Neurotransmission gamma aminobutyric acid

So far attention has concentrated on the effects of lithium on excitatory transmitters. There is evidence that the drug can also facilitate inhibitory transmission, an effect that has been attributed to a desensitization of the pres)maptic gamma-aminobutyric acid (GABA) receptors, which results in an increase in the release of this inhibitory transmitter. The increased conversion of glutamate to GABA may also contribute to this process. Thus it would appear that lithium has a varied and complex action on central neurotransmission, the net result being a diminution in the activity of excitatory transmitters and an increase in GABAergic function. 

Mechanism of Action A benzodiazepine that enhances action of gamma-aminobutyric acid (GABA) neurotransmission in the central nervous system (CNS). Therapeutic Effect Produces depressant effect at all levels of CNS. 

Inhibitory modulation of neurotransmission in the CNS is carried out by two substances, gamma-aminobutyric acid (GABA) and glycine. They are differentially distributed, GABA being found primarily in the brain and glycine primarily in the spinal cord. 

Glutamate is the primary excitatory transmitter substance in brain and spinal cord, and gamma-aminobutyric acid (GABA) is responsible for the majority of inhibitory neurotransmission in the brain (Lam et al 2006 Carlson, 2001 Kandel et al.,... 

Benzodiazepines all bind to a specific binding site on the gamma-aminobutyric acid (GABA) A chloride channel. The GABA chloride channel is a multi-subunit protein complex that is found in the plasma membrane of nerve cells in various parts of the CNS. When the neurotransmitter GABA binds to the chloride channel, the channel opens, allowing the influx of chloride ions into the cell. This causes hyperpolarization of the nerve cell and diminishes its response to excitatory input. The GABAa chloride channel is considered the major inhibitory system to neurotransmission in the CNS. 

Enhances action of neurotransmitter gamma-aminobutyric acid (GABA) neurotransmission at CNS producing anxiolytic effect. Enhances presynaptic inhibition elevating seizure threshold in response to electrical/chemical stimulation. Inhibits spinal afferent pathways, producing skeletal muscle relaxation. 

Schwartz-Bloom RD, SahR. 2001. Gamma-aminobutyric acid(A) neurotransmission and cerebral ischemia. J Neurochem 77 353-371. 

---