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R J Krieg

Publications and source records attributed to R J Krieg.

At least 73 records · Page 4Linked to original sources
PubMed1989

Growth hormone (GH) secretion in the pituitary-grafted male rat: in vivo effects of GH-releasing hormone and isoproterenol and in vitro release by individual somatotropes.

Although the pituitary-grafted rat is a classic model of chronic PRL excess, the presence of somatotropes in grafted pituitary tissue indicates a potential for GH secretion. The current study was designed to investigate GH-releasing hormone (GRH)-induced GH secretion and beta-adrenergic inhibition of GH release in animals bearing ectopic pituitary tissue free from hypothalamic control. Positive findings with regard to these in vivo experiments led us to an initial determination of GH secretion by individual somatotropes from transplanted pituitary tissue. In litters of 10 30-day-old Fisher rats, 2 male animals received subcapsular renal grafts of 3 littermate pituitary glands each. Thirty-five days after grafting, 1 group received saline (SAL) followed by GRH, and the other received the beta-adrenergic agonist isoproterenol (ISO) followed by GRH. Blood samples were taken before and after SAL or ISO treatment, GRH was then infused, and sampling was continued. Plasma was assayed for GH and PRL, and the reverse hemolytic plaque assay was used to determine GH release by individual somatotropes from transplanted pituitary tissue. Plasma PRL was clearly elevated in pituitary-grafted compared to muscle-grafted animals, but there was no difference in either body weight gain or basal GH levels between the groups. As shown previously, ISO itself induced a brief release of GH due to its direct effect on the pituitary gland. The GH response to GRH was greater in pituitary-grafted animals than in muscle-grafted controls after both SAL and ISO. GRH-induced GH release was suppressed by ISO pretreatment in muscle-grafted animals, but not in pituitary-grafted animals. The reverse hemolytic plaque assay unequivocally showed that transplanted pituitary tissue was capable of tonic as well as GRH-stimulated GH release. These results demonstrate that despite similar basal GH levels, animals bearing pituitary grafts release significantly greater amounts of GH in response to GRH. The evidence for GH secretion by individual somatotropes from transplanted pituitary tissue directly shows the grafted tissue to be a source of GRH-stimulated GH. The lack of beta-adrenergic inhibition of GRH-induced GH release in pituitary-grafted animals is consistent with the hypothesis that beta-adrenergic inhibition of GRH-induced GH secretion is mediated by an effect on the hypothalamus.

Animals↗
PubMed1989

Somatostatin inhibition of growth hormone secretion by somatotropes from male, female, and androgen receptor-deficient rats: evidence for differing sensitivities.

To investigate the role of somatostatin (SRIF) in regulating sexually dimorphic GH secretion, we used a reverse hemolytic plaque assay and acutely dispersed somatotropes from age-matched normal male, normal female, and androgen receptor-deficient, testicular feminized (Tfm) rats. Hemolytic plaques were developed after a 90-min incubation in the presence of GH antiserum, 10 nM GH-releasing hormone (GHRH), and the following concentrations of SRIF: 0, 0.001, 0.003, 0.01, 0.03, 0.1, 0.3, 1, 3, 10, 30, and 100 nM. Additional studies were performed with 0 or 100 nM SRIF in the absence of GHRH. The absolute number of somatotropes (x10(6); mean +/- SEM) recovered from the pituitaries of Tfm rats (1.73 +/- 0.18) was significantly greater than that from the males (1.11 +/- 0.13; P = 0.01); the number from female rats (1.30 +/- 0.15) was not different from that of either male or Tfm animals. GHRH-stimulated GH secretion, as estimated by the mean GH plaque area (micron2 x 10(4); mean +/- SEM) in the absence of SRIF, was greater for somatotropes from male rats (3.36 +/- 0.41) than that for either Tfm (2.27 +/- 0.32; P = 0.02) or female (1.78 +/- 0.24; P = 0.001) rats; values for the latter two groups did not differ. However, mean GH plaque areas for each group during maximal SRIF inhibition in either the presence or absence of GHRH were indistinguishable from each other and from mean plaque areas obtained under basal conditions. As demonstrated by a lesser EC50 value (0.04 +/- 0.02 nM; mean +/- SEM), somatotropes from female rats were more sensitive to the inhibitory effect of SRIF than were those from either male (EC50 = 1.82 +/- 0.45; P = 0.0001) or Tfm (EC50 = 0.74 +/- 0.22, P = 0.0001) rats; values for the latter two groups were indistinguishable. These observed differences suggest that gender and/or the gonadal hormone environment may be important determinants of the inhibitory effects of SRIF on GH secretion by the somatotrope. While these gender-associated differences may represent effects of the gonadal hormones directly on the somatotrope, they could reflect modulation of the secretion of hypothalamic SRIF and/or GHRH by the prevailing gonadal hormone environment. Such gender-related differences may contribute to the overall sex-dependent patterns of GH secretion in the intact animal.

