Kainic acid

Kainic acid
Stereo, skeletal formula of kainic acid
Names
IUPAC name
(3S,4S)-3-(Carboxymethyl)-4-(prop-1-en-2-yl)-L-proline
Systematic IUPAC name
(2S,3S,4S)-3-(Carboxymethyl)-4-(prop-1-en-2-yl)pyrrolidine-2-carboxylic acid
Other names
2-Carboxy-3-carboxymethyl-4-isopropenyl-pyrrolidine[citation needed]
Identifiers
3D model (JSmol)
86660
ChEBI
ChEMBL
ChemSpider
KEGG
MeSH Kainic+acid
UNII
  • InChI=1S/C10H15NO4/c1-5(2)7-4-11-9(10(14)15)6(7)3-8(12)13/h6-7,9,11H,1,3-4H2,2H3,(H,12,13)(H,14,15) ☒N
    Key: VLSMHEGGTFMBBZ-UHFFFAOYSA-N ☒N
  • OC(=O)[C@H]1NC[C@H](C(C)=C)[C@@H]1CC(=O)O
Properties
C10H15NO4
Molar mass 213.233 g·mol−1
Melting point 215 °C (419 °F; 488 K) (decomposes)
log P 0.635
Acidity (pKa) 2.031
Basicity (pKb) 11.966
Structure
Monoclinic
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Kainic acid, or kainate, is an acid that naturally occurs in some seaweed. Kainic acid is a potent neuroexcitatory amino acid agonist that acts by activating receptors for glutamate, the principal excitatory neurotransmitter in the central nervous system. Glutamate is produced by the cell's metabolic processes and there are four major classifications of glutamate receptors: NMDA receptors, AMPA receptors, kainate receptors, and the metabotropic glutamate receptors. Kainic acid is an agonist for kainate receptors, a type of ionotropic glutamate receptor. Kainate receptors likely control a sodium channel that produces excitatory postsynaptic potentials (EPSPs) when glutamate binds.[1]

Kainic acid is commonly injected into laboratory animal models to study the effects of experimental ablation. Kainic acid is a direct agonist of the glutamic kainate receptors and large doses of concentrated solutions produce immediate neuronal death by overstimulating neurons to death. Such damage and death of neurons is referred to as an excitotoxic lesion. Thus, in large, concentrated doses kainic acid can be considered a neurotoxin, and in small doses of dilute solution kainic acid will chemically stimulate neurons.[2] In fact, kainate seems to regulate serotonergic activity in the vertebrate retina.[3]

Electrical stimulation of designated areas of the brain are generally administered by passing an electric current through a wire that is inserted into the brain to lesion a particular area of the brain. Electrical stimulation indiscriminately destroys anything in the vicinity of the electrode tip, including neural bodies and axons of neurons passing through; therefore it is difficult to attribute the effects of the lesion to a single area. Chemical stimulation is typically administered through a cannula that is inserted into the brain via stereotactic surgery. Chemical stimulation, while more complicated than electrical stimulation, has the distinct advantage of activating cell bodies, but not nearby axons, because only cell bodies and subsequent dendrites contain glutamate receptors. Therefore, chemical stimulation by kainic acid is more localized than electrical stimulation. Both chemical and electrical lesions potentially cause additional damage to the brain due to the very nature of the inserted electrode or cannula. Therefore, the most effective ablation studies are performed in comparison to a sham lesion that duplicates all the steps of producing a brain lesion except the one that actually causes the brain damage, that is, injection of kainic acid or administration of an electrical shock.

  1. ^ Carlson NR (2013). Physiology of Behavior. Pearson. pp. 121. ISBN 978-0-205-23939-9.
  2. ^ Carlson NR (2013). Physiology of Behavior. Pearson. pp. 152. ISBN 978-0-205-23939-9.
  3. ^ Passos AD, Herculano AM, Oliveira KR, de Lima SM, Rocha FA, Freitas HR, et al. (October 2019). "Regulation of the Serotonergic System by Kainate in the Avian Retina". Cellular and Molecular Neurobiology. 39 (7): 1039–1049. doi:10.1007/s10571-019-00701-8. PMID 31197744. S2CID 254384979.