Alcohol increases the activity of Gaba receptors.
Ethanol (ethyl alcohol) affects many areas of the brain. However, the most pronounced impact is found in the cerebrum, hippocampus, and cerebellum. Ethanol affects the GABA (gamma-aminobutyric acid) neurotransmitter system, binding to GABA-A and GABA-B receptors, and increasing their ability to hyperpolarize neuronal cell membranes. So, it inhibits (slows, reduces) brain activity. When this happens in the cerebral cortex, higher thought is slowed or inhibited. In the hippocampus (where a large number of GABA receptors exist), memory storage is impaired. In the cerebellum (also containing large numbers of GABA receptors to allow for fine-tuning of activities related to coordination), coordination is impaired.
Alcohol's primary effect is central nervous system depression. With repeated heavy consumption of alcohol, certain chemical receptors in the brain (GABAa receptors) are desensitized and reduced in number. The absence of GABA is what causes the CNS depression. When alcohol is stopped, especially abruptly, the person's nervous system suffers from uncontrolled synapse firing because there is not enough GABA to control it. This causes the shakes, and can result in anxiety, life threatening seizures, delirium tremens and hallucinations and possible heart failure.
The drug acamprosate is one such substance that is used to treat alcohol dependence and can cause dystonia. It binds with GABA-A receptors, which is an inhibitory system, reducing neurotransmission and muscle contraction, and can result in dystonia.
They affect GABA, NMDA, opiod, adrenergic, histamine and acetylcholine receptors in your brain. Depressants can effect other parts of your brain aswell, these are just the parts of it that actually cause the depressant effects of the drugs. Alcohol for example effects the GABA, NMDA, acetylcholine and serotonin receptors but it's effect on the serotonin receptor doesn't cause any depressant effect but rather adds to the euphoric effects of alcohol.
GABA (gamma-aminobutyric acid) is an inhibitory neurotransmitter in the brain that helps regulate neuronal excitability. It plays a role in reducing anxiety, promoting relaxation, and improving sleep quality. GABA is also involved in modulating muscle tone and may have potential therapeutic applications for conditions like insomnia and anxiety disorders.
Cocaine blocks the reuptake of dopamine and, to a lesser extent, norepinephrine and serotonin in the brain. This causes the accumulation of dopamine, leading to euphoria and excitation. The increased stimulation of dopaminergic neurons in the mesolimbic (reward) circuit leads to addiction. Alcohol binds with GABA receptors producing inhibitory effects on neural activity. This produces cognitive impairment and reduced anxiety (disinhibition). Activation of GABA receptors also produces postsynaptic dopamine release, which stimulates the mesolimbic circuit in the brain, producing euphoria and addiction.
These are the main factors influencing inebriation from a given amount of alcohol: 1) Eating while drinking slows the absorption rate of alcohol into the bloodstream, and also dilutes it with other substances ingested, reducing the propensity to become drunk. 2) Since the human liver can convert ethanol (remove it from bloodstream) at a rate of about .015 of BAC per hour, if you do not exceed this absorption rate, you don't get drunk as easily. 3) Increased liver enzymes (such as alcohol dehydrogenase) can allow the liver to metabolize more ethanol at a given time, increasing the rate at which the liver converts ethanol to acetaldehyde, and reducing the blood alcohol concentration (reducing the blood sent into the brain). These enzymes are typically increased (upregulated) as a person drinks more alcohol. And this gives a person the majority of their tolerance to alcohol. However, this can also be genetic. 4) GABA receptor variation - some people are predisposed to alcoholism due to variation in their genes that code for GABA (gamma-aminobutyric acid) receptors in the brain, which are responsible for anxiolytic (anxiety-reducing) and inhibitory effects of GABA, benzodiazepines (such as Xanax, Valium, etc.), and ethanol. For those that have "mutant" forms of GABA receptors, they may have reduced binding affinity or reduced activity in the presence of ethanol, which can make them more tolerant to ethanol. 5) GABA receptor downregulation/downmodulation - often times, however, excessive drinking over time will cause the brain to reduce GABA receptor density (decrease the number of GABA receptors), which reduces the effect that GABA, benzodiazepines, and ethanol have on brain cells...which causes a receptor-based, rather than metabolic, tolerance for ethanol.
GABA binds to GABA receptors on the postsynaptic neuron, leading to an influx of negatively charged chloride ions into the neuron. This hyperpolarizes the neuron, making it less likely to generate an action potential and thereby inhibiting its activity.
No, Zofran is a 5-HT3 receptor antagonist while benzodiazapines are GABA-a agonists. The 5-HT3 receptor controls inhibitory processes for the GABA sites, so antagonizing the 5-HT3 site, as Zofran does, may result in GABA stimulation as a byproduct, however it does not directly stimulate the GABA receptors, unlike Benzos.
Gabapentin is structurally related to the neurotransmitter GABA (gamma-aminobutyric acid) but it does not modify or directly act upon GABA(A) or GABA(B) receptors. As with most brain chemical altering drugs they don't completely understand how gabapentin works in the brain but it is theorized that it probably causes brain cells to make more GABA. For those with epilepsy this increase in GABA helps control seizures.
Heavy alcohol use accustoms the brain and the rest of the central nervous system (CNS) to functioning with alcohol present. That is what addiction is. The body becomes unable to function anywhere close to normally without the drug, and all sorts of things happen when it is withdrawn.Alcohol's primary effect is central nervous system depression. With repeated heavy consumption of alcohol, certain chemical receptors in the brain (GABAa receptors) are desensitized and reduced in number. The absence of GABA is what causes the CNS depression. When alcohol is stopped, especially abruptly, the person's nervous system suffers from uncontrolled synapse firing because there is not enough GABA to control it. This causes the shakes, and can result in anxiety, life threatening seizures, delirium tremens and hallucinations and possible heart failure.