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I Assenmacher

Publications and source records attributed to I Assenmacher.

At least 55 records · Page 3Linked to original sources
PubMed1987

The corticotropin-releasing factor release in rat hypophysial portal blood is mediated by brain catecholamines.

In order to study the involvement of the hypothalamic corticotropin-releasing factor (CRF) in catecholamine-induced adrenocorticotropin (ACTH) secretion, we have measured CRF levels in rat hypophysial portal blood (HPB) after the pharmacological destruction of the ventral noradrenergic bundle (VNAB), using 6-hydroxydopamine (6-OHDA) stereotaxically injected into the VNAB. CRF levels in HPB were measured by radioimmunoassay, and the effects of 6-OHDA injection were controlled by the determination of catecholamine concentrations in the total hypothalamus. VNAB lesions induced a dramatic decrease in norepinephrine and epinephrine hypothalamic concentration. The CRF levels in HPB were also significantly reduced. These results suggest that central catecholamines exert a direct stimulatory control on the CRF release and play a major role in stress-induced ACTH secretion.

Adrenocorticotropic Hormone↗
PubMed1987

Further evidence for a central stimulatory action of catecholamines on adrenocorticotropin release in the rat.

Catecholamines may stimulate ACTH secretion during stress. To investigate the nature and site of such an action, plasma ACTH was measured in four groups of unanesthetized adult female rats with an indwelling carotid cannula. Sequential 300-microliter blood samples were taken 60 min, 30 min, and immediately before an intracerebroventricular (icv) infusion of 2.5 microliter adrenaline or noradrenaline and 5, 15, 45, 60, and 120 min after the infusion. The four groups were: 1) intact rats; 2) rats infused 7 days after undergoing a discrete bilateral lesion of the ventral noradrenergic ascending bundle caused by 6-hydroxydopamine, which depleted their hypothalamic adrenaline and noradrenaline levels by 90% and 80%, respectively; 3) rats infused 30 min after pretreatment via the icv route with either prazosin or propranolol; and 4) rats infused 16 and 2 h after two successive intracarotid injections of an anti-rCRH-41 serum. In another group, the effects of icv catecholamine administration were compared with those of an intracerebral (ic) microinfusion close to a single paraventricular nucleus (PVN). Finally, in two additional groups blood was sampled at the above-mentioned times before and after a 2-min ether inhalation by intact rats or prazosin- and/or propranolol-pretreated rats. In the intact rats (group 1), a stress-like stimulatory dose response was noted after both adrenaline and noradrenaline infusions, with a half-maximal effect at concentrations of about 0.6 nmol and a maximal effect at 2.7 nmol or more. At maximally effective doses, adrenaline was significantly more active than noradrenaline. In the rats with ventral noradrenergic ascending bundle lesions (group 2), 2.7 nM adrenaline or noradrenaline stimulated ACTH release as in the controls without lesions. In group 3, prazosin blocked the ACTH responses to both adrenaline and noradrenaline, whereas propranolol only blocked the response to adrenaline. In group 4, i.e. rats pretreated with an anti-rCRH-41 serum, the amplitude of the ACTH surge after icv adrenaline or noradrenaline infusion was halved. A unilateral ic catecholamine microinfusion next to the PVN (half the icv dose given in group 1) led to a rapid ACTH release that peaked at half the response measured in the icv infused rats. Ether stress-induced ACTH release was decreased by 50-60% after icv pretreatment with 1 or 10 micrograms prazosin, 1 or 6.5 micrograms propranolol, or a combined dose comprising 1 microgram of both. The following conclusions were reached.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenocorticotropic Hormone↗
PubMed1987

[Secretion of TRH in the third cerebral ventricle during acute cold exposure in the unanesthetized rat. Effect of alpha-adrenergic drugs].

