Widespread reductions in cerebral blood flow and metabolism elicited by electrical stimulation of the parabrachial nucleus in rat. Academic Article uri icon

Overview

abstract

  • We have studied the effect of electrical stimulation of the parabrachial nucleus (PBN) and adjacent areas of dorsal pons on regional cerebral blood flow (rCBF) and glucose utilization (rCGU) in anesthetized (chloralose), paralyzed (tubocurarine) rats. rCBF and rCGU were measured in dissected tissue samples of 9 brain regions by the [14C]iodoantipyrine and [14C]2-deoxyglucose method, respectively. Electrical stimulation restricted to the medial parabrachial nucleus (PBNm, n = 5) elicited significant (P less than 0.05) reductions in rCBF in 7 out of 9 brain regions. Reductions were greatest in cerebral cortex (up to 35% in occipital cortex) and least in the white matter of the corpus callosum (23%). The effect on rCBF persisted after transection of the cervical sympathetic trunk (n = 5). In contrast, stimulation of the lateral portion of PBN (n = 5), periventricular gray (n = 5) and interestingly, the nucleus locus coeruleus (n = 5) failed to elicit similar changes in rCBF. PBNm stimulation also elicited decreases in rCGU (n = 4) in 5 out of 9 brain areas, most notably regions of cerebral cortex. The decreases in rCGU (delta rCGU) were linearly related to the decreases in rCBF (delta rCBF) according to the equation delta rCBF = 2.37 delta rCGU + 2.1 (r = 0.72; P less than 0.001). We conclude that excitation of neural pathways originating in, or passing through, PBNm elicits a widespread reduction in cerebral metabolism and secondarily in blood flow (secondary vasoconstriction). Since projections of the PBNm do not involve the entire cortex, it seems likely that the effect is mediated via inhibition of diffuse cortical projections through a subcortical site.

publication date

  • August 26, 1985

Research

keywords

  • Brain
  • Cerebrovascular Circulation
  • Glucose
  • Pons

Identity

Scopus Document Identifier

  • 0022391563

Digital Object Identifier (DOI)

  • 10.1016/0006-8993(85)91067-4

PubMed ID

  • 4041796

Additional Document Info

volume

  • 341

issue

  • 2