GABA and alcohol have mutual functions in the human body. The chief relationship between them is that alcohol has similar effects to those of GABA on the nervous system. This is because alcohol binds to and activates the same receptors that suppress the firing of neurons, which slows down activity in the central and peripheral nervous systems. In alcoholics, 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 principal inhibitory neurotransmitter in the brains of humans and all other mammals. When GABA is released by one neuron into 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 different subtypes, where they moderate neuronal communication by inhibiting signals between neurons. GABA neurons are essential to neurological function, from basic control of breathing and walking ability to vision. Like most sedatives, alcohol increases 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 by themselves. When it binds to GABA-A receptors, alcohol is thought to increase their ion conductance, causing the neuron to become even less excitable. Alcohol also enhances GABA absorption. Combined with other GABA agonists like barbituates, alcohol can increase 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 this indirectly by preventing cells from firing. Alcohol opposes glutamate action by binding to glutamate receptors, but not activating them. It blocks the receptor so that glutamate cannot bind to it and excite the neuron. By doing this, 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 quantities of it to respond, while glutamate receptors become hypersensitive to even smaller amounts. If an alcoholic enters alcoholism treatment, he or she may experience withdrawal symptoms that reflect the depressed function of GABA receptors that have become dependent on alcohol. Shaking, hallucinations, even violent seizures can result from diminished GABA response and hyperactive glutamate receptors.