A brainstem area mediating cerebrovascular and EEG responses to hypoxic excitation of rostal ventrolateral medulla in rat

E. V. Golanov, D. A. Ruggiero, D. J. Reis

Research output: Contribution to journalArticle

37 Scopus citations

Abstract

1. We sought to identify the medullary relay area mediating the elevations of regional cerebral blood flow (rCBF) and synchronization of the electroencephalogram (EEG) in the rat cerebral cortex elicited by hypoxic excitation of reticulospinal sympathoexcitatory neurons of the rostral ventrolateral medulla (RVLM). 2. In anaesthetized spinalized rats electrical stimulation of RVLM elevated rCBF (laser-Doppler flowmetry) by 31 ± 6%, reduced cerebrovascular resistance (CVR) by 26 ± 8%, and synchronized the EEG, increasing the power of the 5-6 Hz band by 98 ± 25%. Stimulation of a contiguous caudal region, the medullary cerebral vasodilator area (MCVA), had comparable effects which, like responses of RVLM, were replicated by microinjection of L-glutamate (5 nmol, 20 nl). 3. Microinjection of NaCN (300 pmol in 20 nl) elevated rCBF (17 ± 5%) and synchronized the EEG from RVLM, but not MCVA, while nicotine (1.2 nmol in 40 nl) increased rCBF by 13 ± 5% and synchronized the EEG from MCVA. In intact rats nicotine lowered arterial pressure only from MCVA (101 ± 3 to 52 ± 9 mmHg). 4. Bilateral electrolytic lesions of MCVA significantly reduced, by over 59%, elevations in rCBF and, by 78%, changes in EEG evoked from RVLM. Bilateral electrolytic lesions of RVLM did not affect responses from MCVA. 5. Anterograde tracing with BDA demonstrated that RVLM and MCVA are interconnected. 6. The MCVA is a nicotine-sensitive region of the medulla that relays signals elicited by excitation of oxygen-sensitive reticulospinal neurons in RVLM to reflexively elevate rCBF and slow the EEG as part of the oxygen-conserving (diving) reflex initiated in these neurons by hypoxia or ischaemia.

Original languageEnglish (US)
Pages (from-to)413-429
Number of pages17
JournalJournal of Physiology
Volume529
Issue number2
DOIs
StatePublished - Dec 1 2000

ASJC Scopus subject areas

  • Physiology

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