Androgen-Insensitivity Syndrome↗
PubMed1988

Beta-adrenergic stimulation of growth hormone (GH) release in vivo, and subsequent inhibition of GH-releasing factor-induced GH secretion.

In vivo and in vitro studies of beta-adrenergic influences on GH secretion have produced apparently conflicting data in which the in vivo effect seems to be inhibitory and the in vitro effect to be stimulatory. The present studies were designed to observe the in vivo effect of isoproterenol (ISO), a beta-adrenergic agonist, on 1) GH release during a brief interval after intraatrial infusion, and 2) GH release in response to GRF infused 10 min after ISO. ISO was found to stimulate GH release in both intact and hypothalamus-lesioned animals within 2 min after infusion, but GH returned to control levels within 10 min. ISO also profoundly inhibited the release of GH in response to GRF. Pretreatment of animals with somatostatin (SRIF) antiserum prevented the inhibitory action of ISO on GRF-induced GH release. No change in peripheral levels of SRIF was detected. Also, there was no suppression of GRF-induced GH release by ISO when the treatments were applied in vitro to dispersed perifused pituitary cells. These data show that beta-adrenergic systems can stimulate a rapid but brief release of GH in vivo, and that the subsequent inhibitory action on GRF-induced GH release might be by means of SRIF release.

Adrenergic beta-Agonists↗
PubMed1988

Effects of gonadal steroids on somatotroph function in the rat: analysis by the reverse hemolytic plaque assay.

The mechanism by which gonadal steroids modulate GH secretion is not known. We have used the reverse hemolytic plaque assay to examine whether gonadal steroid-induced modulation of GH secretion is effected by changes in the population of somatotrophs and/or alterations in their secretory properties. Two groups of Sprague-Dawley rats were studied: group 1 (n = 6) comprised male (M), castrate (Cx), and testosterone-replaced castrate male (Cx + T) rats and group 2 (n = 5) consisted of male (M), female (F), and 17 beta-estradiol-replaced castrate male (Cx + E) rats. The number of plaque-forming cells (expressed as both absolute number and a percentage of all cells) was determined, and secretory status was assessed by measuring plaque areas in response to 0, 0.01, 0.1, 1, 10, and 100 nM GHRH. While mean basal GH plaque areas were similar among the treatment groups of group 1, the maximal GH plaque area was significantly decreased in Cx [16.8 +/- 2.4 vs. 26.4 +/- 3.9 X 10(6) microns2 (mean +/- SEM); P less than 0.05], but not in Cx + T (27.5 +/- 4.1 microns2) rats. The GHRH EC50 was unaffected by castration or T replacement. The percentage and absolute population of somatotrophs were reduced in Cx, but not in Cx + T, rats, while the numbers of lactotrophs remained unchanged in these treatment groups. For group 2, the mean peak GH plaque area was reduced in Cx + E (16.5 +/- 2.9 microns2; P less than 0.001) compared to that in M rats (36.2 +/- 2.3 microns2), but was not significantly different from that in F (13.0 +/- 1.5 microns2) rats. The EC50 was significantly (P less than 0.025) greater in Cx + E (10.9 +/- 2.3 nM) and F (7.9 +/- 1.6 nM) compared to M rats (2.8 +/- 0.7 nM). The absolute somatotroph and lactotroph populations were increased in Cx + E compared to M and F rats, as were the populations of other pituitary cell types. Testosterone enhances GH secretion by increasing the secretory capacity, but not the sensitivity, of somatotrophs to GHRH and by recruiting the function of a subpopulation of somatotrophs. Estradiol reduces the secretory capacity and sensitivity of somatotrophs to GHRH, but increases the population of somatotrophs, lactotrophs, and non-GH- and non-PRL-secreting cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Influence of a prolactin- and ACTH-secreting tumour on oestrous cyclicity, the pro-oestrous surges of LH and prolactin and ovarian hypertrophy in the rat.

