Please enable JavaScript.
Coggle requires JavaScript to display documents.
Biological explanation for alcohol addiction (Mode of action (1.…
Biological explanation for alcohol addiction
Mode of action
1. Inhibitory neurotransmitters, GABA, are active throughout the brain, controlling neural activity along brain pathways and reducing energy levels.
2. Glutamate acts as the brain's excitatory neurotransmitter.
3. When alcohol enters the brain, it delivers a double sedative punch, interacting with GABA receptors to make them even more inhibitory and slowing down the CNS.
4. It binds to glutamate receptors, preventing the glutamate from exciting the cell.
5. Reduces serotonin activity - serotonin associated with emotions, low levels in the brain create feelings of depression, alcohol considered a depressant.
6. Increased release of dopamine in the brain's reward centre. Continuation of drinking occurs to get more dopamine release, till the effect is gone.
Empirical evidence
Li et al (2014)
GABA as an inhibitory neurotransmitter in the brain of mammals
Carried out a meta-analysis of GABA-a receptor genes using 4,739 people dependent on alcohol, opioids or methamphetamine and 4,924 controls
Found associations between variants of GABA-a receptor genes and alcohol dependence (GABRA2) and associations between GABRAG2 and both alcohol and heroin dependence
Concluded that give GABA-a receptor genes were implicated
This is evidence for genetic involvement in alcoholism
Many clinical drugs target GABA-a receptors, such as benzodiazepines and barbiturates and GABA is known to be an inhibitory neurotransmitter
The evidence that GABA is involved in alcohol dependence confirms a role for neurotransmission in alcohol addiction
Study of twins showed a genetic link to alcohol and smoking
Maes et al (1999)
looked at 1,412 MZ and DZ twins pairs and found genetic influence in smoking and drinking alcohol
If there is a genetic link to alcohol addiction, this doesn't mean a neurotransmitter explanation is wrong
There can be a neurotransmitter explanation that can be explained by looking at genes
Weiner et al (1997)
Alcohol works to reduce glutamate activity at the NMDA glutamate receptor and increases the inhibiting effect of GABA at the GABA-a receptor, reducing brain activity in general
Roberto et al (2004b)
Alcohol suppressed the transmission of signals using glutamate in the central nucleus of the amygdala
Evaluation
Strengths
A lot of evidence that neurotransmitter functioning, particularly in the brain's reward system, relates to drug misuse, including alcoholism
Noble (1996)
confirmed there are reduced dopamine levels and reduced numbers of D2 dopamine receptors in animals that prefer alcohol, suggesting a neurotransmitter explanation for alcoholism as well as a genetic one
Studies often animal lab experiments with strong controls and careful testing
Cause-and-effect conclusions drawn and conclusions have credibility
Studies using human support animal studies, lending credibility to findings
Noble (1996)
used animal studies as evidence and also showed that brain scanning in humans shows lowered dopamine in alcoholics
Treating alcoholics with a dopamine receptor agonist reduces alcohol drinking, giving evidence for dopamine in alcoholism
Weaknesses
Use of animal lab experiments can be seen as a strength, but there is the criticism that humans aren't the same as animals in their brain functioning
Evidence for an explanation from animal studies might not be generalisable to humans
Neurotransmitter functioning as an explanation for alcohol misuse doesn't seem to be separate from genetic or learning explanations
Genes can affect neurotransmitter functioning
The reward system in the brain rewards the individual in a positive way, which leads to more of the behaviour that gives the reward, relates to operant conditioning
Neurotransmitter, genetic and learning explanations seem to link