axonal connections in the brain. In particular, our aim is to uncover the principles underlying thalamocortical axonal wiring, maintenance and ultimately the rewiring of connections, through an integrated and innovative experimental programme. The development of the thalamocortical wiring requires a precise topographical sorting of its connections. Each thalamic nucleus receives specific sensory information from the environment and projects topographically to its corresponding cortical. A second level of organization is achieved within each area, where thalamocortical connections display an intra-areal topographical organization, allowing the generation of accurate spatial representations within each cortical area. Therefore, the level of organization and specificity of the thalamocortical projections is much more complex than other projection systems in the CNS. The central hypothesis of our laboratory is that thalamocortical input influences and maintains the functional architecture of the sensory cortices. We also believe that rewiring and plasticity events can be triggered by activity-dependent mechanisms in the thalamus. Three major questions are been focused in the laboratory: i) the role of spontaneous patterns of activity in thalamocortical wiring and cortical development, ii) the role of the thalamus and its connectivity in the neuroplastic cortical changes following sensory deprivation, and iii) reprogramming thalamic cells for sensory circuit restoration. Within these projects we are using several experimental programmes, these include: optical imaging, manipulation of gene expression in vivo, cell and molecular biology, biochemistry, cell culture, sensory deprivation paradigms and electrophysiology. The results derived from our investigations will contribute to our understating of how reprogramming of cortical wiring takes place following brain damage and how cortical structure is maintained.

Striatal circuits for reward learning and decision-making

How are actions linked with subsequent outcomes to guide choices? The nucleus accumbens (NAc), which is implicated in this process, receives glutamatergic inputs from the prelimbic cortex (PL) and midline regions of the thalamus (mTH). However, little is known about what is represented in PL or mTH neurons that project to NAc (PL-NAc and mTH-NAc). By comparing these inputs during a reinforcement learning task in mice, we discovered that i) PL-NAc preferentially represents actions and choices, ii) mTH-NAc preferentially represents cues, iii) choice-selective activity in PL-NAc is organized in sequences that persist beyond the outcome. Through computational modelling, we demonstrate that these sequences can support the neural implementation of temporal difference learning, a powerful algorithm to connect actions and outcomes across time. Finally, we test and confirm predictions of our circuit model by direct manipulation of PL-NAc neurons. Thus, we integrate experiment and modelling to suggest a neural solution for credit assignment.

ROLE OF NEURONAL OSCILLATIONS IN HUMAN THALAMUS AND SUBTHALAMIC NUCLEUS IN EVIDENCE INTEGRATION AND MOTOR EXECUTION DURING PERCEPTUAL DECISION-MAKING

FENS Forum 2026

STATE-RELATED NEURAL DYNAMICS IN THE VISUAL THALAMUS OF FREELY MOVING MICE

FENS Forum 2026

PARAVENTRICULAR THALAMUS INPUTS TO THE NUCLEUS ACCUMBENS MODULATE DOPAMINE SIGNALING AND OPIOID RESPONSES IN CHRONIC PAIN

FENS Forum 2026

PAIN-ACTIVE CENTROLATERAL THALAMUS NEURONS PROJECTING TO ANTERIOR CINGULATE CORTEX MEDIATE PAIN-INDUCED SLEEP DISRUPTION IN MICE

FENS Forum 2026

REWIRING PAIN: INVESTIGATING THE ROLE OF THE CENTROLATERAL THALAMUS IN CHRONIC NEUROPATHIC PAIN

FENS Forum 2026

INVESTIGATION OF FEEDING-STATUS DEPENDENT MODULATION OF GABA<SUB>A</SUB>RΑ5 AND GAT3 PROTEINS IN THE VENTROMEDIAL HYPOTHALAMUS

FENS Forum 2026

AGE-DEPENDENT CHANGES OF GHRELIN-SENSITIVE NEURONS IN THE DORSOMEDIAL AND VENTROMEDIAL NUCLEI OF THE HYPOTHALAMUS IN RATS

FENS Forum 2026

SEX- AND DOSE-DEPENDENT MODULATION OF MOUSE BEHAVIOR BY FOXP2 IN THE MEDIODORSAL THALAMUS

FENS Forum 2026

GENOTYPE-DEPENDENT ENGAGEMENT OF ANTERIOR AND POSTERIOR PARAVENTRICULAR NUCLEUS OF THE THALAMUS IN CONDITIONED FEAR INCUBATION

FENS Forum 2026

LEPTIN-SENSITIVE NEURONS IN LATERAL HYPOTHALAMUS COUNTERACT ANXIETY TO ENABLE ADAPTIVE BEHAVIORAL RESPONSES UNDER ANXIOGENIC CONDITIONS AND IN AN ANOREXIA NERVOSA MOUSE MODEL

FENS Forum 2026

ELECTROPHYSIOLOGICAL ALTERATIONS ACROSS MEDIODORSAL THALAMUS SUBDIVISIONS IN THE SCHIZOPHRENIA <EM>GRIN2A<SUP>+/-</SUP></EM><SUP> </SUP>MOUSE