The concentrations of TRH in the cerebrospinal fluid (CSF) of the 3rd ventricle were measured with push-pull cannulae in 12 conscious rats. In the basal state the level of TRH in 15 min perfusion samples (210 microliters) were low (2.69 +/- 0.05 pg) and mostly undetectable with the RIA available. However, 70 to 80 min after exposure of the rats to cold (4 degrees C) a short lived but significant rise of TRH was measured in all animals. Post cold peaks amounted to 5.15 +/- 0.5 pg/15 min (p less than 0.001 vs baseline levels). This cold response to CSF TRH was influenced neither by pretreatment of rats with the alpha-adrenergic blocker phentolamine, administered i.p. (40 mg/kg) or i. c. v. (10(-5) M) 1 h before cold exposure, nor by i. c. v. infusion of the alpha 1-adrenergic blocker prazosin (10(-5) M). In rats receiving the blockers the post-cold TRH peaks were 6.76 +/- 1.61 pg/15 min and 5.70 +/- 0.70 pg/15 min, respectively. The possible origin of CSF TRH and the resistance of its cold stimulation to alpha-adrenergic blockers, compared to TRH released into the median eminence are discussed.

Animals↗
PubMed1987

[Adrenergic activation of the liberation of corticotropin-releasing hormone (CRH41) in the median eminence of unanesthetized rats].

To shed light on the persistent controversy concerning the role of central adrenergic systems in the corticotropic axis, we measured the effects of adrenaline on the release of IR-rCRH41 into a push-pull cannula stereotaxically implanted in the median eminence. Eight days before experimentation, the cannula was implanted, under deep anesthesia, at which time a standard cannula was additionally placed in the lateral ventricle (i.c.v.). The rats were not anesthetized during the main experiment. An i.c.v. injection of 5 microliter of solvent only slightly affected the release of CRH41, whereas an i.c.v. infusion of 1.4 micrograms adrenaline bitartrate under the same conditions led to an instantaneous, but short-lived, 8-fold rise in the CRH41 release above baseline. The data provide the first demonstration of a central stimulatory effect of adrenaline on the secretory activity of CRH41 producing neurons, in unanesthetized, free-moving rats.

Animals↗
PubMed1986

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.

The regulation, by catecholaminergic innervation, of parvocellular neurons of the paraventricular nuclei (PVN) secreting corticotropin releasing hormone (CRH) and vasopressin (Vp) was studied by immunocytochemical visualization of both neurohormones in control rats and in rats given discrete injections of 6-hydroxydopamine in the ventral noradrenergic ascending bundle (VNAB). In both groups, the changes in immunostaining intensities observed in axon terminals of the external median eminence and in PVN perikarya 48 h after a blockade of axoplasmic transport by intraventricular injections of colchicine, served as an index for hormonal release and synthesis. In controls, this treatment induced a strong decrease in CRH and Vp immunoreactivity within the terminals, together with intense labeling of PVN perikarya containing CRH. By contrast, bilateral VNAB lesions strikingly inhibited both the colchicine-induced reduction of the CRH and Vp immunoreactivity in axons and the accumulation of CRH in the perikarya. Unilateral VNAB lesions induced similar alterations but these were restricted to the ipsilateral PVN and median eminence. Comparison of these immunocytochemical data with earlier physiological observations on the effects of VNAB lesions on ACTH secretion indicates that the catecholaminergic afferents to the PVN conveyed by the VNAB stimulate the release and the synthesis of CRH and Vp by parvocellular neurons projecting into the external median eminence.

Afferent Pathways↗
PubMed1986

Radioautographic evidence that axons from the area of supraoptic nuclei in the rat project to extrahypothalamic brain regions.

The axonal efferents of neurons of the supraoptic nucleus area were studied by radioautography in the rat after discrete stereotaxic injections of [3H]leucine into this nucleus. Beside a densely labeled pathway running from the nucleus to the posterior pituitary through the internal median eminence, several of the visualized labeled axonal bundles were found to project into various extrahypothalamic regions, including the olfactory bulb, the cortex, the lateral habenula, the subcommissural organ, the amygdala, the mammillary bodies and the locus coeruleus. These results suggest that part of the vasopressin- or oxytocin-containing perikarya located in the supraoptic nucleus constitute the cells of origin of axons which also contain these peptides and which have already been shown to be present in the above extrahypothalamic areas. This also implies that, like the paraventricular nucleus, the supraoptic nucleus is also involved in central extrahypothalamic regulations.

Animals↗
PubMed1986

Effects of morphine on cold-induced TRH release from the median eminence of unanesthetized rats.

