摘要:

Morphological characteristics of LHRH neurons identified by immunocytochemistry were studied using light and electron microscopy in female rats in which estradiol was replaced at the time of ovariectomy (‘pseudo-intact’ rats) or 3 weeks after ovariectomy (long-term ovariectomized, estradiol-treated). While estradiol levels were equivalent in these two groups, the rise in LH after ovariectomy was prevented by the immediate administration in the pseudo-intact rats, while the augmented plasma LH levels present three weeks following ovariectomy were only reduced by 50% as a result of delayed estradiol treatment. The LHRH content of the medial basal hypothalamus (MBH) including the median eminence (ME) was greater in pseudo-intact females than in untreated long-term ovariectomized control females or long-term ovariectomized, estradiol-treated females, both 1 and 14 days after estradiol exposure. Immunocytochemistry revealed fewer LHRH-immunopositive neuronal processes coursing throughout the MBH and terminating in the ME of long-term ovariectomized, estradiol-treated rats compared to those in pseudo-intact rats. However, within individual neurovascular terminals in the ME, image analysis revealed that the area of reaction product was greater in long-term ovariectomized, estradiol-treated animals. Equivalent amounts of LHRH were assayed in the MBH within each group of animals by several LHRH antisera regardless of their different binding requirements (R42, IJ29 and A-R743), suggesting that the predominant moiety present in neuronal terminals is the fully mature decapeptide. In contrast, in the preoptic area-anterior hypothalamus (POA-AH) these antisera assayed amounts of LHRH that varied as a function of binding characteristics, although the quantities did not vary with the estradiol treatment schedule. Immunocytochemical results paralleled these assay data; antisera requiring an interior sequence of amino acids (A-R743 and A-R419) detected approximately 3 times as many immunoreactive perikarya in the POA-AH as did an antiserum requiring the free amidated C terminal (IJ29). The estradiol treatment schedules had no effect on the total number of LHRH-immunopositive neurons detected by each antiserum or the distribution of LHRH-immunopositive neuronal perikarya. These data support the hypothesis that the predominant moieties present in neuronal cell bodies are precursor forms. The fine-structural characteristics of LHRH-immunopositive neuronal cell bodies are consistent with greater secretory and biosynthetic activity in LHRH neurons of long-term ovariectomized, estradiol-treated rats. We hypothesize that the activity of LHRH neurons in these females is enhanced in comparison to pseudo-intact females and, secondly, that this increased activity contributes to the augmented secretion of LH in long-term ovariectomized, estradiol-treated fema

ISSN:0028-3835    

DOI:10.1159/000124698

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Using the Falck-Hillarp methodology in combination with quantitative microñuorimetry, catecholamine (CA) levels and utilization in discrete hypothalamic CA nerve terminal systems in the male rat have been analyzed 24 h, 1, 2 and 4 weeks following thyroidectomy as well as after T3 or T4 restitution therapy 4 weeks after thyroidectomy. By means of high pressure liquid chromatography (HPLC), dopamine (DA) and noradrenaline (NA) levels and utilization 4 weeks after thyroidectomy have been analyzed in various brain regions. Triiodothyronine treatment (10 µg/kg, s.c, twice daily during 10 days) of 4-week athyroidic rats increased serum T3 levels, but not T4 serum levels. Thyroxine treatment (36 µg/kg, s.c, twice daily during 10 days) of 4-week athyroidic rats increased serum T4 levels and the T3 levels were found to be even slightly higher than those found in normal animals. Triiodothyronine or T4 restitution therapy reversed the changes induced by thyroidectomy on the anterior pituitary hormones (TSH, prolactin and growth hormone) and corticosterone secretion. It is suggested that removal of thyroid hormones may be responsible for the changes in the anterior pituitary hormones and corticosterone secretions. In the quantitative microfluorimetrical analysis 24 h, 1,2 and 4 weeks after thyroidectomy, decreases in DA levels and utilization and increases in NA levels and utilization were found in the lateral palisade zone (LPZ) of the median eminence and in the parvocellular and magnocellular parts of the paraventricular hypothalamic nucleus (PA), respectively. In addition, 1-, 2- and 4-week decreases were found in DA levels and turnover in the medial palisade zone (MPZ) as well as in NA turnover in the dorsomedial hypothalamic nucleus (DM) and in the ‘border zone’ (BZ) between the medial and lateral hypothalamus ventral to the fornix. In the HPLC analysis it could be demonstrated that 4 weeks after thyroidectomy decreases in DA levels and utilization in the mediobasal hypothalamus and increases in DA levels as well as NA levels and utilization in the hypothalamus had developed. The T3 or T4 restitution therapies after 4 weeks of thyroidectomy counteracted the effects on CA levels and utilization in all hypothalamic CA nerve terminal systems except for the reduced NA utilization found in the DM following 4 weeks after thyroidectomy. The demonstrated reductions in DA levels and utilization in the MPZ and LPZ of the median eminence and the increases in NA levels and utilization in the PA are suggested to reflect the existence of an inhibitory dopaminergic mechanism in the median eminence and a facilitatory noradrenergic mechanism in the PA involved in the regulation of TSH secretion. These mechanisms seem to be directly or indirectly regulated by thyroid hormones. The reduced NA utilization in the DM and in the BZ after thyroidectomy is suggested to be related to the lowering of growth hormone secretion and reduction of its pulsatile release in this endocrine