FENS Forum 2026

LEVERAGING A NOVEL HYPOTHALAMUS-BRAINSTEM NEUROCIRCUIT FOR URINARY AND FECAL INCONTINENCE

FENS Forum 2026

FUNCTIONAL DISSECTION OF MEDIODORSAL THALAMUS SUBDIVISIONS IN SOCIAL BEHAVIOR

FENS Forum 2026

INCREASING SLOW-OSCILLATION-SPINDLE COUPLING WITH TEMPORAL INTERFERENCE STIMULATION OF THE THALAMUS IN A COMPUTATIONAL MODEL OF DEEP SLEEP

FENS Forum 2026

NEURAL REPRESENTATION OF DIVERSE TACTILE TEXTURES IN THE MOUSE VENTRAL POSTERIOR LATERAL THALAMUS

FENS Forum 2026

ACTING OR REACTING? DISENTANGLING MOTOR THALAMUS CIRCUITS IN SELF-PACED VERSUS CUED MOVEMENT INITIATION

FENS Forum 2026

ADOLESCENT SOCIAL ISOLATION INDUCED TRANSCRIPTOMIC CHANGES IN THE HYPOTHALAMUS DRIVES ALTERED NEUROENDOCRINE AND BEHAVIOURAL OUTCOMES

FENS Forum 2026

LAMINAR PARVALBUMIN AND SOMATOSTATIN ACTIVATION IN ACC TRACKS MEDIODORSAL THALAMUS CONTROL OF PAIN BEHAVIOR

FENS Forum 2026

SUB-SECOND DOPAMINE FLUCTUATIONS IN HUMAN THALAMUS DURING AUDITORY-MOTOR SYNCHRONISATION

FENS Forum 2026

THE REUNIENS NUCLEUS OF THE THALAMUS: THE CORNERSTONE OF BEHAVIORAL FLEXIBILITY AND SPATIAL MEMORY CONSOLIDATION IN RATS

FENS Forum 2026

STRESS ATTENUATES THE EXCITABILITY OF ACCUMBAL NEURONS PROJECTING TO THE LATERAL HYPOTHALAMUS: POTENTIAL CONSEQUENCES FOR BINGE EATING

FENS Forum 2026

A ROLE OF PREFRONTAL CORTICAL INPUTS ONTO LATERAL HYPOTHALAMUS IN ANXIETY-RELATED BEHAVIOR IN HEALTH AND IN ACTIVITY-BASED ANOREXIA NERVOSA MODEL

FENS Forum 2026

FIBER PHOTOMETRY OF NEURAL ACTIVITY IN PROJECTION-SPECIFIC SUBPOPULATIONS OF THE ANTERO-MEDIAL (AM) NUCLEUS OF THE THALAMUS

FENS Forum 2026

RAB23 CONTROLS APPETITE VIA CILIARY REGULATION OF THE LEPTIN-MELANOCORTIN PATHWAY IN HYPOTHALAMUS NEURONS

FENS Forum 2026

HIGHER-ORDER THALAMUS IS PIVOTAL IN SCHIZOPHRENIA-ASSOCIATED PATHOPHYSIOLOGY

FENS Forum 2026

OPTOGENETIC DISSECTION OF PREFRONTAL–LATERAL HYPOTHALAMUS CIRCUIT IN STRESS-RELATED BEHAVIOURS

FENS Forum 2026

AUDITORY THALAMUS NEURONAL DYNAMICS IN FREE EXPLORATION AND DECISION-MAKING

FENS Forum 2026

DISTINCT NEURONAL CELL POPULATIONS IN THE LATERAL HYPOTHALAMUS PROCESSING ANXIETY-RELATED BEHAVIOR

FENS Forum 2026

MAPPING INPUT-DEFINED MOTOR THALAMUS CIRCUITS USING AAV1-MEDIATED TRANSSYNAPTIC LABELING

FENS Forum 2026

A HYPOTHALAMUS-CORTEX-PRETHALAMIC CIRCUIT DRIVING COURAGE IN AVERSIVE ENVIRONMENTS

FENS Forum 2026

AROUSAL-DEPENDENT SEROTONIN DYNAMICS IN THE POSTPARTUM THALAMUS DURING BEHAVIORAL TRANSITION

FENS Forum 2026

SEX-DEPENDENT MODULATION OF FEAR MEMORY BY TAC2-POSITIVE NEURONS IN THE LATERAL HYPOTHALAMUS

FENS Forum 2026

SEX-DEPENDENT HYPOEXCITABILITY IN THE VISUAL THALAMUS OF A FRAGILE-X SYNDROME MOUSE MODEL

FENS Forum 2026

SUB-SECOND DOPAMINE AND SEROTONIN DYNAMICS IN HUMAN THALAMUS DURING REINFORCEMENT LEARNING UNDER UNCERTAINTY

FENS Forum 2026

Role of the anterior and posterior Paraventricular Nucleus of the Thalamus on Sign-Tracking in inbred C57BL/6J and DBA/2J mice

Regulation of the apoptosis/autophagy switch by propionic acid in ventromedial hypothalamus of rats with type 2 diabetes mellitus

The hepatic Estrogen receptor alpha potential role in the in mediobasal hypothalamus plasticity

Quantitative, automated detection of excitatory afferents in the anterior human thalamus

Propagating spiking activity in the thalamus of anesthetized rodents

H3K27 demethylase Kdm6a/Utx controls Ngn3, Pomc and Npy expression in a sex-specific way in the developing neuroendocrine hypothalamus