The effect of morphine perfusion into the median eminence on cold-induced TRH secretion was studied in unanesthetized rats by push-pull cannulation. Perfusion with 10(-6)M morphine blocked the cold-induced TRH peak occurring about 40 min after the transfer of rats from 24 degrees C to 4 degrees C. This inhibition by morphine was blunted by concomitant administration of naloxone (10(-6)M or 10(-5)M), but naloxone alone had no effect on either basal or cold-induced TRH release. We conclude that specific opiate receptors may be located on TRH nerve endings in the ME, and that endogenous opiates may not have any physiological role in the cold-induced TRH response, at least during the two hours that follow cold exposure.

Animals↗
PubMed1986

Immunoreactivity of hypothalamo-neurohypophysial neurons which secrete corticotropin-releasing hormone (CRH) and vasopressin (Vp): immunocytochemical evidence for a correlation with their functional state in colchicine-treated rats.

The specific immunoreactivity of neurons containing corticotropin-releasing hormone (CRH) or vasopressin (Vp) was studied both centrally, in the parvocellular division of the paraventricular nucleus, and distally, in the external median eminence. Control rats were compared with adrenalectomized rats and with animals supplemented with corticosterone or dexamethasone, either without additional treatment, or 24, and 48 h after an intraventricular injection of colchicine. In all groups of animals, colchicine induced a progressive and parallel decrease in both CRH and Vp immunoreactivity within the axons of the external median eminence. A semi-quantitative estimation of this axonal immunostaining showed that the decrease was clearly correlated with the axons' releasing activity according to the different functional states of the adrenocorticotropic system. Increased rates of hormonal release induced by adrenalectomy could be seen in the accelerated depletion of axonal immunoreactivity whereas corticosteroid supplementation had the opposite effect. Correspondingly, the progressive intensification of the CRH and Vp immunoreactivity within the perikarya following colchicine treatment was further markedly enhanced in adrenalectomized rats and diminished after corticosteroid supplementation. Taken together, these data suggest that in these neurons, perikaryal hormone synthesis may be closely related to the releasing activity of the axon terminals. They further point to appropriate colchicine treatment as useful tool for evaluating the functional state of CRH and Vp neurons of the parvocellular paraventricular nucleus under various experimental conditions.

Animals↗
PubMed1986

Plasma ACTH and corticosterone responses to limbic kindling in the rat.

Changes in plasma ACTH and corticosterone concentrations were measured in individual cannulated rats at stages 1 and 5 of limbic kindling induced by electrical stimulation of the basolateral amygdala or the dorsal hippocampus. At both stages, a stimulation of either structure produced swift surges, first of ACTH and then of corticosterone. At stage 5 of hippocampal stimulation, ACTH baseline concentrations were four times higher than in the controls. The results are discussed in relation to the central control of the adrenocorticotropic system and to the neuroendocrine correlates of the kindling process.

Adrenocorticotropic Hormone↗
PubMed1986

The endocrine control of reproduction and molt in male and female emperor (Aptenodytes forsteri) and adelie (Pygoscelis adeliae) penguins. I. Annual changes in plasma levels of gonadal steroids and LH.

Changes in plasma LH, testosterone, and estrogens were investigated throughout reproduction and molt in free-living male and female emperor (Aptenodytes forsteri) and adelie (Pygoscelis adeliae) penguins. In both sexes and species, plasma LH and gonadal steroids were severalfold above basal level at the time of arrival on the breeding grounds, suggesting that environmental cues (especially decreasing daylength in emperors) rather than mating and courting primarily stimulate gonadal development and reproduction. In both species a marked increase in plasma LH (both sexes), testosterone (males), and estrogens (females) corresponded with the time of maximum gonadal size, and peak values were obtained at the time of copulation, i.e., in emperors about 10-15 days prior to egg laying. In females, plasma LH and estrogens dropped to low levels between copulation and egg laying. Similarly, following copulation in males plasma testosterone fell to lower levels that in emperors were maintained during incubation and brooding of the non-thermally emancipated chick. Plasma LH levels followed the same trend as testosterone, falling after copulation and falling further prior to molt. Though lower than at copulation, plasma LH was higher in incubating (males) and brooding (males and females) emperors than during rearing of the thermally emancipated chicks, suggesting that plasma LH might be related to incubating, brooding, and territorial behavior. In male and female emperors and in male adelies, plasma gonadal steroids and LH were at basal levels throughout molt.

