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Physical dependence is indicated by signs of withdrawal that result from the absence of alcohol in the body when drinking is discontinued. An individual suffering from alcohol withdrawal may experience a host of symptoms ranging from profound anxiety, tremors, hyperthermia, and sleep disturbances to hallucinations and seizures. It has been hypothesized that physically dependent individuals drink to avoid or alleviate these aversive symptoms of withdrawal. However, as clinicians can attest, abstinent alcoholics often resume drinking alcohol long after the signs of physical dependence have disappeared. This fact suggests that recovering alcoholics who resume drinking do so for reasons other than to alleviate withdrawal symptoms. Studies have shown that animals that are repeatedly given doses of alcohol sufficient to produce physical dependence do not necessarily begin to self-administer alcohol voluntarily once the forced alcohol adminis tration is discontinued (Cappell and LeBlanc 1981; Winger 1988). These and other studies indicate that physical dependence is not a requisite condition for the initiation of voluntary alcohol self-administration (Deneau et al. 1969). In fact, physical dependence is viewed now as an important adverse medical consequence of excessive alcohol consumption rather than as a primary cause of abusive drinking. Researchers have begun to examine the reinforcing properties of drugs in their efforts to understand the processes responsible for alcohol-seeking behavior. In contrast to physical dependence, psychological dependence is characterized by compulsive craving and drinking that is independent of the presence or absence of physical dependence and withdrawal (Eddy et al. 1965). Studies with other drugs of abuse have substantiated the concept of psychological dependence. For example, Jaffe (1985) reported that although cocaine does not produce pronounced physical dependence, it does produce marked psychological dependence and craving. Researchers have begun to examine the reinforcing properties of drugs in their efforts to understand the processes responsible for alcohol-seeking behavior. The term reinforcement describes the process whereby the probability of a response (e.g., drug-taking behavior) Figure 1. Rat in a Skinner box responding for brain stimulation reward. This rat is pressing a lever to deliver a small electric current to the tip of an electrode surgically implanted in its brain. The study of brain stimulation reward potentially can provide information about what neurochemical systems are involved in alcohol and other drug abuse. Drawing courtesy of Robert Czechowski and Clare Little. is increased if it results in the attainment of a particular effect (Skinner 1938, 1953). An individual learns a behavior, such as drinking alcohol, to obtain a particular outcome or reinforcer, such as the euphoric effect or the anxiolytic effect of alcohol. This chapter focuses on the neurobehavioral aspects of alcohol reinforcement. A detailed review of significant findings in studies of the neurophysiological, neuroanatomical, and neuropharmacological effects and actions of alcohol is found in Chapter 4, Actions of Alcohol on the Brain. Alcohol as a Reinforcer: Brain Mechanisms of Reinforcement One theory of the biological or physiological basis for alcohol reinforcement suggests that drugs are self-administered if they affect a specific reinforcement system in the brain. For example, many people state that consuming alcohol is a pleasant experience; yet researchers have questioned whether the pleasant experience stems from alcohol-induced euphoria or from the alleviation of an underlying anxiety. Brain stimulation reward (BSR), also known as intracranial self-stimulation (Olds and Milner 1954), is an experimental procedure that has been used to study the neurobehavioral basis of the euphoric properties of alcohol and other drugs of abuse. In these studies, animals will readily learn to deliver small levels of electric current to specific areas of the brain to elicit rewarding stimulation (figure 1). Study results suggest that the neural structures related to BSR may be a specialized system responsible for the process of reinforcement (Olds and Fobes 1981). It is postulated that drugs of abuse function as reinforcers by imitating, facilitating, or sometimes blocking the various neurochemical messengers (e.g., neurotransmitters) and neural modulators involved in this system (Koob and Bloom 1988; Wise 1980, 1987). Experimental evidence supports this theory: Wise (1987) has reported that drugs of abuse, including psychomotor stimulants (e.g., amphetamine and cocaine) and opiates (e.g., morphine and heroin), facilitate BSR. The administration of these drugs either increases the rate at which the animal self-stimulates (i.e., presses a bar to receive more stimulation) or lowers the threshold for BSR so that a smaller amount of electrical current is required to sustain the same self-stimulation behavior, or both. If an animal's response rate increases after alcohol administration, it may be concluded that alcohol increases the reward, or euphoria, experienced by the animal. A decrease in response rate may indicate diminished reward. Alcohol's Effects on Brain The effects of alcohol on BSR are not as unambig- |