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Localization of ionotropic glutamate receptors in caudate‐putamen and nucleus accumbens septi of rat brain: Comparison of NMDA, AMPA, and kainate receptors
Author(s) -
Tarazi Frank I.,
Campbell Alexander,
Yeghiayan Sylva K.,
Baldessarini Ross J.
Publication year - 1998
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(199810)30:2<227::aid-syn13>3.0.co;2-z
Subject(s) - kainate receptor , ionotropic effect , nucleus accumbens , ampa receptor , chemistry , glutamate receptor , neuroscience , caudate nucleus , putamen , nmda receptor , long term depression , receptor , medicine , biology , biochemistry
Changes in binding of selective radioligands at NMDA ([ 3 H]MK‐801), AMPA ([ 3 H]CNQX), and kainate ([ 3 H]kainic acid) glutamate (GLU) ionotropic receptors in rat caudate‐putamen (CPu) and nucleus accumbens (NAc) were examined by quantitative autoradiography following: 1) unilateral surgical ablation of frontal cerebral cortex to remove descending corticostriatal GLU projections, 2) unilateral injection of kainic acid (KA) into CPu or NAc to degenerate local intrinsic neurons, or 3) unilateral injections of 6‐hydroxydopamine (6‐OH‐DA) into substantia nigra to degenerate ascending nigrostriatal dopamine (DA) projections. Cortical ablation significantly decreased NMDA receptor binding in ipsilateral medial CPu (20%), and NAc (16%), similar to previously reported losses of DA D 4 receptors. KA lesions produced large losses of NMDA receptor labeling in CPu and NAc (both by 52%), AMPA (41% and 45%, respectively), and kainate receptors (40% and 45%, respectively) that were similar to the loss of D 2 receptors in CPu and NAc after KA injections. Nigral 6‐OH‐DA lesions yielded smaller but significant losses in NMDA (17%), AMPA (12%), and kainate (11%) receptor binding in CPu. The results indicate that most NMDA, AMPA, and kainate receptors in rat CPu and NAc occur on intrinsic postsynaptic neurons. Also, some NMDA, but not AMPA or kainate, receptors are also found on corticostriatal projections in association with D 4 receptors; these may, respectively, represent excitatory presynaptic NMDA autoreceptors and inhibitory D 4 heteroceptors that regulate GLU release from corticostriatal axons in medial CPu and NAc. Conversely, the loss of all three GLU receptor subtypes after lesioning DA neurons supports their role as excitatory heteroceptors promoting DA release from nigrostriatal neurons. Synapse 30:227–235, 1998. © 1998 Wiley‐Liss, Inc.