Nitric oxide synthase-containing neural processes on large cerebral arteries and cerebral microvessels. Academic Article uri icon

Overview

abstract

  • We studied whether neural processes containing nitric oxide synthase (NOS) are associated with large cerebral arteries and/or intraparenchymal microvessels. The presence of NOS-positive nerves on large cerebral arteries was examined in whole-mount preparations processed for NADPH diaphorase histochemistry, a procedure that stains NOS-containing neurons. The association between NOS-containing neural processes and intracerebral microvessels was studied by electron microscopy in ultrathin brain sections reacted with antibodies against NOS. A dense perivascular plexus of NADPH diaphorase positive axons was observed in the anterior portion of the circle of Willis and its branches while in the basilar artery the innervation was less dense. Lesions of the major sources of perivascular innervation of the cerebral arteries indicated that these nerve fibers arise from the sphenopalatine ganglia. Within the brain parenchyma, NOS immunoreactivity was observed in dendrites and axonal terminals closely associated with the basal lamina of arterioles and capillaries. We conclude that NOS-containing nerves of peripheral origin innervate large cerebral arteries while NOS-containing neural processes of central origin, especially dendrites, are closely associated with cerebral arterioles and capillaries. The presence of NOS in perivascular dendrites raises the possibility that these structures are a major source of NO during neural activity. These findings, collectively, provide morphological evidence supporting the hypothesis that NOS neurons participate in the mechanisms that match neural activity to cerebral blood flow.

publication date

  • March 19, 1993

Research

keywords

  • Amino Acid Oxidoreductases
  • Cerebral Arteries
  • Cerebrovascular Circulation

Identity

Scopus Document Identifier

  • 0027450259

Digital Object Identifier (DOI)

  • 10.1016/0006-8993(93)91583-e

PubMed ID

  • 7681722

Additional Document Info

volume

  • 606

issue

  • 1