ISSN:0028-3835    

DOI:10.1159/000124699

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

In order to elucidate the possible role of noradrenergic neurons of the nucleus locus coeruleus (LC) in stress responses, the effects of corticotropin-releasing factor (CRF) on LC neuronal activity were characterized. In halothane-anesthetized rats, intracerebroventricular administration of CRF was found to have two distinct actions: (1) A dose-dependent increase in spontaneous discharge activity was observed 3 min after peptide injection, with 1.0 and 3.0 µg CRF increasing activity by 7 ± 2 and 47 ± 12%, respectively; Ala14CRF (3.0 µg), an inactive analogue of CRF, had no effect on LC spontaneous discharge rates. These results confirm and extend previous studies of CRF activation of LC basal discharge activity; (2) additionally, CRF (1.0 and 3.0 µg) disrupted sensory responses of LC cells to sciatic nerve stimulation. As previously reported, responses of LC neurons to electrical stimulation of the sciatic nerve usually consisted of a brief activation beginning 20–40 ms after stimulus followed by a period of relatively suppressed activity lasting 100–200 ms. CRF attenuated both components. Responses plotted as normalized, cumulative histograms became more linear in the presence of CRF (1.0 and 3.0 µg), suggesting that discharge rates during phasic responses to sciatic stimulation were similar to spontaneous rates. Statistical comparison using the Kolmogorov-Smirnoff test or correlation coefficients demonstrated that both 1.0 and 3.0 µg CRF reduced response components, while 0.3 µg CRF and Ala14CRF (3.0 µg) had no effect. The degree of attenuation of LC sensory responses by CRF was not linearly related to the magnitude of CRF-in-duced increases in spontaneous discharge rate, suggesting that these are distinct effects of CRF. These actions of CRF on LC activity may represent an important mechanism in the central mediation of stre

ISSN:0028-3835    

DOI:10.1159/000124700

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Bilateral lesions of the amygdaloid central nucleus (ACE) significantly diminished the secretion of ACTH in response to immobilization stress. Stress is associated with increased noradrenergic activity in the ACE and in the anterior and lateral hypothalamic areas. In comparison with intact stressed animals, lesion of the ACE reduced the noradrenergic activity in response to stress within the anterior and lateral hypothalamic areas, the arcuate and paraventricular nuclei of the hypothalamus and the bed nucleus of the stria terminalis. These results support the hypothesis of a stimulatory role for the noradrenergic system in the ACE on ACTH secretion. Stress decreased dopaminergic activity in the ACE, the cortical nucleus of the amygdala, the dorsomedial and ventromedial nuclei of the hypothalamus and the ventral tegmental area. In comparison with intact stressed rats, lesion of the ACE reduced dopaminergic activity in the anterior and lateral hypothalamic areas. Our results support the hypothesis of an inhibitory role of the dopaminergic system, particularly in the ACE, on ACTH secretion. This study also indicates that, in the control of ACTH secretion in response to immobilization stress, the noradrenergic and dopaminergic systems act in opposition to one another in certain brain structures such as the anterior and lateral hypothalamic areas and the ACE.

