Robust fear learning deficits and decreased tonic activity of NAc cholinergic interneurons caused by depletion of MeCP2 could be attributed to an elevation in α2-containing GABA_A receptors.

Optogenetics and in vivo recordings in mice reveal that pauses in cholinergic interneurons offer an alternative mechanism to inhibit subthreshold and suprathreshold events of spiny projection neurons.

Dopamine neurons make novel glutamatergic connections to striatal cholinergic interneurons in the lateral dorsal striatum that are mediated by metabotropic glutamate receptors coupled to TrpC channels.

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.

Conditional forebrain deletion of Tor1a generates a dystonia model with face, construct, and predictive validity, and demonstrates that striatal cholinergic interneurons are selectively vulnerable to loss of the dystonia protein torsinA.

HCN and SK channel currents in striatal cholinergic neurons are decreased with dopamine loss, but only HCN is restored by chronic L-DOPA and SK abnormality persists in dyskinesia.

The pairing of chemogenetic and electrophysiological approaches reveals mechanisms by which cholinergic synapses modulate the final motor output of the nervous system.

Computational modeling suggests that feedback between striatal cholinergic neurons and spiny neurons dynamically adjusts learning rates to optimize behavior in a variable world.

Enhancing levels of the torsinA paralog torsinB prevents essentially all torsinA loss-of-function neuropathological and behavioral phenotypes, identifying torsinB as a novel therapeutic target for DYT1 dystonia.

M2 cortex-dorsolateral striatum circuit is functionally altered in Huntington's disease and, by boosting its activity, we reverse symptoms at behavioral, physiological, and morphological level in symptomatic mice.