The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Chemical Compound Review

SureCN975038     3-(carboxymethyl)-4-prop-1- en-2-yl...

Synonyms: AG-G-89179, BSPBio_002382, KBioGR_002077, KBioSS_000890, CCG-38820, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of kainic acid

  • Serotonergic denervation partially protects rat striatum from kainic acid toxicity [1].
  • More importantly, the combination of this secretory signal with the coding sequence for the active galanin peptide significantly attenuated in vivo focal seizure sensitivity, even with different promoters, and prevented kainic acid-induced hilar cell death [2].
  • When A1 noradrenergic neurons in the caudal ventrolateral medulla of rabbits are destroyed electrolytically or by local injection of the neurotoxin kainic acid, the concentration of vasopressin in plasma increases, causing hypertension [3].
  • Kainic acid lesions of the striatum dissociate amphetamine and apomorphine stereotypy: similarities to Huntingdon's chorea [4].
  • Kainic acid (KA)-induced status epilepticus in adult rats leads to delayed, selective death of pyramidal neurons in the hippocampal CA1 and CA3 [5].

Psychiatry related information on kainic acid


High impact information on kainic acid

  • PGC-1alpha null mice are much more sensitive to the neurodegenerative effects of MPTP and kainic acid, oxidative stressors affecting the substantia nigra and hippocampus, respectively [11].
  • Although c-fos is induced by neuronal activity, including kainic acid-induced seizures, whether and how c-fos is involved in excitotoxicity is still unknown [12].
  • We found that these mutant mice have more severe kainic acid-induced seizures, increased neuronal excitability and neuronal cell death, compared with control mice [12].
  • Neuropathological studies in the four patients who died after mussel-induced intoxication demonstrated neuronal necrosis and loss, predominantly in the hippocampus and amygdala, in a pattern similar to that observed experimentally in animals after the administration of kainic acid, which is also structurally similar to glutamate and domoic acid [13].
  • Powerful inhibition of kainic acid seizures by neuropeptide Y via Y5-like receptors [14].

Chemical compound and disease context of kainic acid


Biological context of kainic acid

  • Synaptic localization of kainic acid binding sites [19].
  • Here we report that disruption of the gene encoding Jnk3 in mice caused the mice to be resistant to the excitotoxic glutamate-receptor agonist kainic acid: they showed a reduction in seizure activity and hippocampal neuron apoptosis was prevented [20].
  • Although application of kainic acid imposed the same level of noxious stress, the phosphorylation of c-Jun and the transcriptional activity of the AP-1 transcription factor complex were markedly reduced in the mutant mice [20].
  • BDNF mRNAs containing exons I, II, and III are expressed predominantly in the brain, whereas exon IV transcripts predominate in the lung and heart. mRNAs containing exons I, II, and III increase markedly in the brain after kainic acid-induced seizures, whereas exon IV mRNA increases only slightly [21].
  • The genomic regions responsible for the in vivo upregulation of BDNF expression in the axotomized sciatic nerve and in the brain after kainic acid-induced seizures and KCl-induced spreading depression were mapped [22].

Anatomical context of kainic acid


Associations of kainic acid with other chemical compounds

  • Zinc ions are contained in high concentrations in mossy fibres of the hippocampal formation, and it is the postsynaptic neurones of these fibres which are most susceptible to the toxic effects of kainic acid, a potent convulsant, or to chronic exposure to organometallic compounds [26].
  • Furthermore, a prior microinjection in the RVLM of gallamine, digoxinspecific antibody Fab fragments, or kainic acid or intravenous injection of hexamethonium all prevented the pressor and sympathoexcitatory effects induced by a subsequent microinjection of ouabain [27].
  • In vivo excitatory stimulation with kainic acid (KA) resulted in an increase in luciferase activity and phosphorylated Smad2 (Smad2P), and nuclear translocation of Smad2P in hippocampal CA3 neurons correlated significantly with luciferase activity [28].
  • Injection of kainic acid, a rigid analog of the excitatory neurotransmitter glutamic acid (glu), into the neostriatum of rats produces a condition that mimics Huntington disease (HD) in at least 12 different morphological and biochemical parameters [29].
  • The partial denervation of the CA1 area induced by the kainic acid led to both an enhanced NMDA-mediated excitatory phase and a decrease in postsynaptic inhibition, resulting in the pronounced hyperexcitability noted in the lesioned slices [30].

