Effect of Electrical Stimulation of the Neurohypophysis on ACTH Release in Rats with Hypothalamic Lesions

Makara, Gábor B.; Stark, E.; Kárteszi, M.; Fellinger, Erzsébet; Rappay, G; Szabó, Dorottya

doi:10.1159/000123081

Cited by 18 publications

(4 citation statements)

References 27 publications

(38 reference statements)

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“…The privileged role of the PVN in ad renocorticotropic regulations shown here adequately fits the concept discussed earlier of specific innervation of the external zone of the median eminence by the PVN rather than by the SON, and of this system's selective responsive ness to stress and adrenalectomy. In the same line of re search, electrical stimulation of only the PVN raised plasma corticosterone [8,9,16] and short-term PVN lesions were re ported to lower the CRF concentrations in the median emi nence as well as basal plasma ACTH levels, and to reduce the increase in plasma ACTH and corticosterone after adre nalectomy, ether stress, and electrical stimulation of the me diobasal hypothalamus [16,17]. Curiously, after longer post operative periods of up to 4 weeks, the impaired adrenal reactivity to ether stress was restored [16], a finding which may indicate that the central regulation system is extremely flexible.…”

Section: Discussionmentioning

confidence: 91%

“…In the same line of re search, electrical stimulation of only the PVN raised plasma corticosterone [8,9,16] and short-term PVN lesions were re ported to lower the CRF concentrations in the median emi nence as well as basal plasma ACTH levels, and to reduce the increase in plasma ACTH and corticosterone after adre nalectomy, ether stress, and electrical stimulation of the me diobasal hypothalamus [16,17]. Curiously, after longer post operative periods of up to 4 weeks, the impaired adrenal reactivity to ether stress was restored [16], a finding which may indicate that the central regulation system is extremely flexible. Our present data are in fairly good agreement with those of the Hungarian team, except that the depressed stress responses by plasma ACTH and corticosterone were still significant 3 weeks after PVN ablation.…”

Section: Discussionmentioning

confidence: 91%

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Adrenocorticotropic Regulations after Bilateral Lesions of the Paraventricular or Supraoptic Nuclei and in Brattleboro Rats

et al. 1982

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The circadian rhythm and ether stress responsiveness of plasma ACTH and corticosterone were explored in chronically cannulated female Sprague-Dawley rats with bilateral lesions of either the paraventricular nuclei (PVN) or supraoptic nuclei and also in female Brattleboro rats. 3 weeks after PVN lesions, the circadian ACTH rhythm had dropped by at least half. Less drastic alterations were measured for the corticosterone rhythm, and only its diurnal maximum and amplitude diminished by one third. Although the kinetics of plasma ACTH and corticosterone stimulation after ether stress were essentially normal, the peaks for both hormones, 5–15 min after stress, were only half as high as the control peaks. The effects of bilateral abolition of supraoptic nuclei on the circadian rhythm of the adrenocorticotropic system were slight, and only the diurnal minimum and mean level of ACTH dropped significantly. Intriguingly, both ACTH and corticosterone levels in rats with supraoptic lesions rose to twice the control levels after ether stress. In Brattleboro rats, neither the circadian rhythm nor stress-induced stimulation of ACTH and corticosterone differed from those of the controls. These data indicate that vasopressin is not essential for either of the regulations of the adrenocorticotropic system. The production of corticotropin-releasing factor (CRF) involved in both types of regulation clearly originates, at least partly, from the PVN area and no significant contribution is made by the region of the supraoptic nuclei, a finding which conforms to neuroanatomical data. However, it is not yet clear whether the PVN area is the site of origin of the recently characterized 41 amino-acid CRF or of other CRF fractions distinct from vasopressin.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 91%

Adrenocorticotropic Regulations after Bilateral Lesions of the Paraventricular or Supraoptic Nuclei and in Brattleboro Rats

et al. 1982

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“…Furthermore, it has been proposed that the paraventricular nuclei might be of significance in the regulation of the release of CRF, from the neurohypophysis at least [16]. In our animals bearing AHD as well as CHD, the neural ties between the paraventricular nuclei and the mediobasal hypothalamus are transected, as is the lateral retrochiasmatic area.…”