These studies were designed to investigate the effects of a prolactin- and ACTH-secreting tumour (7315a) on reproductive cyclicity, pro-oestrous surges of LH and prolactin and ovarian hypertrophy in the rat. Normal adult Buffalo rats, which are syngeneic to the 7315a tumour, were found to have a significant pro-oestrous prolactin surge and a relatively low-level preovulatory LH surge. Within 14 days of s.c. injection of dispersed tumour cells, a small tumour was detectable by palpation in one rat, but measurable tumours were not observed until day 18. The pro-oestrous surge of LH, but not of prolactin, was effectively suppressed by day 17. Cessation of reproductive cyclicity (anoestrus) was apparent within 19.4 +/- 1.1 days of injection of tumour cells. Removal of a single ovary showed that there was no change in ovarian weight before anoestrus in the tumour-bearing animals. Subsequent hypertrophy of the second ovary was augmented during the early stages of tumour development (days 8 and 13), and this corresponded to the unexpected finding that the gonadotrophin surges on days 8 and 13 were significantly increased when compared with controls. Ovarian hypertrophy was not significantly different from that in controls after suppression of the gonadotrophin surge (day 17). The results suggest that inhibition of the preovulatory LH surge might be a critical event in the tumour-induced cessation of reproductive cyclicity. The fact that pre-surge concentrations of prolactin did not increase substantially until the conspicuous onset of tumour prolactin secretion on day 21 indicated that the preovulatory LH surge might be inhibited by relatively low levels of tonically secreted prolactin.

Adrenocorticotropic Hormone↗
PubMed1986

Sex differences in beta-adrenergic stimulation of growth hormone secretion in vitro.

In previous in vitro studies we have shown that the amounts of GH released by pituitary cells in response to human GH-releasing factor -40 (hGRF-40) are significantly related to the sex and gonadal hormone environment of the donor animals. The present studies were designed to determine whether the beta-adrenergic stimulation of GH release is sex related and to compare the response to that observed after hGRF-40. Dispersed pituitary cells from male or female rats were exposed to sequential pulses of isoproterenol (ISO) and epinephrine (EPI), followed by a single pulse of 10 nM hGRF-40. In a second series of experiments, the cells were exposed to sequential pulses of norepinephrine (NE), followed by a single pulse of 10 nM hGRF-40. ISO and EPI stimulated GH secretion at concentrations as low as 10(-8) M, but NE required a concentration of 10(-6) M to cause significant GH release. GH release after ISO, EPI, and NE was concentration dependent, and the order of potency was ISO greater than EPI greater than NE. The amounts of GH secreted by pituitary cells from male rats were significantly greater than those from female rats, and the magnitude of the difference was directly comparable to that observed in response to hGRF-40. These results confirm the beta-adrenergic stimulation of GH release, and the order of potency is consistent with mediation by a beta 2-adrenergic receptor. The significantly greater capacity for pituitary cells from male rats to secrete GH supports the possibility that individual somatotropes in the pituitaries of male rats might have a greater responsiveness and/or sensitivity to beta-adrenergic and hGRF-40 stimulation.

Adrenergic beta-Agonists↗
PubMed1985

Modulation of prolactin binding sites in vitro by membrane fluidizers. Effects on male prostatic and female hepatic membranes in alcohol-fed rats.

