Alcohol and basal ganglia circuitry: Animal models

Abstract

Brain circuits that include the cortex and basal ganglia make up the bulk of the forebrain, and influence behaviors related to almost all aspects of affective, cognitive and sensorimotor functions. The learning of new actions as well as association of existing action repertoires with environmental events are key functions of this circuitry. Unfortunately, the cortico-basal ganglia circuitry is also the target for all drugs of abuse, including alcohol. This makes the circuitry susceptible to the actions of chronic alcohol exposure that impairs circuit function in ways that contribute to cognitive dysfunction and drug use disorders. In the present review, we describe the connectivity and functions of the associative, limbic and sensorimotor cortico-basal ganglia circuits. We then review the effects of acute and chronic alcohol exposure on circuit function. Finally, we review studies examining the roles of the different circuits and circuit elements in alcohol use and abuse. We attempt to synthesize information from a variety of studies in laboratory animals and humans to generate hypotheses about how the three circuits interact with each other and with the other brain circuits during exposure to alcohol and during the development of alcohol use disorders. This article is part of the Special Issue entitled "Alcoholism".

Keywords: Alcohol; Cortex; Dopamine; Globus pallidus; NMDA receptors; Striatum; Synaptic transmission; Ventral tegmental area.

Figure 1

Diagram of the cortex-basal ganglia-cortex loop showing the main projections that will be discussed in this review. Blue arrows represent all main glutamatergic inputs to the striatum and purple arrows the monoamine innervation from the midbrain dopamine neurons and the noradrenergic projection from the nucleus of the solitary tract (NST). Green and red arrows represent the two main output projections that form the direct- and indirect-pathway, respectively.