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This thesis involves a comprehensive review of the personality, psychiatric, and genetic risk factors for alcoholism and drug abuse. Based on this review, it is hypothesised that specific risk factors cluster together to represent separate vulnerability pathways to substance abuse and that differential susceptibility to the pharmacological effects of drugs of abuse (reinforcement and intoxication) mediates the relationship between such risk characteristics and drug-taking behaviour. A series of four studies are presented indicating that groups of individuals characterized by different risk factors for alcoholism are differentially sensitive to the reinforcing properties of alcohol. Non-alcoholic young adult men presumed to be at genetic risk for alcoholism (due to high genetic loading for alcoholism) were shown to be sensitive to the effects of alcohol on resting and stress-induced physiological states hypothesized to reflect activity within a brain reward system involved in the activation of approach and avoidance behaviour. Non-alcoholic young adult males self-reporting a personality profile that has been associated with increased risk for the development of panic disorder also demonstrated idiosyncratic responses to alcohol intoxication in that they appeared particularly sensitive to the. fear-dampening effects of alcohol. Finally, a group of non-alcoholic males were identified as being particularly susceptible to elevated and problematic alcohol and drug use in early adulthood due to a disinhibited/antisocial personality profile. These findings were interpreted as reflecting separate vulnerability pathways to substance use/abuse in which differential sensitivity to drug reinforcement and disinhibited personality are thought to play an important role in determining liability to seek out behavioural reinforcement from drugs of abuse. A second set of studies tested whether these factors are implicated in the maintenance of problematic alcohol and drug consumptio

Alcohol use disorders are a public health issue related to adverse effects for individuals and society. A low level of response, or decreased sensitivity, to alcohol has been identified as a heritable risk factor for development of alcohol use disorders. One method for researching level of response to alcohol is through the use of rodent models, which are developed to mimic human conditions while eliminating barriers to conducting research with people. Current rodent models used to evaluate effects of ethanol on motor performance have been criticized for not being well matched to human tasks that measure level of change in body sway after alcohol consumption. This study looks at oromotor behavior as a potential alternative to gross motor performance in hopes of increasing correspondence between human and rodent measures of intoxication. To evaluate rodent oromotor performance a force transducer lickometer is used to measure several dimensions of licking behavior after administration of different concentrations of ethanol solution via gavage. Results show that force of licking is not sensitive to dose of ethanol. The total number of licks per session show dose related decreases and licking rhythm, evaluated by the length and distribution of interlick intervals, either increased or decreased for three of the four subjects. Recommendations are made for procedural modifications in order to reduce variability in data and further investigate oromotor performance and level of response to alcohol.

This thesis encompasses studies that examine autonomic reactivity and neuropsychological function in preadolescent boys who are at-risk for developing alcoholism and conduct disorder. The literature suggests an association between cognitive impairments and behavioural undercontrol, and that autonomic hyperreactivity may facilitate the use of alcohol to dampen stress. Thus, either factor may contribute to early alcohol use. In the first study, preadolescent sons of male multigenerational alcoholics were found to be cardiovascularly reactive during cognitive stress, and impaired on tests of executive function. Furthermore, reactivity was correlated with anxiety, and executive function deficits with conduct problems. In the second study, reactivity during a laboratory aggression task was monitored and cognitive functions (attentional or memory processes and executive functions) were assessed among aggressive boys rated as disruptive, or anxious-disruptive. During the aggression task, anxious-disruptive boys, unlike disruptive boys or controls, moderated their aggression when their opponent engaged in retaliatory behaviour. Anxious-disruptive boys were more highly aroused throughout the task, and the neuropsychological assessment found they were impaired on tests of executive function, independent of attention and memory. In the third study, anxious-disruptive boys exhibited greater cardiovascular, electrodermal, and muscle tension reactivity than disruptive or control boys during cognitive stress, while disruptive boys were electrodermally underaroused. These studies suggest it is possible to delineate specific neuropsychological profiles among at-risk youth, using either a behavioural genetics model, or selecting for personality traits. There were consistent autonomic reactivity patterns across tasks among groups defined by similar behavioural profiles. Thus, while cognitive impairments and hyperreactivity may comprise a vulnerability among sons of alcoholics, thes

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