The objectives of this study were (i) to determine if in vivo administration of ethanol to rats produced changes in apparent lipid fluidity and prolactin binding capacity of male prostatic and female hepatic membranes and (ii) to compare the effects of membrane fluidizers (aliphatic alcohols) in vitro on prolactin binding of prostatic and hepatic membranes in control and alcohol-fed animals. In vitro ethanol has been shown by us previously to increase prolactin receptor levels presumably by unmasking cryptic prolactin receptors. The degree of fluidization was monitored by a fluorescence polarization method using 1,6-diphenylhexatriene. Adult male and female rats were given either water or 4% ethanol as the sole source of drinking fluid for a period of 6 weeks. No significant changes in plasma prolactin were observed between control and ethanol-treated groups of either sex. However, the microviscosity parameter, inversely related to lipid fluidity, was increased approx. 34% and 40%, respectively, in male prostatic and female rat hepatic membranes after ethanol feeding. Furthermore, 125I-prolactin binding capacity was decreased approx. 30% and 26%, respectively, in prostatic and hepatic membranes of alcohol fed animals. In vitro treatment with aliphatic alcohols had no effect on either microviscosity or prolactin binding in hepatic or prostatic membranes from ethanol-fed rats, but both fluidized and increased prolactin binding in the same membrane preparations from control rats. Our observations are consistent with the direct relationship between membrane fluidity and prolactin receptor levels. The changes in prostatic and hepatic membranes after alcohol feeding, namely decreased prolactin receptor levels, decreased fluidity and increased resistance to the fluidizing effects of in vitro aliphatic alcohols may reflect a fundamental membrane defect.

1-Butanol↗
PubMed1985

Effects of in vivo gonadal hormone environment on in vitro hGRF-40-stimulated GH release.

The effects of gender and the gonadal hormone environment on basal and stimulated growth hormone (GH) release by dispersed and continuously perifused rat anterior pituitary cells were examined. Cells from intact male and diestrus day 2 female rats and from castrate male rats either untreated or treated with testosterone (T) or 17 beta-estradiol (E2) were used. Basal GH release (ng/min per 10(7) cells; mean +/- SE) by cells from diestrus day 2 female rats was less than by cells from castrate rats treated with T (4.3 +/- 0.6 vs. 11.4 +/- 2.7, respectively; P less than 0.025). No other differences in basal release were detected. Concentration-response relationships were documented between human GH-releasing factor 40 (hGRF-40; 0.03-100 nM given as 2.5-min pulses every 27.5 min) and GH release. Mean (+/- SE) overall GH release (ng/min per 10(7) cells) above base line was greater by cells from intact male rats (496 +/- 92) than by cells from castrate (203 +/- 37.3; P less than 0.0001), castrate and T-treated (348 +/- 52.8; P = 0.008), or castrate and E2-treated (58.1 +/- 6.8; P less than 0.001) male rats or by diestrus day 2 rats (68.6 +/- 9.5; P = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Counteraction of the haloperidol blockade of ovulation by bromocriptine, and the effect of bromocriptine on LH and prolactin secretion.

Previous experiments showed that haloperidol (Haldol) blocked LH release and ovulation when injected on the day of proestrus in the female rat. The present studies were designed to investigate the mechanism of Haldol blockade and the possibility that bromocriptine (CB) might counteract the effect. One hour prior to subcutaneous injection of an effective dose of Haldol (0.25 mg/kg at 09.30 h), CB was injected intraperitoneally at one of four doses (2.5, 5.0, 7.5, or 10.0 mg/kg at 08.30 h). Bromocriptine was effective at restoring LH release and ovulation, and the optimal dose for this particular experiment was found to be 7.5 mg/kg. The highest dose (10.0 mg/kg), however, resulted in no significant increase in ovulation. Treating animals with CB (5.0, 10.0, or 20.0 mg/kg at 08.30 h) followed by control vehicle showed that high doses of CB caused a significant inhibition of LH release and ovulation. After 20.0 mg/kg there was no significant surge of LH, and although ovulation did occur it was significantly suppressed when compared to control animals (p = 0.017). These results showed that appropriate doses of CB counteract the Haldol blockade of LH release and ovulation. The suppression of Haldol-induced PRL secretion by low-dose CB, without the significant restoration of ovulation, supported the hypothesis that the Haldol blockade was mediated via a direct effect of Haldol on central nervous system control mechanisms. While CB alone exerted a profound inhibition of PRL at low doses, it had no effect on LH release. CB at high doses, however, was inhibitory to both LH release and ovulation.

