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Chemical Compound Review

AC1NSXA4     (2S)-3-(carboxymethyl)-4- prop-1-en-2-yl...

Synonyms: AG-J-06442, CTK5B4396, 62137-25-1, 3-(Carboxymethyl)-4-isopropenylproline
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Disease relevance of kainic acid

  • Although this activation was most prominent at 24 h after KA administration in neurons, Smad2P immunoreactivity gradually increased in astrocytes and microglial cells at 3 and 5 days, consistent with reactive gliosis [1].
  • The NMDA receptor-specific antagonist MK-801 completely blocked toxicity of NMDA, and the nonNMDA antagonist CNQX preferentially blocked the toxicity of Quis- and KA-type agonists in the spinal cord [2].
  • Kainic acid (KA) induces status epilepticus and delayed neurodegeneration of CA3 hippocampal neurons [3].
  • Unilateral injection of kainic acid (KA) into the dorsal hippocampus of adult mice induces spontaneous recurrent partial seizures and replicates histopathological changes observed in human mesial temporal lobe epilepsy (MTLE) (Bouilleret V et al., Neuroscience 1999; 89:717-729) [4].
  • KA produced the highest number of altered cells in the ganglion cell layer (GCL) and in the inner nuclear layer (INL), with an almost complete depletion of ChAT activity [5].

Psychiatry related information on kainic acid


High impact information on kainic acid


Chemical compound and disease context of kainic acid


Biological context of kainic acid

  • The high density of KA binding sites in the inner molecular layer of the dentate gyrus was unaffected by the ischemic insult, despite an extensive degeneration of cells in the hilus of dentate gyrus which projects glutamatergic afferents to this area.(ABSTRACT TRUNCATED AT 250 WORDS)[19]
  • At the dosage used, the KA produced a 52% decline in the cell density of the inner nuclear layer (INL), a 37% decline in the retinal ganglion cell layer (RGC), and no significant change in the density of cells in the outer nuclear layer (ONL) [20].
  • To determine whether this is a general phenomenon of the developing retina, the neurotoxin kainic acid (KA) was injected intraocularly in midlarval-stage Rana pipiens tadpoles to produce selective lesions of certain retinal cell types [20].
  • These results raise the possibility that the phosphorylation of KA receptor/channels in their cellular environment is negatively regulated by KA [21].
  • Intracellular recordings from CA3 pyramidal cells in irradiated rats revealed recurrent bursts of action potentials on top of large depolarizing waves after KA application [22].

Anatomical context of kainic acid

  • These findings suggest that following a KA-seizure, the intrahippocampal ability to reduce the nitroxide radical is impaired, but the ability is intact in the cerebral cortex [23].
  • In the juvenile rat, no significant changes in NF-kappaB binding activity were observed in piriform cortex, hippocampus, and cerebellum after KA injection [24].
  • Removal of mossy fiber input can therefore reduce KA induced hyperexcitability of CA3 pyramidal cells, but quantitative factors such as proportional loss of granule and hilar cells may explain the considerable differences found among cells and slices [22].
  • The prominent GABA(A)-receptor alpha1 subunit staining of interneurons also disappeared after KA treatment, suggesting acute degeneration of these cells [4].
  • When added to retinal cultures, both KA and BBT caused developmental stage- and concentration-dependent degeneration without affecting the number or qualitative properties of photoreceptors [25].

Associations of kainic acid with other chemical compounds

  • However, pilocarpine-induced seizures result in a more widespread neuronal death in both WT and D2R -/- brains in comparison to KA [26].
  • Furthermore, down-regulation of PKC inhibited the increase in TRE-binding activity by NMDA and KA [27].
  • Systemic administration of kainic acid (KA), an analogue of glutamic acid, causes limbic seizures and pathophysiological changes in adult rats that are very similar to human temporal lobe epilepsy [28].
  • However, this fraction from microsomes contained levels of the 52,000 Mr PSD protein and binding sites for L-glutamate (L-Glu) and L-aspartate (L-Asp) similar to true synaptic junctions, although the Con A binding glycoproteins and KA binding sites were nearly absent [29].
  • The saturation curve for glutamate uptake in slices from KA-seized rats killed 2 hours after the first forelimb clonus was displaced to the left, suggesting a compensatory change for the enhanced excitation [30].