Animals↗
PubMed1986

Effects of castration and thyroidectomy on the annual biological cycles of the edible dormouse Glis glis.

The annual cycle of hibernation, body weight, and plasma testosterone and thyroxine levels were compared in 7 orchidectomized and 16 intact dormice under natural conditions, and in 21 thyroidectomized and 23 intact dormice exposed to a 12-hr light and 12-hr darkness photoperiod under natural temperatures. Hibernation was not affected by either orchidectomy or thyroidectomy, nor did thyroidectomy alter the annual body weight cycle, which, however, was obliterated by orchidectomy. As regards endocrine cycles, orchidectomy had no significant effects on the annual thyroxine cycle, whereas thyroidectomy obliterated the annual testosterone cycle, which was replaced by short-lived, infradian plasma thyroxine cycles. As the latter resembled the fluctuations previously observed in intact animals exposed to constant ambient temperatures, it is proposed that in edible dormice, the annual thyroid cycle, which is thermoperiodically entrained, in turn entrains the testosterone cycle.

Animals↗
PubMed1986

Probable extrapituitary source of the immunoreactive prolactin measured in the cerebrospinal fluid of unanesthetized rats by push-pull cannulation of the 3rd ventricle.

The dynamic pattern of the immunoreactive prolactin (PRL) concentrations in the cerebrospinal fluid (CSF) of the 3rd ventricle was explored by push-pull cannulation during either stimulation or blocking of PRL production in the plasma, which itself was sampled by chronic cannulation of the carotid. Some of the results were compared to the PRL concentrations in CSF samples obtained by 3rd-ventricle puncture. Ether stress, which induced a 4- to 6-fold rise in plasma PRL, altered neither the pulsatile circhoral pattern of PRL in the CSF nor the mean level and amplitude of its pulses. However, the sustained intense hyperprolactinemia induced by haloperidol increased the mean PRL level in the CSF and possibly its pulse rate. Surprisingly, hypophysectomy, which suppressed production of PRL in the plasma, did not alter its baseline level or cycling pattern in the CSF. The possibility that tuberal adenohypophysial cells and/or CNS prolactinergic neurons supply the CSF with PRL is discussed.

Animals↗
PubMed1985

Reserpine inhibits release of vasopressin from the neural lobe of the pituitary in dehydrated rats.

The effects of reserpine on the osmotically induced release of pituitary vasopressin were studied (i) by measuring the urinary excretion and the vasopressin content of the neural lobe of pituitary, and (ii) by examining the ultrastructural morphology of axons in the neural lobe of dehydrated rats. After water deprivation for two days, control rats displayed characteristic antidiuretic response including a 75% reduction of urinary excretion and a six-fold decrease in vasopressin content of the neural lobe associated with a dramatic depletion of neurosecretory granules in corresponding axons. In contrast, when they received two dialy injections of reserpine, animals dehydrated for two days showed both urinary excretion and vasopressin contents in the neural lobe that remained at levels comparable to those measured in the normally hydrated rats. Additionally, neural-lobe axons of such dehydrated, reserpine-treated rats displayed a normal amount of neurosecretory granules. These data indicate that reserpine inhibits release of vasopressin from the neural lobe and favour the concept of a facilitatory role of the catecholaminergic innervation in the control of hypothalamo-neurohypophysial vasopressin-secreting neurons.

Animals↗
PubMed1985

Electron microscopic immunocytochemical study of somatostatin neurons in the periventricular nucleus of the rat hypothalamus with special reference to their relationships with homologous neuronal processes.

The neurons containing somatostatin in the rat periventricular nucleus were studied by using a modified electron microscopic immunocytochemical technique that improves both the penetration of immunoreagents into unembedded immunostained tissues and the preservation of ultrastructural morphology. Inside perikarya and dendrites, immunostaining was not only associated with neurosecretory granules but also with ribosomes and saccules of the cis face of the Golgi apparatus. In the axonal profiles found in this region the labeling was observed both on neurosecretory granule cores and on the limiting membrane of small synaptic-like vesicles. Throughout the periventricular nucleus, both non-synaptic and synaptic relationships were shown between labeled neurons. Non-synaptic relationships mainly consisted of direct apposition of the membranes of neighboring neurons by dendrosomatic, somasomatic or dendrodendritic contacts. These labeled perikarya and dendrites were also synaptically contacted by labeled axonal endings containing numerous aggregated synaptic-like vesicles. The physiological significance of the synaptic and non-synaptic relationships between somatostatinergic neurons is discussed in terms of possible synchronization between homologous neurons of the somatostatin neuroendocrine system and control of these neurons by a central ultra-short loop feedback mechanism.