Animals↗
PubMed1984

Paradoxical suppression of prolactin secretion: involvement of catecholaminergic mechanisms and the adrenal gland.

Prolactin (Prl) secretion is normally elevated on the afternoon of pro-oestrus in the rat. Studies have shown that ether stress caused a 'paradoxical inhibiting effect' on these high Prl levels. The present study was designed to investigate whether the paradoxical suppression of Prl was mediated by the central nervous system or the adrenal glands. Plasma was obtained from adult female rats after sampling via intra-atrial catheters from 16.25-18.45 h on the afternoon of pro-oestrus. Restraint stress administered between 16.45-17.00 h induced the expected precipitous decrease in plasma Prl in intact animals. Pre-treatment of intact animals with the catecholamine receptor blocking agent haloperidol (1.0 mg/kg at 13.00 h) resulted in a further elevation of plasma Prl levels as compared with untreated controls, but eliminated the decrease of Prl in response to restraint stress. Although acutely adrenalectomized (ADX) animals proved to be highly sensitive to the bleeding procedures, initial Prl levels on the afternoon of pro-oestrus were not different from those of intact animals. Restraint stress under conditions of acute ADX was not found to induce the expected suppression of high Prl levels. Rather, the response was opposite to that which occurred in intact animals. These results indicate that the paradoxical suppression of Prl by restraint stress was mediated by catecholaminergic mechanisms, and that the adrenal gland was essential for the effect.

Adrenal Glands↗
PubMed1982

Unremitting suppression of the postovariectomy rise in plasma LH by tumor-induced hyperprolactinemia.

The plasma LH response to ovariectomy was studied at different periods in the development of hyperprolactinemia in rats bearing the transplantable prolactin-secreting pituitary tumors 7315a or MtTW15. Rats were subcutaneously inoculated with tumor cells and ovariectomy was performed at 3 times during the subsequent growth of the solid tumor: (1) coincident with tumor cell implantation; (2) when solid tumors first became palpable, and (3) when solid tumors were large. The values for circulating prolactin and LH were serially determined following ovariectomy for 63, 35 and 28 days, respectively. In other studies, tumor cells were implanted into animals which had undergone ovariectomy 3 months earlier. In the presence of hyperprolactinemia caused by the prolactin secreting tumors, the plasma LH following ovariectomy was either reduced following an initial increase, prevented from increasing, or reduced from chronically elevated levels. Hyperprolactinemia of approximately 7-50 micrograms/ml caused marked suppression of LH secretion, while hyperprolactinemia in the range of 0.2-6 micrograms/ml resulted in significant but slower and lesser suppression of LH which did not reach noncastrate levels. The inhibitory effect of hyperprolactinemia on plasma LH after ovariectomy was persistent and unremitting for the duration of each experiment, and there was no tendency for suppressed LH to return to levels expected for the ovariectomized state. The model of hyperprolactinemia induced with transplantable prolactin-secreting tumors in the ovariectomized rat may prove to be valuable in understanding the mechanism of depression of gonadal function by hyperprolactinemia.

Animals↗
PubMed1981

Differential time- and dose-dependent effects in the haloperidol blockade of luteinizing hormone release and ovulation.

The capacity of haloperidol (Haldol) to block luteinizing hormone (LH) release and ovulation was investigated with particular reference to its effectiveness during the "critical period" on the afternoon of proestrus in normal, cycling female rats. Haldol was injected subcutaneously at 13.30 h in one of five dosage levels (0.125, 0.25, 0.5, 1.0, or 4.0 mg/kg), or at 09.30 h in a single dose of 1.0 mg/kg. Control animals received the corn oil vehicle at 13.30 or 09.30 h. Blood samples were taken by means of intra-atrial catheters which had been implanted on the day prior to Haldol treatment. Oviducts were examined for the presence of ova at 10.00 h on the day following the experiment (estrus). Haldol was found to be ineffective at 13.30 h when given at dosage levels which were shown by previous authors, and in the present experiment, to be capable of blocking LH release and ovulation after injection at 09.30 h. Although LH levels and the numbers of ova released were inversely related to the dose of Haldol administered at 13.30 h, well-defined LH surges were still present and the occurrence of ovulation was not significantly inhibited. Haldol was found to block LH release and ovulation, however, when injected at 13.30 h at the highest dosage level (4.0 mg/kg). The fact that low doses of Haldol blocked in the morning but not in the afternoon indicates that the morning blockade must be mediated by a secondary action of the drug which required a certain period of time to be effective. The blockade by the high dose of Haldol in the afternoon, however, was probably due to a direct action on LH releasing mechanisms.