ISSN:0028-3835    

DOI:10.1159/000124701

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

This study was designed to examine the effects of short photoperiod (SP) exposure on gonadotropin and PRL levels in the presence and absence of estrogen treatment in ovariectomized LSH/SsLak hamsters. In experiment I, regularly cycling hamsters maintained in long photoperiod (14L:10D) were ovariectomized and Silastic capsules containing 2.0-mm columns of estradiol benzoate (EB) implanted simultaneously into half of the animals. On the following day, half of the animals in each treatment group were transferred to SP (8L:16D). After 20 days of SP or long photoperiod (LP) exposure, all animals were sacrificed by decapitation and their sera and pituitaries saved for hormonal determinations. The experimental protocol in experiment II was similar, except that two groups in each photoperiod received estrogen treatments; one group received 2.0-mm implants of 17-beta-estradiol (E2), whereas a second group received 10.0-mm E2 implants. SP treatment effected a reduction in serum LH and FSH levels in the absence of steroid replacement treatment. EB treatment depressed serum gonadotropin levels in LP animals, but did not alter levels in SP hamsters. In experiment II, LP- and SP-treated animals showed similar responses to E2 treatment, although different responses were noted in the two dosage groups. Pituitary gonadotropin contents became progressively decreased with increasing steroid levels and in certain groups showed SP-induced reductions. Serum and pituitary PRL levels increased in response to steroid treatment, but were not affected by SP treatment. In summary, 20 days of SP treatment caused gonad-independent reductions in gonadotropin levels and appeared to reduce the steroid feedback sensitivity of the hypothalamo-pituitary axis. PRL levels were not affected by SP exposure in the absence of the ovaries, and the interaction of PRL and estrogen appeared to be similar in both photoperiods.

ISSN:0028-3835    

DOI:10.1159/000124702

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Adrenal catecholamine secretion after stimulation of trigeminal nucleus caudalis (Vc) was compared to that evoked from more ventrolateral brain stem areas (VLM) by sampling adrenal venous blood in anesthetized cats. The effect of stimulus pattern on catecholamine secretion was assessed by presenting an equal number (300 pulses over 15 s) of electrical stimuli (75 µA, 0.2 ms) as a continuous pattern and as a burst pattern pulse train at each electrode site. Epinephrine secretion increased promptly by 1 min after burst pattern stimulation of Vc, whereas continuous pattern stimuli had no consistent effect. Burst pattern stimulation of VLM sites caused a small decrease in epinephrine secretion, whereas continuous pattern stimuli had no significant effect. Adrenal norepinephrine increased equally after Vc or VLM stimulation regardless of stimulus pattern. The adrenal catecholamine secretory responses could not be explained by the transient evoked changes in adrenal venous plasma flow or arterial pressure. The data indicate that stimulation of Vc evokes a pattern-dependent increase in epinephrine secretion, whereas the increase in norepinephrine secretion is equal after burst or continuous pattern stimuli. Further, adrenal activation by brief neural stimuli cannot be assessed adequately in the cat by measuring epinephrine secretion alone, since stimulation of many ventrolateral brain stem sites caused a significant increase in norepinephrine secretion with no corresponding increase in epinephrine secretion

ISSN:0028-3835    

DOI:10.1159/000124703

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

To determine whether the anorexic and the hyperglycemia actions of somatostatin were mediated through the hypothalamic nuclei, rats were infused with somatostatin and normal saline through previously implanted hypothalamic cannulae. Administration of somatostatin (0.5–1.5 µg in 1.0 µl) into the lateral hypothalamus, but not the ventromedial or the anterior hypothalamus, caused a reduction in food consumption without affecting relative water intake (or water-to-food ratio) in conscious rats in a freely moving state. On the other hand, administration of somatostatin into the lateral hypothalamus, but not the anterior or the ventromedial hypothalamus, caused an increase in blood glucose level in rats. This hyperglycemia was antagonized by vagotomy, but not by spinal transection or adrenalectomy. The data indicate that the lateral hypothalamus is the most sensitive site of the somatostatin-induced anorexia and the action of somatostatin on the lateral hypothalamus-vagus efferent activity is also a possible mechanism mediating hyperglycemia in r

