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The discovery of somatostatin-positive inhibitory neurons projecting from mouse cortex to striatum shows that corticostriatal pathways are not exclusively excitatory.

Our work demonstrated that eye opening differentially modulates inhibitory synaptic transmission from Sst-INs and FS-INs to excitatory neurons in the mammalian cortex.

Cortical interneurons inhibit pyramidal cells to a greater degree when they form synapses with the pyramidal cell body than when they form synapses with dendrites.

Most ChAT-expressing interneurons are a subset VIP+ interneurons that differentially release GABA and acetylcholine onto different post-synaptic targets, while a separate population of non-VIP ChAT+ neurons release acetylcholine in mPFC.

A brain-wide mapping of the direct inputs to striatal cholinergic and parvalbumin interneurons reveals connectivity differences and implies their distinct roles in regulating striatal function.

Mice that lack the autism- and schizophrenia-linked gene MEF2C in cortical neurons have an imbalance of excitatory and inhibitory synapses, and impaired social and cognitive abilities.

Pcdhg determine survival of the GABAergic cortical interneuron population that is necessary to establish and maintain proper excitatory to inhibitory balance in the cerebral cortex.

Biophysically realistic computational model reveals how inhibitory interneurons initiate paroxysmal discharges and how changes in the ionic concentrations shape electrographic features of human seizures.

Neuregulins control the integration of specific excitatory and inhibitory synapses through subcellular sorting.

Demyelination disrupts fast inhibition of pyramidal neurons, thereby changing neocortical rhythms and causing the emergence of brief epileptic-like discharges.