alpha1B adrenoceptors in rat paraventricular nucleus overlap with, but do not mediate, the induction of c-Fos expression by osmotic or restraint stress.

A role has been suggested for hypothalamic alpha1 adrenoceptors in the acute stress-induced activation of the hypothalamic-pituitary-adrenal axis. Using a polyclonal antiserum against the rat alpha1B adrenergic receptor protein, we have demonstrated alpha1B receptor immunoreactivity in neurons and especially in punctate cell processes in the rat paraventricular nucleus. The distribution of alpha1B receptor immunoreactivity overlapped in part with the distributions of c-Fos immunoreactivity induced in the paraventricular nucleus by either restraint stress or hypertonic saline administration. However, intraperitoneal pretreatment with the alpha1 receptor antagonist prazosin (0.5 or 5.0 mg/kg) failed to attenuate stress-induced c-Fos expression in the paraventricular nucleus. Prazosin also failed to attenuate the secretion of corticosterone following restraint stress. Thus, we conclude that neither acute secretory activity nor activation of gene transcriptional responses mediated by c-Fos in the hypothalamic pituitary adrenal axis following these stressors are dependent upon hypothalamic alpha1 adrenergic receptors.