ISSN:0028-3835    

DOI:10.1159/000124704

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

In a double-blind study in normal subjects, methoxamine, a highly selective agonist at alpha-1-adrenoceptors, significantly increased circulating ACTH and cortisol. The stimulant effect of methoxamine on cortisol secretion was dose dependent in the range 3.5–7 µg/kg/min, was abolished by concomitant administration of the strong alpha-1-adrenergic (and weak HI) antagonist thymoxamine but unaffected by the antihistamine, chlorpheniramine. In order to test whether the action of methoxamine on ACTH secretion was exerted centrally or peripherally, the effects of norepinephrine (NE), an alpha-1-agonist that does not cross the blood-brain barrier, were studied. Doses of NE (1–12 µg/min) that increased systolic blood pressure by amounts similar to the changes produced by methoxamine, did not result in any rise in plasma cortisol in normal subjects. The effect of methoxamine, which is more lipid soluble than NE, on plasma ACTH and cortisol, appears to be exerted on the CNS and not at the pituitary or via nonspecific peripheral mechanisms. In addition to its water solubility, NE differs from methoxamine in its beta-1-, beta-2- and alpha-2-agonist actions. However, prenalterol (2 mg) and salbutamol (250 µg), respectively beta-1- and beta-2-adrenergic agonist drugs, had no effect on the secretion of ACTH or cortisol and the alpha-2-antagonist yohimbine in an effective dose did not unmask a stimulant effect of intravenous NE on plasma cortisol. At high infusion rates, NE significantly inhibited cortisol secretion. Stimulation of central alpha-1-adrenergic mechanisms results in secretion of ACTH in man, presumably by increased release of a corticotropin-releasing

ISSN:0028-3835    

DOI:10.1159/000124705

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

The effects of electrical stimulation of the Al noradrenergic cell group on the extracellular activity of medial preoptic-medial septal (MPO-S) neurons were studied in ovariectomized (OVX) female rats under different hormonal conditions [estrogen and progesterone (E-P)-primed or unprimed] via conventional electrophysiological techniques. In addition, MPO-S neurons responding to the Al noradrenergic cell group stimulation were characterized by examining their connections with the arcuate nucleus/median eminence (ARC/ME). With respect to stimulation of the Al noradrenergic cell group, a large proportion of MPO-S neurons exhibited one of the following three types of orthodromic responses: orthodromic excitation (OD + ), orthodromic inhibition (OD-), or complex orthodromic response (OD comp). The predominant type of response was OD +. Although E-P-priming did not change the relative proportion of neurons displaying a specific type of orthodromic response, it did increase the overall percentage of MPO-S neurons orthodromically responding to Al stimulation (39% of MPO-S neurons responded to Al stimulation in the E-P-primed group whereas only 25% of the neurons did so in the unprimed group). Neurons responsive to Al stimulation were more likely to respond orthodromically to ARC/ME stimulation than were those neurons which were unresponsive to Al stimulation. About one fifth of MPO-S neurons identified as projecting to the ARC/ME [putative luteinizing hormone-releasing hormone (LHRH) neurons] orthodromically responded to Al stimulation. The predominant type of response was OD + . The present study indicates that Al noradrenergic input to MPO-S neurons is predominantly excitatory. Furthermore, the findings that (1) the proportion of neurons which responded to Al stimulation was increased by E-P-priming, a treatment used to induce a surge in luteinizing hormone (LH) secretion in an OVX rat, (2) the neurons responding to Al stimulation had a tendency to receive input from the ARC/ME, a brain site intimately involved in the control of LH release, and (3) the activity of putative LHRH neurons was able to be affected by Al stimulation suggest that Al input to MPO-S area may be involved in the control of LH secretion.

ISSN:0028-3835    

DOI:10.1159/000124706

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

In this work the ability of angiotensin II (AII) to potentiate the corticotropin-releasing activity of ovine CRF41 (CRF) and the intracellular mechanism responsible for this effect are described. In perfused rat anterior pituitary cells, AII (10–8M) was found to potentiate the corticotropin-releasing activity of CRF producing a parallel shift of the dose-response curve. Similar results for ACTH release were observed in monolayer cell cultures. In this system, the concentration of cAMP was measured and was shown to be increased in the presence of CRF with a maximal value (2.5-fold greater than control) after 5–10 min incubation. On the other hand, AII at a dose inducing ACTH release (10–7M), had no effect on basal cAMP concentration, but when given simultaneously with CRF, potentiated the CRF-induced cAMP production (1.9-fold greater than CRF value). These results indicate that AII potentiates the corticotropin-releasing activity of CRF and that this effect is preceded by a similar increase in the CRF-induced cAMP produ

ISSN:0028-3835    

DOI:10.1159/000124707

出版商:S. Karger AG    

年代:1987

数据来源: Karger