Animals↗
PubMed1981

A light and electron microscopic study of the pineal body of the nutria (Myocastor coypus).

Light and electron microscopic studies of the nutria (Myocastor coypus) pineal gland revealed pinealocytes interspersed among glial, vascular, and neuronal elements. Each pinealocyte possessed a single process that terminated within the parenchyma near the perivascular region. The eccentrically located nucleus in these cells contained euchromatic chromatin, a prominent nucleolus, and a highly infolded nuclear envelope. The cytoplasm was rich in mitochondria, Golgi complexes, and glycogen particles. The smooth endoplasmic reticulum (SER) was better developed thant he rough endoplasmic reticulum (RER) and polyribosomes were not abundant. Long profiles of subsurface cisterns constituted prominent cytoplasmic features, and these were most conspicuous in the regions of soma-somatic apposition. The bulbous endings of the pinealocyte processes were filled with clear, round, secretory vesicles. Dense-cored vesicles were rarely observed. Glia reminiscent of protoplasmic astrocytes displayed cytoplasmic processes that enveloped blood vessels, invested the pineal periphery, and intervened among the pinealocytes. They thus seemed to form a barrier between the meningeal capsule and vascular space on the one hand and the parenchyma on the other.

Animals↗
PubMed1976

Spontaneous and electrochemically stimulated changes in plasma LH in the female rat following hypothalamic deafferentation.

Plasma LH levels in adult female rats were studied by radioimmunoassay 6 weeks after making frontal cuts (FC) at the optic chiasm with Halász knives of various sizes. Cuts made with a small knife (radius 1.3 mm) permitted a spontaneous rise in plasma LH during proestrus from a mean of 96 +/- 25 ng/ml at 14:00 h to 545 +/- 207 ng/ml at 18:00 h in 13 rats. Seven of the latter, with a mean plasma LH of 967 +/- 281 ng/ml at 18:00 h exhibited tubal ova at hemicastration (hemi-ovx) the following morning. In a similar experiment 6 FC females lesioned with a 1.5 mm knife had plasma LH levels of 53 +/- 7 ng/ml at 14:00 h, but showed neither detectable changes at 2 h intervals through 20:00 h nor ovulation at hemi-ovx. Similar results were obtained in 13 rats deafferented with a 2.0 mm knife. Nine weeks after FC and 3 weeks following hemi-ovx all animals were given pentobarbital (32 mg/kg i.p.) at 13:30 h and stimulated bilaterally in the medial preoptic area (MPO) passing 20 muA anodal DC X 60 sec through concentric bipolar steel electrodes placed 0.8 mm from the midline. All 3 groups of FC animals showed increases in plasma LH to comparable levels (range: 197 +/- 45-357 +/- 156 ng/ml) 1 h after stimulation. Electrochemical stimulation sites extended lateral to the cut locations on at least one side in all animals. The results of these studies suggest that chronically (9 week) deafferented female rats have the capacity to release pituitary LH in response to MPO electrochemical stimulation in spite of retrochiasmatic deafferentation, but that the ovaries of the persistent estrus rat are unresponsive to these amounts of circulating LH.

Animals↗
PubMed1976

Differential effects of intraventricular luteinizing hormone releasing hormone (LH-RH) and norepinephrine on electrical activity of the arcuate nucleus in the proestrous rat.