Animals↗
PubMed1985

Diurnal-stimulated and stress-induced ACTH release in rats is mediated by ventral noradrenergic bundle.

Female rats were bilaterally injected with 3 micrograms of 6-hydroxydopamine (6-OHDA) dissolved in 0.2 microliter saline, via a glass micropipet stereotaxically implanted into the ventral noradrenergic-ascending bundle (VNAB). This bundle conveys most of the catecholaminergic innervation to the paraventricular nuclei and originates from the locus coeruleus and from two medullary groups of neurons (A1 and A2). Two weeks after injection, and 1 wk after the subsequent implantation of an arterial cannula, serial blood samples were taken from each rat over a 36-h period for assay of basal secretion patterns of ACTH and corticosterone (C) by radioimmunoassay and radiocompetition, respectively. Other blood samples were collected at short intervals over a 2-h period to explore the stress-ether responses of both hormones. Effects of 6-OHDA injections on catecholaminergic innervation were attested by the striking decrease in the histofluorescence of hypothalamic catecholamines and by the 86% drop in the hypothalamic noradrenaline concentrations measured by high-performance liquid chromatography at constant dopamine titers. Compared with control, sham-lesioned rats, pharmacological destruction of the VNAB by 6-OHDA led to 1) obliteration of the circadian patterns for ACTH and C and the emergence in their place of ultradian fluctuations of reduced amplitude above base-line levels and 2) 80% inhibition of the ACTH stress response which correlated with a short-lived, depressed C response. These results are discussed within the framework of the controversial literature on the mechanisms by which catecholamines may control corticotropic function.

Adrenocorticotropic Hormone↗
PubMed1985

[Passive immunization with an anti-oCRF41 immune serum inhibits the circadian increase of plasma ACTH in rats].

For 24 hrs. after i.v. injection of 1 ml of an undiluted immune serum raised against oCRF41, the diurnal surge of plasma ACTH dropped to a short-lived limited rise above baseline level. On the second day after injection, the ACTH level in treated rats rose to a subnormal level, although both plasma dilution of the immune serum and its binding capacity in the plasma remained unchanged throughout the experiment. Plasma corticosterone, on the contrary, displayed a normal circadian rhythm during the entire experiment. However, in animals given a second injection of 0.5 ml oCRF41 immune serum 32 hrs. after the first, both ACTH and corticosterone titers fell rapidly below their circadian minimal levels in controls. Concomitantly, the concentration of immune serum in the peripheral plasma, and its capacity to bind to oCRF, rose by 50%. The major role of CRF41 as a diurnal trigger of the circadian rhythm of ACTH is discussed, as well as the limits of passive immunization.

Adrenocorticotropic Hormone↗
PubMed1985

[Evaluation of the inhibitory effect of circulating corticosteroids on circadian stimulated and stress induced secretion of ACTH in rats].

Male rats were bilaterally adrenalectomized in order to measure the extent of inhibition exerted by endogenous corticosteroids on both basal ACTH secretion along its circadian rhythm and ether-stress induced ACTH secretion. In intact controls, plasma ACTH levels at the circadian maximum exceeded by 4 times the circadian minimum, and ACTH response 15 min after ether-stress surpassed the circadian minimum by 20 times. In adrenalectomized rats, the daily minimum was 8 times that of the controls. Nevertheless the circadian maximum was 3 times above the rhythm's minimum, while the maximal stress response (15 min) surpassed the circadian minimum by 8 times. In adrenalectomized rats supplemented with a solid source of corticosterone inducing a stable plasma corticosterone level equivalent to the controls' circadian minimum (3 micrograms/100 ml), the ACTH rhythm still fluctuated twice as high as in intact controls. The tonic feed-back inhibition exerted by endogenous corticosteroids on ACTH secretion appeared thus significantly stronger than the GABAergic inhibition to the corticotropic system which was previously studied under similar standard conditions.

Adrenalectomy↗