Topic: Vglut2

A growing body of evidence indicates a functional dichotomy between the dorsal (dHC) and ventral poles of the hippocampus (vHC). Specifically, the dorsal region is implicated in encoding spatial information and episodic memories, whereas the ventral region is recognized for its role in processing the emotional aspects associated with those memories. The medial septum/diagonal band of Broca complex (MSDB) plays pivotal role in both cognitive and emotional functions, implying anatomically distinct pathways of MSDB efferents conducting information to dHC and vHC, respectively. To test this, we tr

Neurons of the paraventricular thalamic nucleus (PVT) regulates emotional and motivational behavior via highly collateralized axon arbour innervating several forebrain areas. Maintaining an optimal excitation-inhibition balance is vital for PVT function, yet the sources of glutamatergic and GABAergic inputs are presently unclear. We identified subcortical glutamatergic and GABAergic inputs to the PVT by retrograde viral tracing in vGLUT2-Cre and vGAT-Cre mice, respectively. We found distinct retrogradely labelled cell groups containing purely vGLUT2+positive, purely vGAT+ or mixed neurons thro

The hypothalamic, peptide hormone, oxytocin (OXT), is a powerful modulator of social-, stress- and anxiety-related behaviors, as is the brainstem, neuropeptide relaxin-3 (RLN3). Recent studies indicate the involvement of KCNQ potassium channels in neuronal OXT and RLN3 signaling, with these neuropeptides displaying opposing excitatory and inhibitory actions, respectively. OXT receptors (OXTR) and RLN3 receptors (RXFP3) are expressed by neurons in the rat ventral hippocampal CA3 area (vCA3), which is involved in social behavior and anxiety control; but the possible interaction between OXT and R

Midbrain dopamine (DA) neurons are comprised of diverse neuronal subpopulations. For instance, there are subsets of DA neurons that express the vesicular glutamate transporter VGLUT2 and these cells can co-release the excitatory neurotransmitter glutamate. There are also several lines of evidence indicating that the inhibitory neurotransmitter gamma-amino-butyric acid (GABA) can be released from subsets of DA neurons. However, DA neurons do neither express the machinery to synthesize GABA nor the vesicular GABA transporter VGAT typically thought to be necessary for vesicular GABA uptake. Inste

Tetanus Neurotoxin (TeNT) enters the peripheral endings of motor axons in muscles and transports to motoneuron cell bodies where transynaptically translocates to presynaptic inputs blocking inhibitory synapses. This disinhibits motoneurons causing dysregulated firing and tetanic contractions. Preferential actions on inhibitory synapses are usually explained by enrichment in the Vesicle-Associated Membrane Protein 2 isoform (VAMP2). VAMP1 and VAMP2 form part of the SNARE complex and are differentially distributed in different synapses. Nevertheless, the exact VAMP content inside synapses on mot

Medial septal (MS) glutamatergic neurons expressing type 2 vesicular glutamate transporter (VGluT2) are active during theta oscillation and locomotor activity. Optogenetic activation of these neurons at theta frequencies (4-12 Hz) entrains hippocampal theta oscillation and sustains locomotion outlasting the stimulus duration. However, the specific cellular and circuit mechanisms responsible for initiating and sustaining MS VGluT2-driven persistent locomotion and associated hippocampal theta oscillations remain unclear. To address these questions, we optogenetically targeted glutamatergic neuro

The activity of thalamocortical neurons is largely defined by their excitatory inputs. The key determinants of excitatory afferents are the origin, complexity, and density of axon terminals. While some quantitative data are available on these aspects of glutamatergic afferents in animals, organization of excitatory inputs is unknown in the human thalamus. In this study we determined the origin, size and density of glutamatergic axon terminals in the anterior part of the human thalamus, examined their inter- and intra-nuclear heterogeneity as well and s the interindividual variability. We used

When awake, we perceive stimuli from the external world. When asleep, our brain disconnects from the sensory environment. In contrast to these exteroceptive stimuli, little is known about how interoceptive stimuli are processed by the sleeping brain. The vagus nerve is a mixed sensory-motor nerve that interfaces between the autonomic periphery and the brain. We asked whether stimulating specifically vagal sensory afferents modulates sleep. All experiments are based on viral transfection of vGluT2-expressing neurons in the jugular-nodose ganglion of the left vagus nerve, in combination with pol

Knowing how to behave in the presence of an aggressive conspecific is essential for an individual's survival. For many rodents, olfactory cues are crucial for the animal to identify conspecifics and behave properly. An important region for the expression of social defense is the medial amygdala (MeA). This brain region receives projections from neurons in the accessory olfactory bulb (AOB) and processes olfactory cues from conspecifics. The MeA is enriched by glutamatergic (VGLUT2) and GABAergic (VGAT) neurons. Interestingly, GABAergic neurons are predominantly located in the posterodorsal par

In addition to its role in determining sleep need, Salt-inducible kinase 3 (Sik3) is likely to regulate energy homeostasis since mice mutant for exon 13 of the Sik3 gene (Sleepy) display an obese phenotype. The main objective of this project is to identify the role of SIK3 in the central nervous system in the regulation of energy balance. To achieve this, neuron-specific mutant mice lines for the Sleepy gene were generated, as well as viral genetic approaches in Sik3-ex13 floxed mice were used to identify the brain regions involved in SIK3 actions. Our data showed that Vglut2-specific Sleepy m

Though many neuronal populations are affected in Parkinson’s disease (PD), its cardinal motor symptoms are a consequence of dopamine (DA) neuron loss in the substantia nigra (SNc). The precise mechanisms underlying DA neuron vulnerability remain unclear, but include oxidative stress, and aggregation of alpha-synuclein. More recently, a glutamate driven process has been implicated in disease progression, and there is now proof that DA neurons express the vesicular glutamate transporter VGLUT2 and co-release glutamate. In fact, we discovered that the majority of midbrain DA neurons transiently e

Dynamic reorganization of neuronal circuits in the spinal dorsal horn is assumed to cause sensitization in the neuropathic pain. In our previous study, brain-enriched guanylate kinase associated-protein (BEGAIN) was identified as an increased protein in the spinal dorsal horn in the neuropathic pain and the mechanical allodynia was attenuated in the BEGAIN-knockout mice. BEAGIN-expressing neurons have not yet been identified because BEGAIN protein is detected in highly localized dendritic regions, not in the cell body. To identify BEGAIN-expressing neurons, double in situ hybridization with RN