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1 Institute of Physiology, National Yang-Ming University, Taipei 11221, Taiwan; and 2 Department of Medical Education and Research, Veterans General Hospital-Kaohsiung, Kaohsiung 81346, Taiwan, Republic of China
We investigated
the role of glutamatergic projection from the parabrachial nucleus
(PBN) complex to the rostral ventrolateral medulla (RVLM) in the
PBN-induced suppression of reflex bradycardia in adult Sprague-Dawley
rats that were maintained under pentobarbital anesthesia. Under
stimulus conditions that did not appreciably alter the baseline
systemic arterial pressure and heart rate, electrical (10-s train of
0.5-ms pulses, at 10-20 µA and 10-20 Hz) or chemical
(L-glutamate, 1 nmol)
stimulation of the ventrolateral regions and Köelliker-Fuse (KF)
subnucleus of the PBN complex significantly suppressed the reflex
bradycardia in response to transient hypertension evoked by
phenylephrine (5 µg/kg iv). The PBN-induced suppression of reflex
bradycardia was appreciably reversed by bilateral microinjection into
the RVLM of the
N-methyl-D-aspartate (NMDA)-receptor antagonist MK-801 (500 pmol) or the non-NMDA-receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (50 pmol).
Anatomically, most of the retrogradely labeled neurons in the
ventrolateral regions and KF subnucleus of the ipsilateral PBN complex
after microinjection of fast blue into the RVLM were also
immunoreactive to anti-glutamate antiserum. These results suggest that
a direct glutamatergic projection to the RVLM from topographically
distinct regions of the PBN complex may participate in the suppression of reflex bradycardia via activation of both NMDA and non-NMDA receptors at the RVLM.
rostral ventrolateral medulla; N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors; immunohistochemistry; retrograde tract tracing; rat
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