1. MRC Centre for Synaptic Plasticity, Department of Anatomy, University of Bristol, Bristol BS8 1TD, UK

Correspondence to: John T. R. Isaac¹ Correspondence and requests for materials should be addressed to J.I.

Abstract

Most of the fast excitatory synaptic transmission in the mammalian brain is mediated by ionotrophic glutamate receptors, of which there are three subtypes: AMPA (-amino-3-hydroxyl-5-methyl-4-isoxazolepropionate), NMDA (N -methyl-D-aspartate) and kainate. Although kainate-receptor subunits (GluR5–7, KA1 and 2) are widely expressed in the mammalian central nervous system¹,², little is known about their function. The development of pharmacological agents that distinguish between AMPA and kainate receptors has now allowed the functions of kainate receptors to be investigated³,⁴. The modulation of synaptic transmission by kainate receptors⁵,⁶,⁷ and their synaptic activation⁸,⁹,¹⁰,¹¹,¹²,¹³,¹⁴ in a variety of brain regions have been reported. The expression of kainate receptor subunits is developmentally regulated¹,² but their role in plasticity and development is unknown. Here we show that developing thalamocortical synapses express postsynaptic kainate receptors as well as AMPA receptors; however, the two receptor subtypes do not co-localize. During the critical period for experience-dependent plasticity, the kainate-receptor contribution to transmission decreases; a similar decrease occurs when long-term potentiation is induced in vitro. This indicates that during development there is activity-dependent regulation of the expression of kainate receptors at thalamocortical synapses.