Effect of acetylcholine on corticotropin-releasing factor gene expression in the hypothalamic paraventricular nucleus of conscious rats.

Abstract

To examine the physiological role of cholinergic input in the regulation of CRF neurons in the paraventricular nucleus (PVN) of the hypothalamus, acetylcholine (ACh) was microinjected bilaterally into the dorsolateral border of the PVN of conscious rats. Changes in the levels of POMC messenger RNA (mRNA) in the anterior pituitary, CRF mRNA in hypothalamic tissue containing the PVN, and plasma ACTH were assessed. Plasma ACTH concentrations increased in a dose-dependent manner after ACh injection (1-100 pmol/side), reaching a peak 30 min after ACh injection and returning to baseline within 120 min. The POMC mRNA level in the anterior pituitary and the hypothalamic CRF mRNA level increased in a dose-dependent manner 120 min after ACh (0.1-10 pmol/side) injection. Intracerebroventricular pretreatment with atropine completely abolished the ACh-induced increase in plasma ACTH concentrations, whereas pretreatment with hexamethonium was without significant effect. The intracerebroventricular injection of ACh also increased plasma ACTH concentrations in a dose-dependent manner in conscious rats, but not in pentobarbital-anesthetized animals. Thus, cholinergic hypothalamic input stimulates CRF gene expression in the PVN and CRF secretion into the portal circulation under physiological conditions. The use of conscious animals is essential in elucidating the physiological roles of neurotransmitters and other modulators regulating CRF neurons.

Centrally Administered Murine-Leptin Stimulates the Hypothalamus-Pituitary- Adrenal Axis through Arginine-Vasopressin

“…or saline (10 µl/rat i.c.v. ), as previously described [30]. Then, coronal hypothalamic slices containing the PVN (400 µm in thickness) were cut with a vibrating slicer.…”

Dual-Level Afferent Control of Growth Hormone-Releasing Hormone (GHRH) Neurons in GHRH–Green Fluorescent Protein Transgenic Mice

“…A neuromodulator such as acetylcholine can orchestrate several peptidergic functions within and beyond the arcuate nucleus. For example, it can regulate GHRH (Magnan et al, 1993;Rigamonti et al, 1998), tuberoinfundibular dopaminergic neurons (Shieh and Pan, 1995;Chu et al, 2001), orexin neurons (lateral hypothalamus) (Yamanaka et al, 2003;Sakurai et al, 2005), CRH neurons (paraventricular area) (Tizabi and Calogero, 1992;Ohmori et al, 1995), and possibly SRIH neurons (periventricular area) (Giustina and Veldhuis, 1998;Müller et al, 1999). Furthermore, monosynaptic inputs to neuropeptidecontaining neurons can undergo functional remodelling (Horvath and Diano, 2004;Sternson et al, 2005), which implies the existence of an upper-level stratum of afferent control.…”

Pituitary-Adrenal Cortical Responses to Low-Dose Physostigmine and Arginine Vasopressin Administration in Normal Women and Men

“…20 , NO . 5 Pituitary-Adrenal Responses to Physostigmine and AVP 435 and Grossman 1990;Michels et al 1991;Okuda et al 1993;Whitnall 1993;Coiro et al 1995;Calogero 1995;Ohmori et al 1995), both of which stimulate ACTH secretion (Rivier et al 1990;Antoni 1993). Several studies in humans, however, suggest that the hypothalamo-pituitary-adrenal cortical (HPA) axis is activated only by doses of cholinergic agonists that produce noxious side effects, especially nausea (Carroll et al 1980;Davis et al 1982;Doerr and Berger 1983;Nurnberger et al 1983;Lewis et al 1984;Krieg et al 1987;Freeman et al 1990), and, by inference, a nonspecific stress response, nausea being a powerful stimulus to AVP release (Nussey et al 1988;Koch et al 1990;Kohl 1992).…”