Gene context of kainic acid


Analytical, diagnostic and therapeutic context of kainic acid

  • This pattern of results parallels that found in patients suffering from Hungtington's chorea, thus strengthening the parallels between the kainic acid animal model and the human disease state initially suggested on biochemical gounds [4].
  • Differential display PCR was used to identify mRNAs that are differentially expressed between degenerating and nondegenerating tissues in the brain after kainic acid-induced seizure activity [36].
  • Intraventricularly administered kainic acid, which selectively destroys CA3-4 pyramidal cells, results in an increase of enkephalin immunostaining in mossy fibers and a significant increase in enkephalin-ir by radioimmunoassay in whole hippocampus [37].
  • Here we report that certain strains of mice, including strains that are used for gene targeting studies, do not exhibit excitotoxic cell death after kainic acid seizures [38].
  • Renal SNA inhibition evoked with AVP at doses of 1 and 3 mU/kg/min in rabbits after sinoaortic denervation and vagotomy was totally blocked by chemical lesions with kainic acid of the bilateral NTS or the area postrema [39].


  1. Serotonergic denervation partially protects rat striatum from kainic acid toxicity. Berger, M., Sperk, G., Hornykiewicz, O. Nature (1982) [Pubmed]
  2. Attenuation of seizures and neuronal death by adeno-associated virus vector galanin expression and secretion. Haberman, R.P., Samulski, R.J., McCown, T.J. Nat. Med. (2003) [Pubmed]
  3. Destruction of noradrenergic neurons in rabbit brainstem elevates plasma vasopressin, causing hypertension. Blessing, W.W., Sved, A.F., Reis, D.J. Science (1982) [Pubmed]
  4. Kainic acid lesions of the striatum dissociate amphetamine and apomorphine stereotypy: similarities to Huntingdon's chorea. Mason, S.T., Sanberg, P.R., Fibiger, H.C. Science (1978) [Pubmed]
  5. Status epilepticus decreases glutamate receptor 2 mRNA and protein expression in hippocampal pyramidal cells before neuronal death. Grooms, S.Y., Opitz, T., Bennett, M.V., Zukin, R.S. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  6. Lesion of striatal neurones with kainic acid provides a model for Huntington's chorea. Coyle, J.T., Schwarcz, R. Nature (1976) [Pubmed]
  7. Aphagia and adipsia after preferential destruction of nerve cell bodies in hypothalamus. Grossman, S.P., Dacey, D., Halaris, A.E., Collier, T., Routtenberg, A. Science (1978) [Pubmed]
  8. Plasticity of hippocampal circuitry in Alzheimer's disease. Geddes, J.W., Monaghan, D.T., Cotman, C.W., Lott, I.T., Kim, R.C., Chui, H.C. Science (1985) [Pubmed]
  9. The basal forebrain-cortical cholinergic system: interpreting the functional consequences of excitotoxic lesions. Dunnett, S.B., Everitt, B.J., Robbins, T.W. Trends Neurosci. (1991) [Pubmed]
  10. Sustained induction of prostaglandin endoperoxide synthase-2 by seizures in hippocampus. Inhibition by a platelet-activating factor antagonist. Marcheselli, V.L., Bazan, N.G. J. Biol. Chem. (1996) [Pubmed]
  11. Suppression of Reactive Oxygen Species and Neurodegeneration by the PGC-1 Transcriptional Coactivators. St-Pierre, J., Drori, S., Uldry, M., Silvaggi, J.M., Rhee, J., J??ger, S., Handschin, C., Zheng, K., Lin, J., Yang, W., Simon, D.K., Bachoo, R., Spiegelman, B.M. Cell (2006) [Pubmed]
  12. c-fos regulates neuronal excitability and survival. Zhang, J., Zhang, D., McQuade, J.S., Behbehani, M., Tsien, J.Z., Xu, M. Nat. Genet. (2002) [Pubmed]
  13. Neurologic sequelae of domoic acid intoxication due to the ingestion of contaminated mussels. Teitelbaum, J.S., Zatorre, R.J., Carpenter, S., Gendron, D., Evans, A.C., Gjedde, A., Cashman, N.R. N. Engl. J. Med. (1990) [Pubmed]
  14. Powerful inhibition of kainic acid seizures by neuropeptide Y via Y5-like receptors. Woldbye, D.P., Larsen, P.J., Mikkelsen, J.D., Klemp, K., Madsen, T.M., Bolwig, T.G. Nat. Med. (1997) [Pubmed]
  15. Functional neuronal replacement by grafted striatal neurones in the ibotenic acid-lesioned rat striatum. Isacson, O., Brundin, P., Kelly, P.A., Gage, F.H., Björklund, A. Nature (1984) [Pubmed]
  16. The embryonic form of neural cell surface molecule (E-NCAM) in the rat hippocampus and its reexpression on glial cells following kainic acid-induced status epilepticus. Le Gal La Salle, G., Rougon, G., Valin, A. J. Neurosci. (1992) [Pubmed]
