Vasoactive intestinal peptide

Neural activity in the cortex exhibits a wide range of timescales, allowing animals to respond to rapidly changing sensory stimuli while maintaining information in working memory. Recent studies show how top-down inputs representing locomotive state modulates these timescales differently across visual areas in mice. In particular, the sign of correlations between speed and neural activity varies by region, highlighting the interplay between bottom-up sensory inputs, top-down pathways and connectivity motifs in shaping cortical dynamics. In addition, cortical circuits comprise a large diversity

Neural activity in the cortex exhibits a wide range of timescales, allowing animals to respond to rapidly changing sensory stimuli while maintaining information in working memory. The timescales of neural activity are not only affected by bottom-up sensory inputs, but also by top-down inputs originating from corticocortical and neuromodulatory pathways. In addition, cortical circuits comprise a large diversity of cell types connected in non-random ways, which are the subject of profound plasticity dynamics. Due to this complexity, understanding how top-down projections affect the timescales of

…slices and we studied the effects of peptides expressed in the SCN on the SPZ neurons. Photostimulation of SCN neuromedin-S (NMS) neurons or the vasoactive intestinal peptide (VIP) neurons induced opto-evoked inhibitory post-synaptic currents (oIPSCs) in 60% and 50% of recorded SPZ neurons, respectively. These responses were mediated by GABA

The circuitry underlying the initiation, maintenance, and coordination of wakefulness, rapid eye movement sleep, and non-rapid eye movement sleep is not thoroughly understood. Sleep is thought to arise due to decreased activity in the ascending reticular arousal system, which originates in the brainstem and awakens the thalamus and cortex during wakefulness. Despite the conventional association of sleep-wake states with hippocampal rhythms, the mutual influence of the hippocampal formation in regulating vigilance states has been largely neglected. Here, we focus on the subiculum, the main outp

…(PV+), somatostatin- (Sst+), and vasoactive intestinal peptide- (VIP+) expressing interneurons, in processing information about familiar and novel social stimuli.We employed chemo/optogenetics alongside automated behavioral testing in Eco-HAB®, an RFID-based system for ecologically relevant assessment of social behavior in group-housed mice. This

Rapid eye movement (REM, also called paradoxical) sleep correlates with enhanced cellular activity in region-specific thalamo-cortical circuits and subcortical structures including the hippocampus, midbrain or hypothalamus. This REM sleep specific neuronal activity is hypothesized to promote structural plasticity and provide a window for the consolidation of contextual and emotional memories previously acquired during wakefulness, yet the underlying mechanism remains unclear.Amongst the cortical structures, the activity of neurons located in the retrosplenial cortex (RSC) is increased during R

Sensory experience and perceptual learning changes receptive field properties of cortical pyramidal neurons possibly mediated by long-term potentiation (LTP) of synapses. We have previously shown in the mouse somatosensory cortex (S1) that sensory-driven LTP in layer (L) 2/3 pyramidal neurons is dependent on higher order thalamic feedback from the posteromedial nucleus (POm), which is thought to convey contextual information from various cortical regions integrated with sensory input. We have followed up on this work by dissecting the cortical microcircuitry that underlies this form of LTP

Dravet syndrome is a severe childhood epilepsy due to heterozygous loss-of-function mutation of the gene SCN1A, which encodes the type 1 neuronal voltage gated sodium (Na+) channel alpha-subunit Nav1.1. Prior studies in mouse models of Dravet syndrome (Scn1a+/- mice) at early developmental time points indicate that, in cerebral cortex, Nav1.1 is predominantly expressed in GABAergic interneurons (INs) and, in particular, in parvalbumin-positive fast-spiking basket cells (PV-INs). This has led to a model of Dravet syndrome pathogenesis whereby Nav1.1 mutation leads to preferential IN dysfunction