Search PubMed⌕ Search

Biomedical subjects

A Szafarczyk

Publications and source records attributed to A Szafarczyk.

At least 37 records · Page 2Linked 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↗
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

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↗
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↗
PubMed1983

Acute and delayed effects of picrotoxin on the adrenocorticotropic system of rats.

To investigate the possible effect of GABA on the corticotropic system, the potent GABA antagonist picrotoxin was injected into two groups of 14 female rats at 07.00 h and 19.00 h, respectively. A single subconvulsive I.p. injection dramatically raised plasma ACTH and corticosterone, and thereafter suppressed the circadian rhythm of ACTH, but not of corticosterone, for 24 h in the group injected at 07.00 h and for 48 h in the one injected at 19.00 h and increased mean hormonal levels. Results are discussed in the light of the possibility that inhibition by the GABAergic system and stimulation by the serotoninergic system might be components of the mechanism controlling the circadian rhythm of ACTH.

Adrenocorticotropic Hormone↗
PubMed1983

CNS control of the circadian adrenocortical rhythm.

The effects of various CNS impairments on the circadian rhythm of plasma ACTH and Corticosterone (C) were studied in individual cannulated female Sprague-Dawley rats. Pinealectomy had no effect whatever the light perception (intact or blinded rats). Bilateral ablation of paraventricular nuclei did not obliterate the hormonal rhythms, although the rhythms' amplitude were markedly depressed. On the other hand, destruction of suprachiasmatic nuclei (SCN) or systemic blockade of the serotoninergic (5-HT) system by pCPA blocked ACTH rhythm at baseline levels, although circadian or ultradian fluctuations with normal amplitudes persisted for C. Similar effect was observed in several blinded rats with raphe lesions suppressing 5-HT innervation of SCN. Daily 5-HTP injections, if given 4 h after dawn restored normal ACTH rhythm. The respective role of related structures in the rhythms' control will be discussed.

Adrenal Cortex↗
PubMed1983

[Persistance of phase-coupling between the circadian rhythms of hypophyseal hormones in free-running rats].

The circadian rhythms in plasma ACTH, TSH, LH and PRL were explored in sighted or blind, spayed and estrogen-implanted rats. A marked endogenous circadian rhythmicity was shown to persist in the blind animals for the 4 endocrine rhythms. The endogenous rhythms also kept very close reciprocal phase relationship as in the synchronized state, and they were peaking almost simultaneously, after 60 d. of free-running. Finally the endogenous hormonal rhythm maintained their usual phase relationships with the endogenous activity rhythm, so that the circadian phase of increased hormonal secretion coincided with the circadian resting phase of the sleep/wake rhythm. These results are discussed in the light of the alternate theory of one vs multiple but phase-locked circadian pacemakers driving endocrine and behavioral circadian rhythms.

Adrenocorticotropic Hormone↗
PubMed1983

[Persistence of circadian rhythms of plasma ACTH and corticosterone after pinealectomy in sighted or blind rats].

The possible effects of pinealectomy on the corticotropic system was studied in either sighted or ocular enucleated adult female Rats. Individual ACTH and corticosterone measurements were performed on sequential plasma samples obtained over a 48 hrs period from a carotid implanted cannula. Compared with their respective sighted or blind controls, pinealectomized Rats displayed no alteration in the hormonal rhythms' periodicity, phase, mean level and amplitude. On the other hand, ocular enucleation, whether or not associated with pinealectomy depressed the amplitude and to a lesser extent the mean level of the ACTH rhythm, and paradoxically increased the corticosterone rhythm's mean level. While no pineal factors appear therefore required for a normal corticotropic rhythmicity, the possible regulating role of retinal melatonin may be discussed.

Adrenocorticotropic Hormone↗
PubMed1983

[Extrahypothalamic efferent pathways of the suprachiasmatic nucleus in the rat].

Efferent connections of the suprachiasmatic nucleus (SCN) in the Rat were evidenced using specific silver impregnation techniques designed to explore degenerating nerve fibers and terminals after a unilateral destruction of the suprachiasmatic nucleus. Suprachiasmatic efferences were confirmed and terminal buttons were identified in the septum, habenula and paraventricular nucleus of the thalamus. In addition suprachiasmatic fibers and nerve endings were revealed in the medial, cortical and central nuclei of the amygdala in the hippocampic subiculum, in different areas of the olfactory system and in the area parolfactoria.

Animals↗
PubMed1981

Effects of raphe lesions on circadian ACTH, corticosterone and motor activity rhythms in free-running blinded rats.

Blinded female rats underwent additional midbrain raphe lesions, in order to explore the role of the raphe in the organization of endogenous circadian rhythms for ACTH, corticosterone (B) and motor activity (MA). Amplitudes and mean levels of rhythms were depressed for ACTH and MA, with persistent free-running circadian periodicity for MA and, in several rats, for ACTH and B as well. Other rats exhibited split circadian and ultradian rhythmicity for ACTH and B, whereas other again displayed no detectable ACTH rhythmicity. These results are discussed in the light of the structure of circadian pacemaker systems.

Adrenocorticotropic Hormone↗
PubMed1981

[Effects of the destruction of the suprachiasmatic nuclei on the circadian rhythms of ACTH corticosterone and the general activity of female rats exposed to a aperiodic environment].

The effects of bilateral destruction of suprachiasmatic nuclei (SCN) on the temporal patterns of plasma concentrations in ACTH and corticosterone (sequential blood samples from an aortic cannula, at 4 h intervals over 48 h) and of general activity (stabilimeter recordings) were studied in female rats under constant illumination (LL : 10 lx). Under this arrhythmic environment, the SCN lesions induced a syndrome similar to that previously described in a photoperiodic environment (12 L-12 D). This SCN syndrome included : 1) blockade of the ACTH rhythm at baseline levels ; 2) maintained fluctuations of corticosterone, with either circadian or ultradian profiles ; 3) persistent rhythmicity of general activity, with a circadian periodicity in addition to ultradian periods. The persistence of a circadian rhythmicity in the SCN syndrome under arrhythmic environmental conditions, clearly argues in favour of the occurrence of endogenous components of the circadian pacemaker outside the SCN.

Adrenocorticotropic Hormone↗