  17. Phenobarbital modifies seizure-related brain injury in the developing brain. Mikati, M.A., Holmes, G.L., Chronopoulos, A., Hyde, P., Thurber, S., Gatt, A., Liu, Z., Werner, S., Stafstrom, C.E. Ann. Neurol. (1994) [Pubmed]
  18. Angiotensin converting enzyme in kainic acid--injected striata. Singh, E.A., McGeer, E.G. Ann. Neurol. (1978) [Pubmed]
  19. Synaptic localization of kainic acid binding sites. Foster, A.C., Mena, E.E., Monaghan, D.T., Cotman, C.W. Nature (1981) [Pubmed]
  20. Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene. Yang, D.D., Kuan, C.Y., Whitmarsh, A.J., Rincón, M., Zheng, T.S., Davis, R.J., Rakic, P., Flavell, R.A. Nature (1997) [Pubmed]
  21. Multiple promoters direct tissue-specific expression of the rat BDNF gene. Timmusk, T., Palm, K., Metsis, M., Reintam, T., Paalme, V., Saarma, M., Persson, H. Neuron (1993) [Pubmed]
  22. Identification of brain-derived neurotrophic factor promoter regions mediating tissue-specific, axotomy-, and neuronal activity-induced expression in transgenic mice. Timmusk, T., Lendahl, U., Funakoshi, H., Arenas, E., Persson, H., Metsis, M. J. Cell Biol. (1995) [Pubmed]
  23. Intraventricular kainic acid preferentially destroys hippocampal pyramidal cells. Nadler, J.V., Perry, B.W., Cotman, C.W. Nature (1978) [Pubmed]
  24. Membrane conductance oscillations in astrocytes induced by phorbol ester. MacVicar, B.A., Crichton, S.A., Burnard, D.M., Tse, F.W. Nature (1987) [Pubmed]
  25. A newly identified population of presumptive microneurones in the cat retinal ganglion cell layer. Hughes, A., Wieniawa-Narkiewicz, E. Nature (1980) [Pubmed]
  26. Release of endogenous Zn2+ from brain tissue during activity. Assaf, S.Y., Chung, S.H. Nature (1984) [Pubmed]
  27. Role of ouabain-like compound in the rostral ventrolateral medulla in rats. Teruya, H., Yamazato, M., Muratani, H., Sakima, A., Takishita, S., Terano, Y., Fukiyama, K. J. Clin. Invest. (1997) [Pubmed]
  28. 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]
  29. Huntington disease and Tourette syndrome. II. Uptake of glutamic acid and other amino acids by fibroblasts. Comings, D.E., Goetz, I.E., Holden, J., Holtz, J. Am. J. Hum. Genet. (1981) [Pubmed]
  30. Excitatory synaptic potentials in kainic acid-denervated rat CA1 pyramidal neurons. Turner, D.A., Wheal, H.V. J. Neurosci. (1991) [Pubmed]
  31. Role of the Y5 neuropeptide Y receptor in limbic seizures. Marsh, D.J., Baraban, S.C., Hollopeter, G., Palmiter, R.D. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  32. Changes in neurotrophic factor expression and receptor activation following exposure of hippocampal neuron/astrocyte cocultures to kainic acid. Rudge, J.S., Pasnikowski, E.M., Holst, P., Lindsay, R.M. J. Neurosci. (1995) [Pubmed]
  33. Disruption of the metallothionein-III gene in mice: analysis of brain zinc, behavior, and neuron vulnerability to metals, aging, and seizures. Erickson, J.C., Hollopeter, G., Thomas, S.A., Froelick, G.J., Palmiter, R.D. J. Neurosci. (1997) [Pubmed]
  34. Hypersensitivity to seizures in beta-amyloid precursor protein deficient mice. Steinbach, J.P., Müller, U., Leist, M., Li, Z.W., Nicotera, P., Aguzzi, A. Cell Death Differ. (1998) [Pubmed]
  35. Functional comparisons of three glutamate transporter subtypes cloned from human motor cortex. Arriza, J.L., Fairman, W.A., Wadiche, J.I., Murdoch, G.H., Kavanaugh, M.P., Amara, S.G. J. Neurosci. (1994) [Pubmed]
  36. A novel seizure-induced synaptotagmin gene identified by differential display. Babity, J.M., Armstrong, J.N., Plumier, J.C., Currie, R.W., Robertson, H.A. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  37. Dynorphin is contained within hippocampal mossy fibers: immunochemical alterations after kainic acid administration and colchicine-induced neurotoxicity. McGinty, J.F., Henriksen, S.J., Goldstein, A., Terenius, L., Bloom, F.E. Proc. Natl. Acad. Sci. U.S.A. (1983) [Pubmed]
  38. Genetic determinants of susceptibility to excitotoxic cell death: implications for gene targeting approaches. Schauwecker, P.E., Steward, O. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  39. Central nervous system mechanisms involved in inhibition of renal sympathetic nerve activity induced by arginine vasopressin. Suzuki, S., Takeshita, A., Imaizumi, T., Hirooka, Y., Yoshida, M., Ando, S., Nakamura, M. Circ. Res. (1989) [Pubmed]
WikiGenes - Universities