Immunocytochemical evidence for stimulatory control by the ventral noradrenergic bundle of parvocellular neurons of the paraventricular nucleus secreting corticotropin releasing hormone and vasopressin in rats

Alonso, G.; Szafarczyk, A.; ́zol, Monique Balmefre; Assenmacher, I

doi:10.1016/0006-8993(86)90631-1

Cited by 137 publications

(59 citation statements)

References 30 publications

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“…The results obtained from the MBH-lesioned animals suggest that the ACTH-releasing effect of ci2-antagonists may occur at a central level in the hypothalamus, and here may be also a site of oo-adrenoceptor-CRF-glucocorticoid in teraction. This suggestion is also in harmony with ana tomical evidence showing a dense noradrenergic innerva tion, and synaptic contacts between noradrenergic axons and immunoactive corticotropin-releasing factor-41 (CRF-41) and vasopressin neurons [25][26][27],…”

Section: Discussionsupporting

confidence: 82%

Adrenocorticotropin, Prolactin and Beta-Endorphin Stimulatory Actions of Alpha-2-Adrenoceptor Antagonists

et al. 1995

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We studied the effect of glucocorticoid pretreatment, mediobasal hypothalamus lesion (MBHL) and the interaction between clonidine and yohimbine in male Wistar rats to elucidate the sites and/or mechanisms of endocrine actions of α₂-antagonists. The pretreatment of 1 mg/kg s.c. dexamethasone for 4 days effectively prevented the stimulatory effect of α₂-antagonists yohimbine (5 mg/kg i.p.) and CH-38083 (1 mg/kg i.p.) on adrenocorticotropin (ACTH) secretion, while the action of these antagonists on prolactin (PRL) and β-endorphin (βE) remained unchanged. The central (i.c.v.) pretreatment of 5 µg/ rat clonidine failed to antagonize the prolactin (PRL) and βE releasing effect of yohimbine. However, it inhibited the yohimbine-induced ACTH secretion. MBHL resulted in a significant enhancement in basal plasma PRL and β-endorphin (βE) levels. But basal plasma ACTH levels have not been changed. Yohimbine failed to stimulate ACTH secretion in MBH-lesions rats, while PRL and βE response to the yohimbine was maintained in these animals. This study confirms that the α₂-antagonists stimulate ACTH secretion by a cortico-steroid-sensitive mechanism which is located centrally. In contrast, α₂-antagonists affect PRL and βE secretion via a corticosteroid-insensitive mechanism located at the periphery, possible within the pituitary gland.

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Section: Discussionsupporting

confidence: 82%

Adrenocorticotropin, Prolactin and Beta-Endorphin Stimulatory Actions of Alpha-2-Adrenoceptor Antagonists

et al. 1995

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“…However, knowing the physiological effects of CRF in the LC and knowing what the neuroanatomic projections of the LC are, as well as the behavioral effects of CRF on LC neurons in laboratory animals, one can make some reasonable deductions about the current finding.The LC is the major source of NE to the cortex, hippocampus, and cerebellum and the hypothalamic projection of the LC provides excitatory innervation to CRF neurons of the paraventricular nucleus based upon immunohistochemical evidence (Alonso et al, 1986;Petrov et al, 1993). Intracerebroventricular administration of CRF increases release of NE as measured by microdialysis probes sited in the medial hypothalamus (Lavicky and Dunn, 1993).…”

Section: Discussionmentioning

confidence: 99%

Elevated Concentrations of CRF in the Locus Coeruleus of Depressed Subjects

Bissette

Klimek

Pan

et al. 2003

Neuropsychopharmacol

132

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Research evidence that corticotropin-releasing factor (CRF) plays a role in the pathophysiology of major depressive disorder (MDD) has accumulated over the past 20 years. The elevation of lumbar cerebrospinal fluid (CSF) concentrations of CRF decreased responsiveness of pituitary CRF receptors to challenge with synthetic CRF, and increased levels of serum cortisol in MDD subjects support the hypothesis that CRF is chronically hypersecreted in at least the endocrine circuits of the hypothalamic-pituitary-adrenal (HPA) axis and may also involve other CRF brain circuits mediating emotional responses and/or arousal. One such circuit includes the excitatory CRF input to the locus coeruleus (LC), the major source of norepinephrine in the brain. Furthermore, there are now reports of decreased levels of CRF in lumbar CSF from MDD patients after symptom relief from chronic treatment with antidepressant drugs or electroconvulsive therapy. Whether this normalization reflects therapeutic effects on both endocrine-and limbic-associated CRF circuits has not yet been effectively addressed. In this brief report, we describe increased concentrations of CRF-like immunoreactivity in micropunches of post-mortem LC from subjects with MDD symptoms as established by retrospective psychiatric diagnosis compared to nondepressed subjects matched for age and sex.

