In: Biology
Prior to beginning work on this discussion, read the required chapters from the text and review the required articles for this week. Alcohol and caffeine have nearly opposite effects on behavior and the nervous system, yet these substances are not used to treat overdose or addiction to the other. Why not use caffeine to treat alcohol addiction? Analyze the issues of pharmacological and physiological antagonism. Explain the receptor systems involved and the central nervous system structures effects with regard to this question. Frame your analysis in terms of drug action first and other consequences second.
Caffeine Affects the Neurotransmitters of the Brain that Fuel Addiction caffeine drinkers which often revert back to alcohol use during their treatment. The consumption of these drinks may lead to serious problems. If co-administration of alcohol and caffeine allow people to drink for longer periods of time because of reduced sedation, they may consume more alcohol; this could lead to serious health risks, such as near-lethal blood alcohol levels.
Alcohol is a sedative it Effects on Acetylcholine, GABA, Serotonin and NMDA receptors . It works in part by potentiating the GABAergic neurotransmitter system. GABA [gamma-aminobutyric acid] is an inhibitory neurotransmitter. When the neurons in the brain release GABA, it acts to slow down or inhibit other neural processes. This can reduce anxiety, increase relaxation while sedating a person. With higher levels of alcohol, problems can arise as important neural and other bodily systems become overinhibited and shut down.
Compared to alcohol, caffeine is on the other end of the spectrum of psychoactive drugs in that it is a stimulant. Caffeine is an antagonist for the neurotransmitter adenosine. Adenosine is an inhibitory neurotransmitter; so similar to GABA, adenosine can dampen or inhibit other neural processors. Caffeine exerts secondary effects on many classes of neurotransmitters, including noradrenaline, dopamine, serotonin, acetylcholine, glutamate, and GABA (Daly, 1993). Caffeine activates noradrenaline neurons and seems to affect the local release of dopamine. Many of the alerting effects of caffeine may be related to the action of the methylxanthine on serotonin neurons.With caffeine, we have a double negative in that it inhibits an inhibitory neurotransmitter and thus increase levels of arousal and alertness—but higher doses can produce nervousness, anxiety and tachycardia. Dr. Florian Koppelstaetter and colleagues from the Medical University Innsbruck in Austria presented a study in 2005 that showed caffeine consumption activates the frontal lobes of the brains. These areas are responsible for short-term memory and attention. Thus, caffeine can increase these functions in a person. However for long term memory loss due to Slowed Hippocampus Function.