Cardiovascular response to group I metabotropic glutamate receptor activation in NTS

Citation
Cm. Foley et al., Cardiovascular response to group I metabotropic glutamate receptor activation in NTS, AM J P-REG, 45(5), 1999, pp. R1469-R1478
Citations number
40
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
45
Issue
5
Year of publication
1999
Pages
R1469 - R1478
Database
ISI
SICI code
0363-6119(199905)45:5<R1469:CRTGIM>2.0.ZU;2-1
Abstract
Glutamate is the proposed neurotransmitter of baroreceptor afferents at the level of the nucleus tractus solitarius (NTS). Exogenous glutamate in the NTS activates neurons through ionotropic and metabotropic glutamate recepto rs (mGluRs). This study tested the hypothesis that group I mGluRs in the NT S produce depressor, bradycardic, and sympathoinhibitory responses. In uret han-anesthetized rats, unilateral 30-nl microinjections of the group I-sele ctive mGluR agonist 3,5-dihydroxyphenylglycine (DHPG) into the NTS decrease d mean arterial pressure, heart rate, and lumbar sympathetic nerve activity . The dose of drug that produced 50% of the maximal response (ED50) was 50- 100 mu M. The response to microinjection of equal concentrations of DHPG or the general mGluR agonist 1-aminocyclopentane-1S,3R-dicarboxylic acid (ACP D) produced similar cardiovascular effects. The cardiovascular response to injection of DHPG or ACPD was abolished by NTS blockade of mGluRs with alph a-methyl-4-carboxyphenylglycine (MCPG). Blockade of ionotropic glutamate re ceptors with kynurenic acid did not attenuate the response to DHPG or ACPD injection. These data suggest that DHPG and ACPD activate mGluRs in the NTS and do not require ionotropic glutamate receptors to produce their cardiov ascular response. In the NTS the group I mGluRs produce responses that are consistent with excitation of neurons involved in reducing sympathetic outf low, heart rate, and arterial pressure.