Understanding alcohol`s effects on inhibition of behaviour; implications for treatment
Lead Research Organisation:
University of Sussex
Department Name: Sch of Psychology
Abstract
Alcohol is highly abused, very harmful and leads to criminal behaviours. Once its use becomes compulsive it is very difficult to stop, and for the few who attempt to stop drinking it becomes very difficult to remain abstinent. We do not know the exact mechanisms that are responsible for this power that alcohol has over some individuals. However, we do know that as an individual?s drinking career advances his/her ability to inhibit drinking becomes weakened, particularly after they have had a small initial drink, or appetizer. This phenomenon occurs despite the fact that alcoholics report obtaining less pleasure from drinking as their drinking career progresses. Thus, it is the ability to inhibit drinking that is at fault specifically, rather than an overactive desire or pleasure in drinking. Our plan is to examine the inhibition failure that occurs after a drink, but for ethical reasons, we cannot study the effects of an appetizer on excessive drinking in alcoholics. Consequently, we need to study the effects of an appetizer on a related normal behaviour, which may shed light on the alcoholic?s case. For this purpose, we plan to study the effects of a small dose of alcohol (the appetizer) on the inhibition of a learned routine that has been established previously in non-alcoholics. We expect the appetizer to produce a failure in the individuals to alter their routine in the light of new information. We regard this failure as analogous to alcoholics? failure to inhibit drinking despite the fact that drinking has become less pleasurable. More importantly, we will study the brain structures and chemicals that we think are responsible for alcohol producing a failure to inhibit the old routine. The hope is that such knowledge will help guide the development of drugs or psychological techniques that will stop alcohol from producing the failure of inhibition, and so stop alcoholics in abstinence from relapsing. In this way, our work may contribute to the treatment of alcoholism in particular, but also drug abuse in general.
Technical Summary
Alcohol impairs the ability to inhibit a pre-potent or over-learned behaviour; alcohol acutely also increases the capture of attention by alcohol related stimuli (the so-called attentional bias) and impairs reward seeking behaviour.
We have proposed that the alcohol-induced disinhibition contributes to alcohol?s effects on attentional bias and on reward seeking behaviour. To test this proposal, we wish to examine whether brain structures associated with inhibitory control are less activated when participants, under alcohol, perform tasks that challenge inhibitory control, or are exposed to alcohol related stimuli or are learning a reward seeking response. We have also proposed that alcohol-induced disinhibition may be mediated by modulation of central glutamatergic neurotransmission, as it is known that alcohol blocks one type of glutamatergtic receptors in the brain. The basis for this latter proposal is further supported by the fact that alcohol and glutamatergic antagonists produce similar disinhibitory behavioural effects.
Understanding the basis of disinhibition is important for human health because effective inhibitory control plays a vital role in protecting an individual from drinking alcohol in excess and compulsive drug use (among other risky behaviours). Specifically, it is thought that compulsive drug abuse, as opposed to drug use or ?natural? reward seeking, is typified by a weakening of inhibitory control, rather than by a strengthening of appetitive motivation. Brain imaging should highlight the involvement of inhibitory control areas (e.g. prefrontal cortex) in the acute effects of alcohol, rather than of areas involved in motivational processes (e.g amygdala). Moreover, we wish to examine whether glutamate agonists, by their ability to correct the inhibition failure, can ameliorate the alcohol effects on the ability to inhibit a pre-learned response, on the attentional biases to alcohol related stimuli, and on reward seeking learning. With the research proposed here it is hoped that a better understanding of the neurobiological basis of prefrontal inhibitory control will be achieved to enable the development of drugs and psychotherapies that selectively activate this function and prevent the general trend for substance-dependent individuals to progress to compulsive drug abuse.
We have proposed that the alcohol-induced disinhibition contributes to alcohol?s effects on attentional bias and on reward seeking behaviour. To test this proposal, we wish to examine whether brain structures associated with inhibitory control are less activated when participants, under alcohol, perform tasks that challenge inhibitory control, or are exposed to alcohol related stimuli or are learning a reward seeking response. We have also proposed that alcohol-induced disinhibition may be mediated by modulation of central glutamatergic neurotransmission, as it is known that alcohol blocks one type of glutamatergtic receptors in the brain. The basis for this latter proposal is further supported by the fact that alcohol and glutamatergic antagonists produce similar disinhibitory behavioural effects.
Understanding the basis of disinhibition is important for human health because effective inhibitory control plays a vital role in protecting an individual from drinking alcohol in excess and compulsive drug use (among other risky behaviours). Specifically, it is thought that compulsive drug abuse, as opposed to drug use or ?natural? reward seeking, is typified by a weakening of inhibitory control, rather than by a strengthening of appetitive motivation. Brain imaging should highlight the involvement of inhibitory control areas (e.g. prefrontal cortex) in the acute effects of alcohol, rather than of areas involved in motivational processes (e.g amygdala). Moreover, we wish to examine whether glutamate agonists, by their ability to correct the inhibition failure, can ameliorate the alcohol effects on the ability to inhibit a pre-learned response, on the attentional biases to alcohol related stimuli, and on reward seeking learning. With the research proposed here it is hoped that a better understanding of the neurobiological basis of prefrontal inhibitory control will be achieved to enable the development of drugs and psychotherapies that selectively activate this function and prevent the general trend for substance-dependent individuals to progress to compulsive drug abuse.
