Activation of brain neurons following central hypervolaemia and hypovolaemia: Contribution of baroreceptor and non-baroreceptor inputs

Citation
Pd. Potts et al., Activation of brain neurons following central hypervolaemia and hypovolaemia: Contribution of baroreceptor and non-baroreceptor inputs, NEUROSCIENC, 95(2), 2000, pp. 499-511
Citations number
65
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROSCIENCE
ISSN journal
03064522 → ACNP
Volume
95
Issue
2
Year of publication
2000
Pages
499 - 511
Database
ISI
SICI code
0306-4522(2000)95:2<499:AOBNFC>2.0.ZU;2-K
Abstract
In the present study we have used the detection of Fos, the protein product of c-fos, to determine the distribution of neurons in the medulla and hypo thalamus that are activated by changes in central blood volume. Experiments were conducted in both barointact and barodenervated conscious rabbits, to determine the contribution of arterial baroreceptors to the pattern of Fos expression evoked by changes in central blood volume, induced either by in travenous infusion of an isotonic modified gelatin solution, or by partial occlusion of the vena cava. These procedures resulted in a significant incr ease and decrease, respectively, in right atrial pressure over a 60 min per iod. In control experiments, barointact and barodenervated rabbits were sub jected to the identical procedures except that no changes in central blood Volume were induced. In comparison with the control observations, central h ypervolaemia produced a significant increase in the number of Fos-immunorea ctive neurons in the nucleus tractus solitarius, area postrema, the caudal, intermediate and rostral parts of the ventrolateral medulla, supraoptic nu cleus, paraventricular nucleus, arcuate nucleus, suprachiasmatic nucleus an d median preoptic nucleus. The overall pattern of Fos expression induced by central hypervolaemia did not differ significantly between barointact and barodenervated animals. Similarly, the overall pattern of Fos expression in duced by central hypovolaemia did not differ significantly between barointa ct and barodenervated animals, but did differ significantly from that produ ced by hypervolaemia. In particular, central hypovolaemia produced a signif icant increase in Fos expression in the same regions as above, but also in the subfornical organ and organum vasculosum lamina terminalis. In addition , compared with central hypervolaemia, hypovolaemia produced a significantl y greater degree of Fos expression in the rostral ventrolateral medulla and supraoptic nucleus. Furthermore, double-labelling for tyrosine hydroxylase immunoreactivity demonstrated that neurons in the Ventrolateral medulla th at expressed Fos following hypovolaemia were predominantly catecholamine ce lls, whereas following hypervolaemia they were predominantly non-catecholam ine cells. Finally, double-labelling for vasopressin immunoreactivity demon strated that the number of Fos/vasopressin immunoreactive cells in the supr aoptic nucleus was approximately 10 times greater following hypovolaemia co mpared with hypervolaemia, but there were very few such double-labelled neu rons in the paraventricular nucleus in response to either stimulus. The results demonstrate that central hypervolaemia and hypovolaemia each in duces reproducible and specific patterns of Fos expression in the medulla a nd hypothalamus. The degree and pattern of Fos expression was unaffected by arterial baroreceptor denervation, indicating that it is primarily a conse quence of inputs from cardiac receptors, together with an increase in the l evel of circulating hormones such as atrial natriuretic peptide, angiotensi n II or vasopressin. Furthermore, the pattern of Fos expression produced by central hypervolaemia and hypovolaemia is distinctly different from that e voked by hypertension and hypotension, respectively [Li and Dampney (1994) Neuroscience 61, 613-634], particularly in hypothalamic regions. These find ings therefore indicate that the central pathways activated by changes in b lood volume are, at least in part, separate from those activated by changes in arterial pressure. (C) 1999 IBRO. Published by Elsevier Science Ltd.