Section: Discussionmentioning

confidence: 99%

Adrenocortical Responses following Limbic Stimulation in Rats with Hypothalamic Deafferentations

1982

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In view of the involvement of limbic structures in adrenocortical regulation, their afferent projections to the mediobasal hypothalamus were investigated. Electrical stimulation via chronically implanted electrodes in the dorsal hippocampus, the medial septal nuclei, the basolateral amygdala or the mesencephalic reticular formation all elicited a significant increment in plasma corticosterone levels in adult male rats under pentobarbital anesthesia. Complete or anterior hypothalamic deafferentation blocked these adrenocortical responses completely, and posterior hypothalamic deafferentation attenuated them to a marked extent. In animals with bilateral medial forebrain bundle lesions, hippocampal stimulation had no effect upon plasma corticosterone levels. These studies demonstrate that extrahypothalamic effects upon adrenocortical secretion are neurally mediated, and that the integrity of neural pathways impinging upon the mediobasal hypothalamus from both the rostral and the caudal directions is essential to these effects.

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“…Following osmotic stimulation of AVP secretion, plasma ACTH levels increased in horses [3]and a significant increase in CRH-stimulated ACTH release was shown in humans [4]. In rats, electrical stimulation of the neural lobe has been shown to increase plasma ACTH levels [33]and recent studies demonstrated an impairment in the ACTH secretory response to various stimuli in neurolobectomized rats [34]. Moreover, Elias et al [35]have recently reported that an acute increase in plasma osmolality amplified ACTH and cortisol responses to CRH in patients with central diabetes insipidus.…”

Section: Discussionmentioning

confidence: 99%

Combined Hypervolemia and Hypoosmolality Alter Hypothalamic-Pituitary-Adrenal Axis Response to Endotoxin Stimulation

et al. 1999

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Changes in corticotropin (ACTH) and glucocorticoid secretion have been described during disturbances of body fluid homeostasis and attributed to alterations in arginine vasopressin (AVP) secretion from magnocellular hypothalamic neurons. In order to further characterize the mechanisms involved in the interactions between body fluid alterations and pituitary adrenal function, we manipulated osmolality and volemia in sheep under stimulation of the pituitary-adrenal axis by acute injection of endotoxin. We have recently shown that endotoxin injection induces a long-lasting release of both corticotropin releasing hormone (CRH) and AVP into hypophysial portal blood, and an early stimulation of AVP secretion into peripheral vessels, thus suggesting a joint activation of magnocellular and parvocellular neurons of the PVN. We used the same experimental model to investigate the effect of combined volume loading and plasma dilution (achieved by 1-deamino-8-D-arginine (dDAVP) administration together with infusion of 2 liters of 2.5% glucose solution) on CRH, AVP, ACTH and cortisol responses to endotoxin stimulation. In volume-loaded animals, ACTH and cortisol responses to endotoxin were significantly blunted and we observed a parallel decrease in portal CRH and jugular and portal AVP levels. These data show that hypoosmolality and/or hypervolemia reduce(s) ACTH and cortisol response to stress in sheep as in other species. They strongly suggest that this reduction in ACTH and cortisol responses to endotoxin involve not only magnocellular hypothalamic neurons secreting AVP, as usually assumed, but also PVN parvocellular neurons secreting both CRH and AVP.

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Effect of Electrical Stimulation of the Neurohypophysis on ACTH Release in Rats with Hypothalamic Lesions

Cited by 18 publications

References 27 publications

Adrenocorticotropic Regulations after Bilateral Lesions of the Paraventricular or Supraoptic Nuclei and in Brattleboro Rats

Adrenocorticotropic Regulations after Bilateral Lesions of the Paraventricular or Supraoptic Nuclei and in Brattleboro Rats

Adrenocortical Responses following Limbic Stimulation in Rats with Hypothalamic Deafferentations

Combined Hypervolemia and Hypoosmolality Alter Hypothalamic-Pituitary-Adrenal Axis Response to Endotoxin Stimulation

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