Topic: inhibitory synaptic transmission

Pathogenic variants in GABAA receptor subunits are a prominent cause of genetic epilepsies. Recent biophysical analysis of pathogenic GABRB3 variants reveals that both loss- and gain-of-function can cause epilepsy. Stratification shows that patients carrying gain-of-function variants experience an earlier onset of seizures that are refractory and have worse developmental delay compared to loss-of-function variant patients. This suggests that distinct pathological mechanisms underlie disease in each GABRB3 functional class. To date, research has only focused on loss-of-function variants. Here,

The hippocampus is crucial for episodic memories and is characterized by unique sharp wave ripple complexes (SWRs). These hallmark oscillations, 150-250 Hz in the local field potential (LFP), are produced by fast signaling between synaptically coupled pyramidal neurons (PNs) and parvalbumin-positive basket cells (PV+BCs). Although much has been learned about the synaptic and microcircuit properties mediating ripple oscillations, whether and how myelination of the hippocampus contributes remains unresolved. Here, we performed LFP measurements in combination with paired recordings between PV+BCs

Mutations in the presynaptic adhesion protein Neurexin-1 (NRXN1) have been repeatedly implicated in cases of autism, schizophrenia, and ADHD. The excitation to inhibition (E:I) imbalance hypothesis posits that behaviours associated with neurodevelopmental disorders such as autism may be driven by the disturbed balance of excitation and inhibition in the cortex. We aimed to identify and characterise the effect of Neurexin-1 mutations on the E:I balance in autism-associated cortical circuits.To assess the effect of Nrxn1 alpha KO on synaptic transmission, whole-cell electrophysiological recordin