Behavioural neuroscienceCardiovascular function of a glutamatergic projection from the hypothalamic paraventricular nucleus to the nucleus tractus solitarius in the rat
Section snippets
General procedures
Experiments were done in adult male Wistar rats (Charles River Laboratories, Wilmington, MA, USA) weighing 300–380 g (n=73). All animals were housed under controlled conditions with a 12-h light/dark cycle. Food and water were available to the animals ad libitum. The experiments were performed according to the NIH guide for “The Care and Use of Laboratory Animals, 7th Edition, 1996” and with the approval of the Institutional Animal Care and Use Committee of this university. Every effort was
Concentration-response of NMDA in the PVN
Unilateral microinjections of NMDA into the PVN elicited increases in MAP and HR (Table 1A). Maximal pressor and tachycardic responses were elicited by 10 mM concentration; therefore, this concentration of NMDA was selected for further studies in other groups of rats. The onset, peak and duration of the responses elicited by 10 mM concentration of NMDA were 5–20 s, 1–2 min, and 10–15 min, respectively. In this and other series of experiments, microinjections of aCSF alone into the PVN and mNTS
Discussion
The following new observations were made in this study: 1) a glutamatergic bilateral projection from the PVN to the mNTS was identified, 2) bilateral blockade of ionotropic glutamate receptors in the mNTS exaggerated the pressor and sympathetic nerve, but not HR, responses to unilateral chemical stimulation of the PVN, and 3) the projection from the PVN to the mNTS was determined to be tonically active.
NMDA has been used to stimulate PVN in only a few investigations (Li et al 2001, Li et al 2006
Conclusion
In summary, using anatomical, physiological and electrophysiological techniques, we have demonstrated the presence of a glutamatergic projection from the PVN to the mNTS. The projection is bilateral with ipsilateral preponderance. Since the blockade of this projection in the mNTS exaggerated the pressor responses to the PVN stimulation, it may be concluded that its normal function is to restrain the excitatory cardiovascular effects of PVN stimulation. The projection from the PVN to the mNTS is
Acknowledgments
This work was supported in part by NIH grants HL024347 and HL076248 awarded to Dr. H. N. Sapru.
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