Principles of NMDA receptor co-agonism at cortical fast-spiking GABAergic interneurons in the adolescent prefrontal cortex

GABAB Receptors Gate Sex-Specific Synaptic Plasticity in the Nucleus Accumbens

Excitatory synaptic plasticity within the nucleus accumbens (NAc) drives motivated behaviors, and dysregulation is implicated in several psychiatric disorders marked by impaired reward processing. The NAc integrates glutamatergic input, which conveys information about reward, context, and behavioral goals, with local G...

NMDA receptor hypofunction on GABAergic interneurons results in input-specific Excitatory/Inhibitory imbalance in pyramidal neurons of medial prefrontal cortex

It is found that circuit dysfunction can selectively bias the processing of specific afferent pathways rather than produce a uniform disruption of cortical excitability, with direct relevance for understanding hippocampal–prefrontal dysconnectivity in neuropsychiatric disorders.

Glycine Transporter 1 Inhibitor, Bitopertin, Changes Excitatory and Inhibitory Network Connectivity in Mouse Medial Prefrontal Cortex.

Cognitive deficits in Schizophrenia (SCZ) are correlated with excitation-inhibition (E/I) imbalance within the medial prefrontal cortex (mPFC). E/I imbalance may arise from N-methyl-D-aspartate receptor (NMDAR) hypofunction and dysfunction of GABAergic neurotransmission. Previous research has shown that bitopertin, a g...

Pharmacological and Physiological Characteristics of Synaptic Transmissions From the Medial Prefrontal Cortex Onto Noradrenergic Neurons and Inhibitory Interneurons in the Mouse Locus Coeruleus

It is proposed that the simultaneous connections onto LC‐NA neurons and LC‐iINs, along with cell type–specific differences in transmitter release plasticity, may enable the mPFC to effectively multiplex information to the LC for adaptive behavioral regulation.

receptors and plasticity of inhibitory neurotransmission in the central

α2δ-2 mediates coupling of presynaptic calcium entry to vesicle release in hippocampal parvalbumin-expressing interneurons

Using electrophysiological recordings from genetically modified mice, α2δ-2 functionally couples calcium entry to vesicle release from parvalbumin-expressing cells, which provides a potential explanation for the seizure phenotype of α2δ-2 mutant mice and illuminates the broader roles of α2δ proteins in neuronal functio...