Topic: PV+ interneurons

How do we learn about experiences while being removed from the experience itself? One solution involves offline learning via reactivations. Sensory reactivation involves the recurrence of a pattern of neural activity during sleep or quiet waking that previously occurred during a sensory experience. Historically, reactivations have been studied in the hippocampus. However, whether reactivations in sensory cortex depend on local activation of neurons during prior experience is not well understood. We hypothesize that such reactivations in sensory association cortex could be important for learnin

For pre-surgical evaluation of patients with focal seizures, stereoelectroencephalographic (SEEG) signals are routinely recorded to identify the epileptogenic zone network (EZN). This network consists of distant brain regions involved in seizure initiation. However, the mechanisms underlying typical SEEG patterns that occur during the transition from interictal to ictal activity in distant brain nodes of the EZN remain elusive.We analyzed SEEG signals recorded from the EZN (involving three distant neocortical brain regions) in 10 patients during the transition from interictal to ictal activity

Single-cell methodologies have improved our understanding of cellular diversity within complex tissues such as the mammalian neocortex. However, despite the unprecedented granularity, sampling of minority yet diverse cell populations remains challenging. Here, we show that many subtypes of cortical inhibitory γ-aminobutyric acid-containing (GABAergic) neurons are poorly represented in current atlases, with most datasets limited to adult stages and not recapitulating cell-state transitions of these rare cell types during development. We address this gap by optimizing experimental techniques and

Early life stress (ELS) is one of the key risk factors in the development of mental health disorders, strongly impacting the limbic system. Kainate receptors and GluK1 specifically have been previously shown to be affected, and potentially mediate some of the effects of ELS on GABAergic interneurons. Aims: To study the effects of the ELS on the circuitry of the ventral hippocampus (vHPC) and assess the potential of GluK1 as a tool for phenotype rescue.Methods: Limited bedding and nesting model of ELS was used in WT and PV-Cre mice and validated using standard behavioral tests in adults. Electr

Autistic spectrum disorder (ASD) has been associated with genetic alterations of synaptic proteins such as the point mutation R451C in neuroligin 3 (NLGN3), a postsynaptic adhesion molecule located at both excitatory and inhibitory synapses. By exploiting the transgenic NLGN3-R451C knock-in (KI) mice, an animal model of ASD, we investigated this mutation in the coordination of excitatory and inhibitory synaptic plasticity. In hippocampal primary cultures, while the NLGN3-R451C protein was less expressed in KI mice with respect to WT, the molecular and functional properties of basal excitatory