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.
The release of acetylcholine in the basolateral amygdala is precisely timed to salient events during reward learning but has long-lasting effects that potentiate learning of cue-reward contingencies.
In vivo deconstruction of reward-related behaviors with circuit and pharmacological specificity using designer, light-controllable nicotinic acetylcholine receptors.
The neuromodulator acetylcholine contributes to state-dependent modulation of motor vigor and variability by direct action on songbird premotor cortex, bypassing basal ganglia circuitry.
Muscarinic acetylcholine receptor type A in adult Drosophila inhibits Kenyon cells, and is required for aversive olfactory learning and learning-associated synaptic depression between Kenyon cells and their output neurons.
Local elimination of acetylcholine synthesis in habenular neurons demonstrates a key role for vesicular synergy and neurotransmitter co-release in nicotine dependence.
Neurons of the cholinergic system, which release the excitatory neurotransmitter acetycholine throughout the cortex, also release the inhibitory transmitter GABA, with potential implications for cognitive function.
Acetylcholine, a common modulator in the brain, controls spike-frequency adaptation by specifically attenuating Ether-a-go-go related K+ currents, thereby explaining many cortical network statistical changes often observed in vivo.
