Gamma-aminobutyric acid, commonly known as GABA, is a chemical messenger in the brain that plays a significant role in the central nervous system. It functions as the primary inhibitory neurotransmitter, meaning it reduces the excitability of nerve cells. This action helps to promote a sense of calmness and can regulate feelings of anxiety, stress, and fear. The unique chemical structure of GABA is fundamental to how it achieves these effects within the brain.
Understanding GABA’s Chemical Identity
GABA is an amino acid with the chemical formula C4H9NO2 and a molar mass of 103.12 g/mol. Unlike protein-building amino acids, GABA’s amino group (-NH2) is attached to the gamma carbon atom of its four-carbon chain.
The molecule has a linear chain structure, featuring a carboxyl group (-COOH) at one end and an amino group (-NH2) at the other. These functional groups are connected by a short carbon chain, making it a “gamma-amino acid.” This molecular architecture defines GABA.
The Shape That Controls Calm
GABA’s specific conformation allows it to bind precisely to specialized protein structures on nerve cells called GABA receptors. Several types exist, with GABAA and GABAB receptors being the most prominent.
When GABA binds to a GABAA receptor, it changes the receptor’s shape, opening an ion channel that allows chloride ions (Cl-) to flow into the neuron. This influx of negatively charged chloride ions makes the neuron’s interior more negative, a process called hyperpolarization, which reduces its excitability and makes it less likely to generate an electrical signal. GABAB receptors, conversely, are coupled to G proteins and indirectly activate potassium channels, leading to potassium efflux and also hyperpolarizing the cell.
Building and Breaking GABA: Structural Transformations
GABA’s presence in the brain is maintained through a dynamic process of synthesis and breakdown. It is primarily synthesized from glutamate, another neurotransmitter, by the enzyme glutamic acid decarboxylase (GAD). GAD modifies glutamate’s structure by removing a carboxyl group, converting the excitatory glutamate into inhibitory GABA.
Once GABA has served its purpose, it is broken down to prevent continuous neuronal inhibition. This metabolism is primarily carried out by the enzyme GABA transaminase (GABA-T). GABA-T converts GABA into succinic semialdehyde, which then enters the citric acid cycle for further metabolism, rendering GABA inactive. This precise regulation of GABA levels maintains brain activity balance.