Introduction

Abuse of alcohol and alcoholism are associated with a risk of toxic damage to the central nervous system (CNS), frequently accompanied by modified behavioral patterns, such as ataxia of the lower extremities associated with alcohol-induced cerebellar degeneration in humans. Most of what is known about alcohol toxicity has been inferred from the study of autopsied human tissues and of in-vitro and in-vivo tissue and animal models. A major advantage of well-characterized animal models is that in them the progress of particular diseases and associated behavioral dysfunction can be documented. The discussion in this chapter focuses primarily on the toxic actions of ethanol in an animal model and on our current understanding of the functional consequences of those actions.

The rodent cerebellum is illustrated schematically in Fig. 21.1. Basic similarities in the organization and synaptic circuitry of the cerebellum in all mammals make nonprimate mammalian species, especially rodents, excellent subjects for experimental studies of cerebellar structure and function. Toxic effects of ethanol on cerebellar structure and function have been studied extensively in rodents, and results from studies not considered here have been reviewed previously (see Hunt and Nixon, 1993).

Neuronal targets of ethanol

As illustrated in Fig. 21.1C–F, there are five major types of resident cerebellar neurons, but only two of these have figured prominently in studies of the effects of ethanol: the granule neurons, the most numerous neurons in the cerebellum, and the Purkinje neurons, the most spectacular neurons in the cerebellum. The discussion that follows focuses on these two cell types. The experimental effects of alcohol on the morphometry and function of these cerebellar cortical cells are summarized in Table 21.1.