Format

Send to

Choose Destination
See comment in PubMed Commons below
Brain Res. 1991 Feb 15;541(2):206-15.

Viscerotopic organization of neurons subserving hypotensive reactions within the midbrain periaqueductal grey: a correlative functional and anatomical study.

Author information

1
Department of Anatomy, University of Sydney, N.S.W. Australia.

Abstract

Microinjection of the excitatory amino acid D,L-homocysteic acid (40 nmol, in 200 nl) made into the ventrolateral part of the caudal half (A2.5-P1.5) of the midbrain periaqueductal gray (PAG) of the decerebrate cat evoked a hypotensive reaction associated with a slowing of the heart and a decrease in either external iliac or renal vascular resistance. The decrease in iliac vascular resistance was elicited from the pretentorial portion (A2.5-A0.6) of the PAG hypotensive area, whereas the decrease in renal vascular resistance was elicited from the subtentorial portion (A0.6-P1.5). Anatomical experiments using the method of retrograde transport of rhodamine-labelled microspheres or wheat germ agglutinin-horseradish peroxidase demonstrated topographically organized projections from the ventrolateral PAG to the subretrofacial (SRF) pressor nucleus in the rostral ventrolateral medulla. The pretentorial part of the ventrolateral PAG projected mainly to the caudal part of the SRF nucleus, which preferentially controls iliac vascular resistance. The subtentorial part of the ventrolateral PAG projected mainly to the rostral part of the SRF nucleus, which preferentially controls renal vascular resistance. Taken together, these findings suggest: (i) that neurons within the ventrolateral PAG are viscerotopically organized; and (ii) that their hypotensive function may be mediated by an inhibition of SRF pressor neurons. The results are discussed in relation to the recently described PAG hypertensive area which also is viscerotopically organized and projects to the SRF nucleus.

PMID:
2054638
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center