Break the cycle of addiction with these strategies to keep dopamine in check : Life Kit : NPR

The activity of the dopamine system depends on the state of one’s dopamine receptors, and in people with these conditions, the chemical interacts with other factors in ways that have yet to be explained. Scientists have long sought the mechanisms by which alcohol acts on the brain to modify behavior. An important finding is the demonstration that alcohol can affect the function of specific neurotransmitters1 (Lovinger et al. 1989). Studies of neurotransmitters and the receptors to which they bind have provided data on both the structure and the mechanism of action of these molecules as well as clues to their role in behavior. However, the function of individual neurotransmitters and their receptors cannot entirely explain a syndrome as complex as alcoholism. Motivational arousal is a state variable; it regulates readiness to respond to external stimuli.

Researchers are also investigating whether drugs that normalize dopamine levels in the brain might be effective for reducing alcohol cravings and treating alcoholism. Marco Leyton, a professor and addiction researcher at McGill University’s Department of Psychiatry, said in a 2013 press release that participants more at risk for developing alcoholism had “an unusually large brain dopamine response” when they took a drink. Other research indicates that some people tend to have a higher release of and response to dopamine than others. In addition, those individuals may be predisposed to drink more heavily and develop an alcohol addiction.

National Institute on Alcohol Abuse and Alcoholism (NIAAA)

In humans, for example, the levels of serotonin metabolites in the urine and blood increase after a single drinking session, indicating increased serotonin release in the nervous system (LeMarquand et al. 1994a). This increase may reflect enhanced signal transmission at serotonergic synapses. For example, increased serotonin release after acute alcohol exposure has been observed in brain regions that control the consumption or use of numerous substances, including many drugs of abuse (McBride et al. 1993).

  • However, in rodent and macaque brain slices, an acute alcohol challenge following chronic alcohol exposure (inhalation or drinking) decreases dopamine release in the nucleus accumbens (NAc) in vivo and ex vivo preparations [24, 38].
  • Increased 5-HT3 activity results in enhanced GABAergic activity, which, in turn, causes increased inhibition of neurons that receive signals from the GABA-ergic neurons.
  • Other lines of research related to alcohol withdrawal reinforce this model of alcohol-related changes in DA.
  • It is one of the most ancient neurotransmitters as it is found in lizard brains, too.
  • They further calculate that an average adult neuron expresses 30% of known neurotransmitter receptors.
  • According to one study published by[67] physical dependence, which refers to the pharmacological tolerance induced by chronic alcohol intake, results in AWS and is neurobiologically supported by the imbalance between GABA and glutamate-NMDA neurotransmission.

Alcohol’s actions on inhibitory neurotransmission in this lower area of the central nervous system may cause some of alcohol’s behavioral effects. Eventually, after three weeks of alcohol abstinence, the number of transporter and receptor sites decreased. This change meant that there was less dopamine available to bind to the receptor sites and more left unused.

General procedure

Fluoxetine reduces alcohol consumption in humans only moderately, however, and does not affect all alcoholics (Litten et al. 1996). Moreover, although increased serotonin levels at the synapses in the brain can moderate alcohol consumption, additional factors contribute to continued alcohol abuse. Consequently, SSRI’s cannot be recommended as the sole treatment for alcoholism. By studying alcohol and dopamine knockout mice that lack a particular receptor, researchers can assess that receptor’s role in specific aspects of brain functioning and behavior, including responses to alcohol and alcohol consummatory behavior. For example, scientists have studied a strain of knockout mice lacking the 5-HT1B receptor with respect to the effects of acute alcohol exposure (Crabbe et al. 1996).

It is also why drugs that flood the brain’s dopamine levels can be so addictive that someone will continue to drink alcohol regardless of the consequences. Alcohol increases dopamine levels while removing the brain’s built-in brake system that limits dopamine receptivity. In lab experiments, dopamine prompts a rat to press a lever for food again and again. This is no different in humans; it’s the reason why we partake in more than one helping of cake.

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