Gene context of kainic acid

  • The excitotoxin KA decreased MR mRNA levels in CA1 and CA3, decreased GR mRNA levels in DG, and negated all antagonist-induced increases of ACR mRNAs [31].
  • Utrophin knockout mice had a normal hippocampal cytoarchitecture but were more sensitive to KA-induced excitotoxicity, as shown by increased mortality and faster progression of the lesion [32].
  • In contrast, the NT-3 concentration was unaltered after KA lesion [33].
  • However, we found that Lingo-1 mRNA was strongly up-regulated while NgR mRNA was down-regulated in the dentate gyrus in both the BDNF and the KA experiments [34].
  • Here, we tested whether the systemic treatment of mice with kainic acid (KA), an amino acid inducing limbic seizures, could elevate in the brain mRNAs encoding uPA and its specific inhibitor, plasminogen activator inhibitor-1 (PAI-1), a major antifibrinolytic agent [35].

Analytical, diagnostic and therapeutic context of kainic acid


  1. Bioluminescence imaging of Smad signaling in living mice shows correlation with excitotoxic neurodegeneration. Luo, J., Lin, A.H., Masliah, E., Wyss-Coray, T. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  2. Excitotoxicity in the embryonic chick spinal cord. Stewart, G.R., Olney, J.W., Pathikonda, M., Snider, W.D. Ann. Neurol. (1991) [Pubmed]
  3. Selective reduction of GluR2 protein in adult hippocampal CA3 neurons following status epilepticus but prior to cell loss. Friedman, L.K. Hippocampus. (1998) [Pubmed]
  4. Early loss of interneurons and delayed subunit-specific changes in GABA(A)-receptor expression in a mouse model of mesial temporal lobe epilepsy. Bouilleret, V., Loup, F., Kiener, T., Marescaux, C., Fritschy, J.M. Hippocampus. (2000) [Pubmed]
  5. Choline acetyltransferase depletion in the rat retina after intraocular injection of neurotoxins. Gómez-Ramos, P., Estrada, C., Pérez-Rico, C. J. Neurochem. (1985) [Pubmed]
  6. Long-term effects of early status epilepticus on the acquisition of conditioned avoidance behavior in rats. de Feo, M.R., Mecarelli, O., Palladini, G., Ricci, G.F. Epilepsia (1986) [Pubmed]
  7. Seizure-induced memory impairment is reduced by choline supplementation before or after status epilepticus. Holmes, G.L., Yang, Y., Liu, Z., Cermak, J.M., Sarkisian, M.R., Stafstrom, C.E., Neill, J.C., Blusztajn, J.K. Epilepsy Res. (2002) [Pubmed]
  8. Plasticity in hippocampal excitatory amino acid receptors in Alzheimer's disease. Geddes, J.W., Cotman, C.W. Neurosci. Res. (1986) [Pubmed]
  9. Lateral preoptic neurons inhibit thirst in the rat. Osaka, T., Kawano, S., Ueta, Y., Inenaga, K., Kannan, H., Yamashita, H. Brain Res. Bull. (1993) [Pubmed]
  10. Different behavioral responses of rats to kainate injections into the dorsal and median raphe nuclei. Przewłocka, B., Stala, L., Scheel-Krüger, J., Przewłocki, R. Polish journal of pharmacology and pharmacy. (1986) [Pubmed]
  11. Transgenic mice neuronally expressing baculoviral p35 are resistant to diverse types of induced apoptosis, including seizure-associated neurodegeneration. Viswanath, V., Wu, Z., Fonck, C., Wei, Q., Boonplueang, R., Andersen, J.K. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  12. EUK-134, a synthetic superoxide dismutase and catalase mimetic, prevents oxidative stress and attenuates kainate-induced neuropathology. Rong, Y., Doctrow, S.R., Tocco, G., Baudry, M. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  13. Expression of synaptopodin, an actin-associated protein, in the rat hippocampus after limbic epilepsy. Roth, S.U., Sommer, C., Mundel, P., Kiessling, M. Brain Pathol. (2001) [Pubmed]
  14. Proechimys guyannensis: an animal model of resistance to epilepsy. Arida, R.M., Scorza, F.A., de Amorim Carvalho, R., Cavalheiro, E.A. Epilepsia (2005) [Pubmed]
  15. Obesity exacerbates chemically induced neurodegeneration. Sriram, K., Benkovic, S.A., Miller, D.B., O'Callaghan, J.P. Neuroscience (2002) [Pubmed]
  16. Neuroprotective effect of GMP in hippocampal slices submitted to an in vitro model of ischemia. Oliveira, I.J., Molz, S., Souza, D.O., Tasca, C.I. Cell. Mol. Neurobiol. (2002) [Pubmed]
