Topic: vasoactive intestinal peptide

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

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