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J Neurophysiol (September 28, 2005). doi:10.1152/jn.00772.2005
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Submitted on July 21, 2005
Accepted on September 26, 2005

Group I metabotropic glutamate receptors on second-order baroreceptor neurons are tonically activated and induce a Na+-Ca2+ exchange current

Shin-ichi Sekizawa1 and Ann C. Bonham1*

1 Medical Pharmacology and Toxicology, University of California Davis, Davis, CA, USA

* To whom correspondence should be addressed. E-mail: ann.bonham{at}ucdmc.ucdavis.edu.

The nucleus tractus solitarius (NTS) is essential for coordinating baroreflex control of blood pressure. The baroreceptor sensory fibers make glutamatergic synapses onto second-order NTS neurons. Glutamate spillover activates Group II and III presynaptic metabotropic glutamate receptors (mGluRs) on the baroreceptor central terminals to inhibit synaptic transmission, but the role of postsynaptic mGluRs is less understood. We used whole-cell patch-clamping in anatomically-identified second-order baroreceptor neurons in a brainstem slice to test whether Group I, II and III mGluRs had postsynaptic effects at this first central synapse in the baroreceptor afferent pathway. The Group I agonist, DHPG, induced a depolarization and spiking that was mimicked by endogenous glutamate. Group I mGluR blockade prevented the depolarization and slightly hyperpolarized the neurons, suggesting a small tonic Group I mGluR activation. The DHPG-induced inward current consisted of voltage-dependent and -independent components; the former was blocked by TEA and the latter was blocked by replacing extracellular NaCl with LiCl or Tris-HCl. The DHPG current was potentiated in a Ca2+ free external solution and was diminished by intracellular dialysis with BAPTA and by perfusion with Na+-Ca2+ exchanger blockers, KB-R7943 or 3',4'-dichlorobenzamil. Intracellular dialysis with GDP{beta}S or heparin and perfusion with the PLC inhibitor, U-73122, or the Ca2+-calmodulin inhibitor, W-7, significantly decreased the DHPG current. The data suggest that Group I mGluRs on baroreceptor neurons are functional, are activated by endogenous glutamate and activate a Na+-Ca2+ exchanger through G-protein, PLC, IP3, Ca2+-calmodulin mechanisms to excite the cell, thus providing postsynaptic mechanisms to enhance or prolong baroreceptor signal transmission.




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