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“…Because there is complete axonal transport blockade at 6 h, it is reasonable to assume that the decrease in immunostaining observed following the experimental manipulations reflects the proportional re lease of the peptide from ME terminals to the portal cir culation. Since axonal blockade is irreversible [23], at longer time periods after colchicine administration the stressor effect of colchicine becomes more evident with depletion of irCRH stored in the ME terminals and in creases in irCRH and CRH mRNA in the perikarya [15,19,25], These effects of colchicine are not seen in other hypothalamic pathways, such as the thyroid axis [ 15], and can be prevented by lesions of the ventral noradrenergic bundle, which carries most of the catecholaminergic in nervation to the PVN [11], Therefore, prolonged col chicine treatment was used as a stress model to study the nature of the catecholaminergic influence on the regula tion of hypothalamic CRH.…”

Section: Discussionmentioning

confidence: 99%

“…Electron microscopic studies have shown that CRH-containing neurons of the PVN form di rect synapses with terminals that contain tyrosine hydrox ylase and phenylethanolamine N-methyltransferase [9,10]. It has been shown that plasma ACTH levels, the re lease of irCRH from the ME, and the increase in CRHstained neurons in the paraventricular nucleus following 48 h colchicine administration, are markedly reduced by selective lesions of the ventral noradrenergic ascending bundle, which carries most of the noradrenergic and ad renergic inputs to the PVN [11,12].…”

mentioning

confidence: 99%

Participation of α<sub>1</sub>-Adrenergic Receptors in the Secretion of Hypothalamic Corticotropin- Releasing Hormone during Stress

Kiss

Aguilera²

1992

Neuroendocrinology

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The role of α₁-adrenergic receptors in the secretion of corticotropin-releasing hormone (CRH) during stress was studied by immunohistochemical analysis of the CRH content of the median eminence (ME) after intracerebroventricular (icv) administration of the αi-adrenergic agonist, methoxamine, or the antagonist, prazosin, in rats pre treated with colchicine. Immunohistochemical staining was performed by the peroxidase technique on 40 µm free-floating sections using a polyclonal antibody specific for CRH. In the first experimental model, rats were implanted with icv cannulae and adapted to the experimental conditions by daily handling and icv injection of artificial CSF. Colchicine (75 µg) was administered through the cannulae 6 h before the experiment, conditions in which axonal transport was blocked with little change in basal immunostaining. Two hours after immobilization stress or a single injection of methoxamine (100 µg, icv), there was a marked decrease in CRH immunoreactivity throughout the ME, reflecting release of the neuropeptide into the portal circulation. The decrease in CRH immunostaining following immobilization was largely prevented by icv injection of the α₁-adrenergic antagonist, prazosin. In the second experimental model, rats were sacrificed 48 h after icv colchicine injection, conditions in which colchicine acts as a stressor and causes marked depletion of irCRH from the ME. This chronic effect of colchicine was also partially prevented by administation of prazosin, 400-ng injection 5 min prior to colchicine, followed by a continuous icv mini-pump infusion of prazosin, indicating that αi-adrenergic stimulation contributes to the action of colchicine. In addition, the increase in the number and immunodensity of CRH cell bodies in the paraventricular nucleus typically observed following 48 h colchicine treatment was markedly reduced by prazosin administration, suggesting that αi-adrenergic stimulation causes an increase in peptide synthesis as well as release. These results indicate that central α₁-adrenergic mechanisms are an important component in the regulation of hypothalamic CRH secretion during stress.

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Immunocytochemical evidence for stimulatory control by the ventral noradrenergic bundle of parvocellular neurons of the paraventricular nucleus secreting corticotropin releasing hormone and vasopressin in rats

Cited by 137 publications

References 30 publications

Adrenocorticotropin, Prolactin and Beta-Endorphin Stimulatory Actions of Alpha-2-Adrenoceptor Antagonists

Adrenocorticotropin, Prolactin and Beta-Endorphin Stimulatory Actions of Alpha-2-Adrenoceptor Antagonists

Elevated Concentrations of CRF in the Locus Coeruleus of Depressed Subjects

Participation of α<sub>1</sub>-Adrenergic Receptors in the Secretion of Hypothalamic Corticotropin- Releasing Hormone during Stress

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