Immunohistochemical detection of Fos, the protein product of the immediate-early gene c-fos, was evaluated as a functional marker of central neurons sensitive to a change of blood pressure/blood volume. Controlled hemorrhage and infusion of the hypotensive agent nitroprusside or hydralazine induced the appearance of Fos-immunoreactivity (Fos-IR) in several prominent groups of central neurons: the piriform cortex, bed nucleus of the stria terminalit, islands of Calleja, subfornical organ, central nucleus of the amygdala, parabrachial nucleus, supraoptic and paraventricular nuclei, pontine A5, locus ceruleus, ventrolateral medulla, the nucleus of the solitary tract, area postrema, and intermediolateral cell column in the spinal cord. Elevation of blood pressure by infusion of phenylephrine caused the appearance of Fos-IR in fewer groups of neurons: the bed nucleus of the stria terminalis, central nucleus of the amygdala, parabrachial nucleus, the nucleus of the solitary tract and area postrema. The differential distribution of Fos neurons in hypotensive versus hypertensive animals underscores the potential application of Fos as a metabolic marker in identifying a network of neurons responding to a specific cardiovascular challenge. Further, simultaneous characterization of the transmitter phenotype of Fos-containing neurons offers an additional advantage of this method over other conventional tract-tracing techniques.

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