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Quisqualamine is the α-decarboxylated analogue of the glutamate receptor agonist and neurotoxin quisqualic acid and an analogue of the neurotransmitter γ-aminobutyric acid (GABA).[1][2]

α-Decarboxylation of excitatory amino acids can produce derivatives with inhibitory effects.[2] Relatedly, unlike quisqualic acid, quisqualamine has central depressant and neuroprotective effects, and appears to act predominantly as an agonist of the GABAA receptor and to a lesser extent as an agonist of the glycine receptor.[1][2][3] Its actions are inhibited by GABAA receptor antagonists like bicuculline and picrotoxin and by the glycine receptor antagonist strychnine in vitro.[1][2][3]

The NMDA receptor antagonists magnesium and DL-AP5, the AMPA and kainate receptor antagonist CNQX, and the GABAB receptor antagonist 2-hydroxysaclofen all do not affect quisqualamine’s actions in vitro.[2] As such, the drug does not appear to interact with the ionotropic glutamate receptors or GABAB receptor.[2]

See also

References

  1. ^ a b c Evans RH, Francis AA, Hunt K, Martin MR, Watkins JC (June 1978). “Quisqualamine, a novel gamma-aminobutyric acid (GABA) related depressant amino acid”. The Journal of Pharmacy and Pharmacology. 30 (6): 364–7. doi:10.1111/j.2042-7158.1978.tb13257.x. PMID 26767. S2CID 84350091.
  2. ^ a b c d e f Herrero JF (March 1994). “GABAergic activity of quisqualamine and homoquisqualamine in hemisected spinal cord in vitro preparation”. Revista Española de Fisiología. 50 (1): 11–7. PMID 7527570.
  3. ^ a b Biraboneye AC, Madonna S, Maher P, Kraus JL (January 2010). “Neuroprotective effects of N-alkyl-1,2,4-oxadiazolidine-3,5-diones and their corresponding synthetic intermediates N-alkylhydroxylamines and N-1-alkyl-3-carbonyl-1-hydroxyureas against in vitro cerebral ischemia”. ChemMedChem. 5 (1): 79–85. doi:10.1002/cmdc.200900418. PMID 19943277. S2CID 39067721.