  17. Effects of status epilepticus on extracellular amino acids in the hippocampus. Lehmann, A., Hagberg, H., Jacobson, I., Hamberger, A. Brain Res. (1985) [Pubmed]
  18. Lesions to Schaffer collaterals prevent ischemic death of CA1 pyramidal cells. Onodera, H., Sato, G., Kogure, K. Neurosci. Lett. (1986) [Pubmed]
  19. Dynamic changes of excitatory amino acid receptors in the rat hippocampus following transient cerebral ischemia. Westerberg, E., Monaghan, D.T., Kalimo, H., Cotman, C.W., Wieloch, T.W. J. Neurosci. (1989) [Pubmed]
  20. Cell-specific regulation of neuronal production in the larval frog retina. Reh, T.A. J. Neurosci. (1987) [Pubmed]
  21. Phosphorylation of the 49-kDa putative subunit of the chick cerebellar kainate receptor and its regulation by kainatergic ligands. Ortega, A., Teichberg, V.I. J. Biol. Chem. (1990) [Pubmed]
  22. Residual granule cells can maintain susceptibility of CA3 pyramidal cells to kainate-induced epileptiform discharges. Czéh, B., Seress, L., Czéh, G. Hippocampus. (1998) [Pubmed]
  23. EPR imaging for in vivo analysis of the half-life of a nitroxide radical in the hippocampus and cerebral cortex of rats after epileptic seizures. Yokoyama, H., Lin, Y., Itoh, O., Ueda, Y., Nakajima, A., Ogata, T., Sato, T., Ohya-Nishiguchi, H., Kamada, H. Free Radic. Biol. Med. (1999) [Pubmed]
  24. Seizure activity results in a rapid induction of nuclear factor-kappa B in adult but not juvenile rat limbic structures. Rong, Y., Baudry, M. J. Neurochem. (1996) [Pubmed]
  25. Generation of enriched populations of cultured photoreceptor cells. Politi, L.E., Adler, R. Invest. Ophthalmol. Vis. Sci. (1986) [Pubmed]
  26. Dopamine D2 receptor signaling controls neuronal cell death induced by muscarinic and glutamatergic drugs. Bozzi, Y., Borrelli, E. Mol. Cell. Neurosci. (2002) [Pubmed]
  27. Involvement of protein kinase C in Ca(2+)-signaling pathways to activation of AP-1 DNA-binding activity evoked via NMDA- and voltage-gated Ca2+ channels. Ohtani, K., Sakurai, H., Oh, E., Iwata, E., Tsuchiya, T., Tsuda, M. J. Neurochem. (1995) [Pubmed]
  28. Long-term expression of Fos-related antigen and transient expression of delta FosB associated with seizures in the rat hippocampus and striatum. Bing, G., Wang, W., Qi, Q., Feng, Z., Hudson, P., Jin, L., Zhang, W., Bing, R., Hong, J.S. J. Neurochem. (1997) [Pubmed]
  29. Identification of synapse specific components: synaptic glycoproteins, proteins, and transmitter binding sites. Mena, E.E., Foster, A.C., Fagg, G.E., Cotman, C.W. J. Neurochem. (1981) [Pubmed]
  30. Plasticity of excitatory amino acid transporters in experimental epilepsy. Claudio, O.I., Ferchmin, P., Velísek, L., Sperber, E.F., Moshé, S.L., Ortiz, J.G. Epilepsia (2000) [Pubmed]
  31. Adrenocorticosteroid receptor blockade and excitotoxic challenge regulate adrenocorticosteroid receptor mRNA levels in hippocampus. McCullers, D.L., Herman, J.P. J. Neurosci. Res. (2001) [Pubmed]
  32. Increased vulnerability to kainate-induced seizures in utrophin-knockout mice. Knuesel, I., Riban, V., Zuellig, R.A., Schaub, M.C., Grady, R.M., Sanes, J.R., Fritschy, J.M. Eur. J. Neurosci. (2002) [Pubmed]
  33. Hippocampal neurotrophin levels after injury: Relationship to the age of the hippocampus at the time of injury. Shetty, A.K., Rao, M.S., Hattiangady, B., Zaman, V., Shetty, G.A. J. Neurosci. Res. (2004) [Pubmed]
  34. Neuronal activity-induced regulation of Lingo-1. Trifunovski, A., Josephson, A., Ringman, A., Brené, S., Spenger, C., Olson, L. Neuroreport (2004) [Pubmed]
  35. mRNAs encoding urokinase-type plasminogen activator and plasminogen activator inhibitor-1 are elevated in the mouse brain following kainate-mediated excitation. Masos, T., Miskin, R. Brain Res. Mol. Brain Res. (1997) [Pubmed]
  36. Stimulation of Cl area neurons globally increases regional cerebral blood flow but not metabolism. Underwood, M.D., Iadecola, C., Sved, A., Reis, D.J. J. Cereb. Blood Flow Metab. (1992) [Pubmed]
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