Effects of intraventricular infusions of LH-RH and norepinephrine (NE) on the electrical activity of the arcuate nucleus were investigated in normally cycling proestrous rats. Under urethane anesthesia, recordings were made of amplitude-discriminated multiple unit spike activity and integated multiunit activity (MUA) in parallel with cortical EEG. Control infusions of saline (2 microliter, isotonic, pH 5.5) were ineffectual, but LH-RH (0.5 microgram) induced a significant increase in both multiunit spike activity and integrated MUA. While the response appeared to be continuous, statistical analysis revealed 2 phases: a quick rise which persisted for approximately 5 min, followed 15 min later by a longer-lasting elevation in activity. The onset of the 2nd increase corresponded with the attainment of peak values of pituitary LH output. Subsequent treatment with 20 microgram NE, on the other hand, resulted in a marked depression of activity. The fact that NE depresses arcuate neuronal activity at dose levels which cause the release of LH and that LH-RH increases activity within the same population of neurons, while possibly mediating an 'ultrashort-loop' negative feedback effect, suggest that this responsive component of the arcuate nucleus, perphaps the tuberoinfundibular dopaminergic system of neurons, is inhibitory to LH release.

Animals↗
PubMed1976

Effects of intraventricular catecholamines on luteinizing hormone release in ovariectomized-steroid-primed rats.

The effects of intraventricular norepinephrine (NE) and dopamine (DA) were studied in the awake, freely behaving rat. In long-term ovariectomized, estrogen-progesterone-primed (OVE E2-P) animals, blood samples were taken via indwelling intra-atrial catheters before and after intraventricular infusion of either pH-adjusted saline, NE )5 mug, 15 mug, 20 mug), or DA (4 mug, 15 mug), and plasma LH was measured by radioimmunoassay. Under urethane anesthesia, records were made of the effects of intraventricular saline and NE on the electrical activity of the arcuate nucleus in the form of multi-unit spike activity. In unanesthetized animals, intraventricular NE caused marked changes in behavior. The typical response consisted of three phases: generalized activation (5-7 min), feeding (5-15 min), and sleep 1-2 h). DA exerted similar behavioral effects but without the marked sleep phase characteristic of the NE response. The effects of the catecholamines on LH output were significant increases in plasma LH levels for all NE doses tested (5 mug, p less than .025; 15 mug, p less than .05; 20 mug, p less than .005), while DA had no effect. The dynamics of the LH response to NEwere similar at all dosage levels, and the increase caused by 20 mug NE was found to be essentially equal to that induced by a quick intravenous infusion of 1.25 ng LHRH. Arcuate nucleus multi-unit spike activity (MUSA) showed a clear response to intraventricular NE at a dosage capable of stimulating the release of LH. In every case, the initial effect was a decrease in spike activity. These results, considered in relation to previous findings, suggest that NE may be stimulatory to neurons secreting LH-releasing hormone (LHRH). The decrease in arcuate nucleus MUSA in response to NE implies that certain elements of this nucleus are inhibited during LH release, perhaps the dopaminergic tuberoinfundibular neurons.

Animals↗
PubMed1975

Limbic system involvement in the increase in plasma prolactin following cortical spreading depression in gonadotropin-treated female rats.

Cortical spreading depression (SD) was induced by applying 25% KCl to the frontal cerebral cortex in female rats under continuous ether anesthesia. Three weeks previously the animals had been subjected to sham operation, bilateral surgical "deefferentation" of the amygdala or transection of the dorsal columns of the fornix. During the week prior to experiment the rats were made "pseudopregnant" by treatment with PMS and hCG. Plasma prolactin was measured by radioimmunoassay in blood samples obtained from the peripheral circulation at 20 min intervals. After two control samples had been taken, KCl was applied to the cortex and sampling continued for another 100 min; In the sham-operated group prolactin levels increased with time following the application of KCl. Fornix-cut animals showed a similar, although briefer, increase with values significantly lower than those found in sham-operated animals at 80 min. The increase in plasma prolactin observed in sham-operated and fornix groups was completely abolished in amygdala-cut animals. These results indicate that limbic structures play a significant role in the mechanisms by which cortical SD elevates plasma prolactin levels under the present experimental conditions.

Amygdala↗