Quinolinic Acid: A Pathogen in Seizure Disorders?

  • R. Schwarcz
  • C. Speciale
  • E. Okuno
  • E. D. French
  • C. Köhler
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 203)


Multiple lines of experimental evidence, exemplified in several chapters of this volume, point to a prominent if not necessarily causative involvement of brain N-methyl-D-aspartate (NMDA) receptors in seizure phenomena. At the present time, the situation is reminiscent of that encountered in schizophrenia research where it appears that dopamine receptors are ‘somehow’ involved in psychiatric symptomatology (Snyder et al., 1974). While the theoretical framework for studies in those two seemingly quite unrelated areas is thus remarkably similar, one considerable difference exists: there is no question as to the identity of the endogenous agonist of the dopamine receptor. In fact, the catecholamine has lent its name to the ’dopamine hypothesis’ of schizophrenia. In contrast, no endogenous NMDA-agonist of similar prominence has emerged, which could be generally accepted as a candidate for a pathogen in human epileptic disorders. Yet the characterization of such an endogenous compound is eminently relevant, given the non-endogenous nature of NMDA and the apparent non-selectivity of glutamate for the NMDA-subtype of excitatory amino acid receptors (Foster and Fagg, 1984). Here we will review the growing body of evidence suggesting that quinolinic acid (pyridine 2,3-dicarboxylic acid; QUIN) may fulfill such a role.


Temporal Lobe Epilepsy Kainic Acid Quinolinic Acid Neuronal Cell Body Nicotinamide Adenine Dinucleotide 
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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • R. Schwarcz
    • 1
  • C. Speciale
    • 1
  • E. Okuno
    • 1
  • E. D. French
    • 1
  • C. Köhler
    • 2
  1. 1.Maryland Psychiatric Research CenterBaltimoreUSA
  2. 2.Department of PharmacologyASTRA-LäkemedelSödertäljeSweden

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