Alcohol and GABA have similar effects on the nervous system as alcohol binds to and activates the same receptors as GABA, slowing activity in the central and peripheral nervous systems. Alcohol enhances the inhibitory effects of GABA, and both oppose the effects of glutamate. In alcoholics, GABA-A receptors become less sensitive to alcohol, while glutamate receptors become hypersensitive, leading to withdrawal symptoms.
GABA and alcohol have mutual functions in the human body. The main relationship between them is that alcohol has similar effects to GABA on the nervous system. This is because alcohol binds to and activates the same receptors that suppress the firing of neurons, which slows activity in the central and peripheral nervous systems. In alcoholics, the normal function of the neurotransmitter GABA becomes dependent on the presence of alcohol in the bloodstream.
The acronym GABA stands for gamma-aminobutyric acid. It is the major inhibitory neurotransmitter in the brain of humans and all other mammals. When GABA is released from a neuron at a synapse, it binds to GABA receptors on adjacent neurons and prevents these cells from firing by reducing their electrical excitability. Many depressants, including alcohol, can bind to GABA receptors and trigger the same inhibitory response.
Alcohol binds the class of GABA receptor known as GABA-A. These receptors are found throughout the brain in several subtypes, where they moderate neuronal communication by inhibiting signals between neurons. GABA neurons are essential for neurological function, from basic control of breathing and the ability to walk to vision. Like most sedatives, alcohol enhances the inhibitory effects of GABA, which explains why alcohol depresses motor skills and perception.
GABA and alcohol enhance each other’s effects. GABA and alcohol together will have a greater effect than the same amount of alcohol or GABA alone. When alcohol binds to GABA-A receptors, alcohol is thought to increase their ionic conductance, making the neuron even less excitable. Alcohol also enhances GABA absorption. In combination with other GABA agonists such as barbiturates, alcohol can enhance the sedative effects of these drugs.
Glutamate is the primary excitatory neurotransmitter in the brain and neurons use it to induce electrical communication between cells. Both GABA and alcohol oppose the effects of glutamate in the nervous system, but GABA does so indirectly by preventing cells from activating. Alcohol opposes the action of glutamate by binding to glutamate receptors, but not by activating them. It blocks the receptor so that glutamate cannot bind to it and excite the neuron. In this way, alcohol further enhances the inhibitory effects of GABA.
Alcoholism changes the relationship between GABA and alcohol. GABA-A receptors become less sensitive to alcohol and require larger amounts to respond, while glutamate receptors become hypersensitive to even smaller amounts. If an alcoholic enters alcoholism treatment, he may experience withdrawal symptoms that reflect the depressed function of the GABA receptors that have become dependent on alcohol. Tremors, hallucinations, and even violent seizures can result from a decreased response to GABA and overactivity of glutamate receptors.
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