Glutamate release in parabrachial nucleus and ...
|Title||Glutamate release in parabrachial nucleus and baroreflex alterations after vagal afferent activation|
|Author(s)||T. Saleh, L. Bauce, Q. Pittman|
|Journal||The American Journal of Physiology|
|Issue||5 Pt 2|
|Abstract||The parabrachial nucleus (PBN) is a regulatory nucleus that relays visceral information from the brain stem to the cortex. Immunohistochemical studies have shown that the levels of various neuropeptides in the PBN were changed after visceral afferent activation. Because the major transmitter relaying visceral information through the PBN is glutamate, the present study asked if glutamate release into the PBN also was changed after vagal afferent activation in anesthetized male rats. The distally crushed vagus was stimulated (50 Hz, 1-2 mA, 1 s on, 2 s off) for 2 h. Dialysates of the PBN were collected every 30 min and assayed for glutamate using high-performance liquid chromatography. Extracellular glutamate concentrations were reduced during the vagal stimulation, increased fourfold compared with prestimulated levels after the stimulation was terminated, and returned to prestimulated levels over the next 2 h poststimulation. These changes were not due to alterations in blood pressure because sodium nitroprusside infusion for the same interval resulted in a similar hypotension, but increased glutamate release. Phenylephrine and sodium nitroprusside were infused intravenously to measure the cardiac baroreflex before, during, and after vagal stimulation. The pressor (but not the depressor) response was elevated during the period of enhanced glutamate release, and the baroreflex curve was shifted to the right (increased threshold) without a change in gain. These changes in the cardiac baroreflex were reduced, but still seen, when the PBNs were dialyzed bilaterally with the glutamate antagonists MK-801 and 6-cyano-7-nitroquinoxaline-2,3-dione. Thus visceral activation alters glutamate release in the PBN and has enduring effects on cardiac baroreflex function.|
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