Reference

Kainic acid and the glutamate receptor

Kainic acid and the glutamate receptor. Hall, J. G.; Hicks, T. P.; McLennan, H. (Dep. Physiol., Univ. British Columbia, Vancouver, B. C., Can.). Neurosci. Lett., 8(2), 171-5 (English) 1978. CODEN: NELED5. ISSN: 0304-3940. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Interactions) On 22 of 25 ventrobasal thalamus neurons of anesthetized rats, the excitatory action of 0.4 M L-glutamic acid (I) [56-86-0] was reduced or abolished by the antagonists 0.5 M glutamic acid di-Et ester (II) [16450-41-2] (12 neurons) and 0.2 M D-a-aminoadipic acid (III) [7620-28-2] (10 neurons) related to the excitatory action of 50 mm kainic acid (IV) [487-79-6] which was usually unaffected or only minimally decreased. When compared to the excitotoxic agent 0.1 M N-methyl-DL-aspartic acid (V) [17833-53-3], I action was reduced by II relative to that of V, and in the presence of III, I was less affected than V. Apparently, I and IV elevate neuronal firing rate by different mechanisms involving different receptor populations.

Glutamic acid and ethanol dependence

Glutamic acid and ethanol dependence. Freed, William J.; Michaelis, Elias K. (Lab. Clin. Psychopharmacol., Natl. Inst. Mental Health, Washington, D. C., USA). Pharmacol., Biochem. Behav., 8(5), 509-14 (English) 1978. CODEN: PBBHAU. ISSN: 0091-3057. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Glutamate di-Et ester [16450-41-2], a specific glutamate [56-86-0] antagonist, attenuated the seizures and decreases in behavioral activity that were obsd. in mice during EtOH [64-17-5] withdrawal. Prior to withdrawal, EtOH-dependent animals were supersensitive to kainic acid [487-79-6], a potent glutamate agonist, but they were not supersensitive to the convulsant drug pentylenetetrazol. Apparently, supersensitivity to glutamate develops during ethanol dependence, and this phenomenon contributes to the signs of EtOH withdrawal.