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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Chemical Compound Review

Kainite     magnesium potassium chloride sulfate...

Synonyms: Kainite(8CI), AG-L-18773, AC1L4VIG, CTK4B7581, AR-1J3744, ...
 
 
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Disease relevance of Kainite

  • Domoic acid (DA), a kainite-receptor agonist and potent inducer of neurotoxicity, has been administered intravenously in adult rats in the present study (0.75 mg/kg body weight) to demonstrate neuronal degeneration followed by glial activation and their involvement with inducible nitric oxide synthase (iNOS) in the hippocampus [1].
  • PURPOSE: To investigate the temporal relation between high-frequency oscillations (HFOs) in the dentate gyrus and recurrent spontaneous seizures after intrahippocampal kainite-induced status epilepticus [2].
  • We have shown previously that corneal inoculation of mice with HSV-1 causes acute spontaneous behavioral and electrophysiological seizures and increases hippocampal excitability and kainite-induced seizure susceptibility [3].
 

High impact information on Kainite

  • Glutamate (Glu)- or kainite (KA)-induced currents were completely inhibited by a specific blocker of AMPA receptor, LY300164, indicating that functional Glu-receptors in cultured microglia are mostly AMPA receptor but not KA receptor in many cells [4].
  • By examining the pharmacological, biochemical, and morphologic features of kainite-induced excitotoxic death, we also determined whether it occurs by apoptosis, necrosis, or both [5].
  • METHODS: Male Wistar rats with cannulae aimed at the dlPAG received vehicle, AP7 (a NMDA receptor antagonist, 2 nmol) or NBQX (an AMPA/kainite receptor antagonist, 100 nmol) injection 10 min before the administration of SIN-1 (an NO donor, 300 nmol) [6].
  • Interestingly, PCs are highly susceptible to a variety of pathological conditions that may involve glutamate-mediated 'excitotoxicity', a term coined to describe an excessive release of glutamate, and a subsequent over-activation of excitatory amino acid (NMDA, AMPA, and kainite) receptors [7].
  • In this study, to elucidate the mechanism of the neuroprotective effect of Zn-ATSM2, we first examined its in vitro protective effects against glutamate-, NMDA- and kainite-induced neurotoxicity in primary cultures of hippocampal neurons [8].

References

  1. Protective role of melatonin in domoic acid-induced neuronal damage in the hippocampus of adult rats. Ananth, C., Gopalakrishnakone, P., Kaur, C. Hippocampus. (2003) [Pubmed]
  2. High-frequency oscillations after status epilepticus: epileptogenesis and seizure genesis. Bragin, A., Wilson, C.L., Almajano, J., Mody, I., Engel, J. Epilepsia (2004) [Pubmed]
  3. Valacyclovir treatment ameliorates the persistently increased pentylenetetrazol-induced seizure susceptibility in mice with herpes simplex virus type 1 infection. Wu, H.M., Liang, Y.C., Chen, S.H., Huang, C.C., Chen, S.H., Tsai, J.J., Hsieh, C.L., Hsu, K.S. Exp. Neurol. (2004) [Pubmed]
  4. Heterogeneity and potentiation of AMPA type of glutamate receptors in rat cultured microglia. Hagino, Y., Kariura, Y., Manago, Y., Amano, T., Wang, B., Sekiguchi, M., Nishikawa, K., Aoki, S., Wada, K., Noda, M. Glia (2004) [Pubmed]
  5. AMPA receptors are the major mediators of excitotoxic death in mature oligodendrocytes. Leuchtmann, E.A., Ratner, A.E., Vijitruth, R., Qu, Y., McDonald, J.W. Neurobiol. Dis. (2003) [Pubmed]
  6. Ionotropic glutamate-receptor antagonists inhibit the aversive effects of nitric oxide donor injected into the dorsolateral periaqueductal gray of rats. Moreira, F.A., Molchanov, M.L., Guimarães, F.S. Psychopharmacology (Berl.) (2004) [Pubmed]
  7. Don't get too excited: mechanisms of glutamate-mediated Purkinje cell death. Slemmer, J.E., De Zeeuw, C.I., Weber, J.T. Prog. Brain Res. (2005) [Pubmed]
  8. Mechanisms of [2,3-butanedione bis(N4-dimethylthiosemicarbazone)]zinc (Zn-ATSM2)-induced protection of cultured hippocampal neurons against N-methyl-D-aspartate receptor-mediated glutamate cytotoxicity. Kubota, M., Iida, Y., Magata, Y., Kitamura, Y., Kawashima, H., Saji, H. Jpn. J. Pharmacol. (2000) [Pubmed]
 
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