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This Article Full Text Full Text (PDF) Supplemental data All Versions of this Article: 575/3/727    most recent jphysiol.2006.112672v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Simms, A. E. Articles by Pickering, A. E. Search for Related Content PubMed PubMed Citation Articles by Simms, A. E. Articles by Pickering, A. E. Related Collections Neuroscience

¹ Department of Physiology, Bristol Heart Institute, School of Medical Sciences, University Walk, University of Bristol, Bristol BS8 1TD, UK
² Department of Anaesthesia, Bristol Royal Infirmary, Bristol BS2 8HW, UK

The nucleus tractus solitarii (NTS) is the first site of integration for primary baroreceptor afferents, which release glutamate to excite second-order neurones through ionotropic receptors. In vitro studies indicate that glutamate may also activate metabotropic receptors (mGluRs) to modulate the excitability of NTS neurones at pre- and postsynaptic loci. We examined the functional role of metabotropic glutamate receptors (mGluRs) in modulating the baroreceptor reflex in the rat NTS. Using the working heart–brainstem preparation, the baroreflex was activated using brief pressor stimuli and the consequent cardiac (heart rate change) and non-cardiac sympathetic (T8–10 chain) baroreflex gains were obtained. Microinjections of glutamate antagonists were made bilaterally into the NTS at the site of termination of baroreceptor afferents. NTS microinjection of kynurenate (ionotropic antagonist) inhibited both the cardiac and sympathetic baroreflex gains (16 ± 5% and 59 ± 11% of control, respectively). The non-selective mGluR antagonist MCPG produced a dose-dependent inhibition of the cardiac gain (30 ± 3% of control) but not the sympathetic gain. Selective inhibitions of the cardiac gain were also seen with LY341495 and EGLU suggesting the response was mediated by group II mGluRs. This effect on cardiac gain involves attenuation of the parasympathetic baroreflex as it persists in the presence of atenolol. Prior NTS microinjection of bicuculline (GABA_A antagonist) prevented the mGluR-mediated attenuation of the cardiac gain. These results are consistent with the reported presynaptic inhibition of GABAergic transmission by group II mGluRs in the NTS and constitute a plausible mechanism allowing selective feed-forward disinhibition to increase the gain of the cardiac limb of the baroreflex without changing the sympathoinhibitory component.

(Received 21 May 2006; accepted after revision 22 June 2006; first published online 29 June 2006)
Corresponding author A. E. Pickering: Department of Physiology, Bristol Heart Institute, School of Medical Sciences, University Walk, University of Bristol, Bristol BS8 1TD, UK. Email: tony.pickering{at}bristol.ac.uk

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