Gamma-aminobutyrate (GABA) is the major inhibitory neurotransmitter found in the CNS and, as such, is important for balancing excitatory action of other neurotransmitters. High levels of GABA may be a result of excitatory overload, or a compensatory mechanism to balance the surplus excitatory neurotransmitter activity. These high levels result in a ‘calming’ action that may contribute to sluggish energy, feelings of sedation, and foggy thinking. Low GABA levels are associated with dysregulation of the adrenal stress response. Without the inhibiting function of GABA, impulsive behaviors are often poorly controlled, contributing to a range of anxious and/or reactive symptoms that extend from poor impulse control to seizure disorders. Alcohol as well as benzodiazepine drugs act on GABA receptors and imitate the effects of GABA. Though these substances don’t cause an increase in GABA levels, understanding their mechanism can give us additional insight into the effects of GABA.
- Low levels in plasma are characteristic of one subset of people with depression. The neurodegenerative condition Huntington's disease, also manifests as lowered levels of GABA as neuron loss proceeds.
- Vitamin B6 deficiency impairs GABA formation, offering one option to help assist people with inadequate GABA production.
- In animal models of seizure, lysine has dose-dependent anticonvulsant effects that appear to be due to GABA receptor modulation.
- May reflect decreased ability to convert to succinate for use in the Krebs (citric acid) cycle for energy generation. Cofactors here are α-KG and vitamin B6.
- Gamma-hydroxybutyric aciduria is characteristic of genetic variants with succinic semialdehyde dehydrogenase deficiency. The inevitable retardation of language development in children with this polymorphism is sometimes accompanied by other autistic features. This disorder constitutes one of potential genetic origins of autism.
- Elevated GABA levels, whether primary to illness or compensatory to another process, may be associated with dysfunctional GABAergic neurotransmission in chronic schizophrenia. [L]
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