GABA agonism

Consider propofol pharmacotherapy, as it agonizes GABA-A receptors and antagonizes NMDA receptors. Phenobarbital can be used as an alternative... 

Alcohol Theories include combination of effects at receptor and Pi adernergic agonism leading to GABA receptor sensitization to ethanol Sedation and hypotension with coadministration Caution patients to avoid coadministration Lin et al., 1994... 

Carbamazepine is licenced as an alternative to lithium for prophylaxis of bipolar affective disorder, although clinical trial evidence is actually stronger to support its use in the treatment of acute mania. Carbamazepine appears to be more effective than lithium for rapidly cycling bipolar disorders, i.e. with recurrent swift transitions from mania to depression. It is also effective in combination with lithium. Its mode of action is thought to involve agonism of inhibitory GABA transmission at the GABA-benzodiazepine receptor complex (see also Epilepsy, p. 417). 

The mode of action of ivermectin has been reviewed (2). It has tentatively been identified as agonism at GABA receptors, with inhibition of ion channels that control specific nerve cell connections. The functioning of chloride channels should thus be altered in most organisms, leading to paralysis and death of parasites. Several sites of action have been proposed ... 

Direct agonism of GABA receptors. This has met with limited success due to tachyphlaxis. 

Hydrocodone and oxycodone are widely prescribed opioid analgesics that are agonists at the mu, kappa, and delta receptors in the central nervous system. The cellular changes that occur with agonism at the opioid receptors are still under investigation. However, it is known that mu opioid receptors are G protein-coupled receptors that decrease intracellular levels of cAMP. This decrease in intracellular cAMP inhibits the release of critical neurotransmitters and hormones including substance P, acetylcholine, GABA, somatostatin, and other substances that activate or sensitize nociceptors. Inhibition of neurotransmitter release causes a subsequent decrease in the perceived level of pain by the patient. Also, activation of opioid receptors modifies specific calcium channels at the surface of cells, which hyperpolarizes and decreases excitability of neurons. 

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