Functional Properties of Kainate Receptors

  • James E. Huettner
Part of the The Receptors book series (REC)


Kainic acid was first isolated from seaweed more than 40 yr ago (see McGeer et al., 1978 for a review of early work). By the mid-1970s, the excitatory and neurotoxic actions of kainate were well established, and the hypothesis that kainate acted on a specific subset of excitatory amino acid receptors had been developed (Watkins and Evans, 1981). More recent work has shown that kainate can activate several different receptor subtypes, including α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors (Patneau and Mayer, 1991), kainate receptors (Agrawal and Evans, 1986; Huettner, 1990), and lower-mol wt kainate binding proteins in some species (see Henley, 1994). The current definition of these subtypes stems from a comparison of physiological responses evoked at native receptors to the behavior of cloned receptor subunits expressed in heterologous cells. AMPA receptors are formed by the subunits GluR1–4, also known as GluR-A-D (Boulter et al., 1990; Keinänen et al., 1990; Nakanishi et al., 1990). A large body of evidence indicates that postsynaptic AMPA receptors mediate fast excitatory transmission throughout most of the central nervous system (CNS) (reviewed by Collingridge and Lester, 1989; Monaghan et al., 1989). Kainate activates these receptors with lower affinity than AMPA, glutamate, or quisqualate, but kainate produces a much larger steady-state current than the other agonists (Patneau and Mayer, 1991).


Glutamate Receptor AMPA Receptor Mossy Fiber Kainic Acid Domoic Acid 
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© Humana Press Inc. 1997

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