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γ-Aminobutyric acid (GABA) is an amino acid produced endogenously and is utilized in the adult brain as the primary inhibitory neurotransmitter. In the brain GABA is produced mostly by GABAergic neurons, also known as inhibitory neurons secondary to their primary role surrounding production of their inhibitory neurotransmitter. GABA is very important to normal physiologic function and the absence of a function system revolving around GABA can have drastic effects to health. Spastic diplegia, also known as Little’s Disease, is a condition noted by hypertonicity and spasticity of muscles secondary to the absence of functional GABA receptors in the brain, indicating that, in the absense of GABA, neuroexcitation goes unmitigated.
The body produces GABA through glutamate (the primary excitatory neurotransmitter) metabolism by the enzyme L-glutamic acid decarboxylase in the presence of a vitamin b6 cofactor. Commercially, this same process is replicated using Lactobacillus hilgardii K-3, a bacteria that is found commonly in wine, cider, cheese and cured meats .
GABA’s Mode of action:
In general, dietary GABA has been shown to have poor transmission across the blood brain barrier (BBB). When, in rats, intraperitoneal radiolabled H3-γ-aminobutyric acid was administered, there was found to be no significant transmission across the BBB. Furthermore, the small amount of radioactivity that was found, was found within the metabolites of radiolabeld GABA and not the molecule itself .
GABA achieves inhibition of neuronal signal propagation by causing hyperpolarization of neurons with GABAa or GABAb receptors, within their synaptic clefts. Hyperpolarization of the neuron is done by causing the potential between the plasma membrane of the neuron to become more negative .
GABA achieves this by allowing the influx of Cl- ions into the neuron or by opening K+ ion channels that remove K+ from the neuron.
Many classes of drugs target the GABA receptor to exert their effects. Benzodiazepines and barbiturates are two common classes that do just this; their effects are the result of their action on the activation of the GABA receptor, although their methods of activation differ. Most every drug, including GABA, that agonizes the GABA receptor, will result in symptoms of reducing neurologic tone. For this reason, GABA receptor agonization results in symptoms such as anxiolysis or sedation.
GABA has been seen in postnatal development to act excitatory. This fact has not been proven, in humans, albeit in mice studies, it has been found that GABA plays a depolarizing effect on the NMDA receptors, it is thought, by triggering Ca(2+) influx via NMDA receptor .
In other studies, GABA has been found to be at levels 12% higher than normal in the occipital regions of people suffering from primary insomnia .
Many other compounds bind to the GABA receptor, as a means of yielding their effect. Benzodiazepines, barbituates and alcohol are the most well known to follow this mechanism. In people who suffer from chronic alcoholism, the GABA receptor becomes downregulated to the point that, normal, indogenous levels of GABA begin to have no effect. In these people, it may happen such that levels of GABA that would cause any non-alcoholic to become comatose, a chronic alocoholic would appear arroused .