Kainic acid

Kainic acid

Names
IUPAC name (2S,3S,4S)-3-(Carboxymethyl)-4-prop-1-en-2-ylpyrrolidine-2-carboxylic acid
Other names (3S,4S)-3-(Carboxymethyl)-4-prop-1-en-2-yl-L-proline; 2-Carboxy-3-carboxymethyl-4-isopropenyl-pyrrolidine
Identifiers
CAS Number	487-79-6 Y
3D model (Jmol)	Interactive image
Beilstein Reference	86660
ChEBI	CHEBI:31746 Y
ChEMBL	ChEMBL27527 N
ChemSpider	9837 Y
KEGG	C12819 N
MeSH	Kainic+acid
PubChem	10255
UNII	SIV03811UC Y
InChI 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
SMILES OC(=O)[C@H]1NC[C@H](C(C)=C)[C@@H]1CC(=O)O
Properties
Chemical formula	C10H15NO4
Molar mass	213.23 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
Crystal structure	Monoclinic
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
N  (what is YN ?)
Infobox references

Kainic acid (kainate) is a natural marine acid present in some seaweed. Kainic acid is a potent neuroexcitatory amino acid 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.

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.

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. It is important to note that 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.