The basal ganglia are involved in complex brain functions and are implicated in numerous neurological and psychiatric disorders. At the heart of both function and dysfunction of basal ganglia circuits is the interaction of dopamine and glutamate. Improved labeling, imaging, recording, and genetic manipulation approaches have yielded new information on how dopamine and glutamate interact to generate the circuit activity underpinning basal ganglia function. This volume synthesizes this research, presenting current insights on individual neurons and synapses, detailed circuit analysis, and learning and action functions of the basal ganglia. The book also discusses compromised dopamine–glutamate interaction in various disorders of basal ganglia function.

The basal ganglia are involved in complex brain functions, from voluntary movement control to learning and reward processing, and they are implicated in numerous neurological and psychiatric disorders. Information from the cerebral cortex and thalamus is conveyed to basal ganglia nuclei via glutamate release, while dopamine from the midbrain is released in close proximity to glutamate. At the heart of both function and dysfunction of basal ganglia circuits is the interaction of these two neurotransmitters, dopamine and glutamate.

Elucidating the relationship between their molecular and cellular effects and behavioural significance has been challenging, but in the past 5–10 years, improved labeling, imaging, recording, and genetic manipulation approaches have yielded new information on how dopamine and glutamate interact to generate the circuit activity underpinning basal ganglia function. Dopamine–Glutamate Interactions in the Basal Ganglia synthesizes this recent research from the level of receptor molecules all the way to complex behaviours and disease.

Current insights from research on individual neurons and synapses, detailed circuit analysis, and learning and action functions of the basal ganglia are presented against a historical perspective. The book also discusses compromised dopamine–glutamate interaction in disorders of basal ganglia function, including Parkinson’s disease, Huntington’s disease, and drug addiction.