Biomedical subjects

R R Gala

Publications and source records attributed to R R Gala.

At least 37 records · Page 2Linked to original sources

PubMed1988

The serotonin 5-HT2 receptor system, but not the alpha 1-adrenergic receptor system, is involved in the estrogen-induced afternoon prolactin surge in the rat.

Ketanserin (Ket), a new serotonergic (5-HT2) antagonist, has recently been shown to block the estrogen-induced afternoon PRL surge (Endocrinology 120: 2070-2077, 1987). It is not certain, however, whether the effect of Ket was due to its serotonergic or adrenergic receptor antagonistic property. Another 5-HT2 receptor antagonist, LY53857, which possesses no alpha 1-adrenergic receptor affinity, as well as an alpha 1-adrenergic receptor antagonist, prazosin, were used in this study to further clarify the mechanism of 5-HT in the control of PRL secretion. Adult female Sprague-Dawley rats ovariectomized for 2-3 weeks and given a single injection of polyestradiol phosphate were studied 6 days later. Ket, LY53857 and prazosin were examined singly or in combination and animals were injected twice on the sampling day at 1200 and 1300h, respectively. The dosages were as follows: Ket and LY53857, 3 mg/kg BW, ip and 2 mg/kg BW, sc; prazosin, 1 mg/kg BW, ip and 0.7 mg/kg BW, sc. Blood samples were drawn from indwelling intraatrial catheters throughout the afternoon PRL surge.

Animals↗

PubMed1988

Clinical value of prolactin bioassay in euprolactinemic reproductive disorders.

To examine the disparity between clinical presentation and prolactin (PRL) measured by radioimmunoassay (RIA), serum samples from 128 patients with galactorrhea and/or reproductive disorders were evaluated by RIA for immunoassayable PRL (RIA-PRL) and by Nb2 lymphoma cell proliferation assay for bioassayable PRL (bioassay-PRL). One hundred fifteen patients had normal RIA-PRL and 13 patients had high RIA-PRL (greater than 25 ng/ml). Twenty patients had galactorrhea, two of whom had hyperprolactinemia. The reproductive disorders in female patients included infertility, amenorrhea, oligomenorrhea, irregular menstrual cycles, and luteal phase defects. Six oligospermic males also were studied. Twenty-three male and female volunteers with no evidence of reproductive disorders served as controls. Appropriate comparisons showed that PRL bioassay/RIA ratio, an index of agreement between the two assay systems, did not differ for the various patient groups compared with controls. It is concluded that Nb2 lymphoma bioassay does not provide additional diagnostic value to RIA in defining the cause of euprolactinemic galactorrhea and/or reproductive disorders.

Biological Assay↗

PubMed1988

The pharmacologic induction of prolactin release in the medial preoptic/suprachiasmatic nuclei-lesioned, estrogen-treated ovariectomized rat.

It has been shown that lesions of the medial preoptic/suprachiasmatic nuclei (MPO/SCN) abolish the estrogen-induced afternoon prolactin (PRL) surge. Recent studies using both dopamine antagonist and thyrotropin-releasing hormone (TRH) successfully induced an increase in plasma PRL in various animal models. The same drug approach was used in this study in the MPO/SCN lesioned rat to determine whether these areas participated in the induced PRL release. It is concluded that a significant PRL release can be induced by DA antagonism, or TRH stimulation preceded by DA antagonism in the MPO/SCN lesioned, estrogen-treated ovariectomized rat.

Animals↗

PubMed1988

The effect of dopamine antagonists and/or VIP on TRH- or VIP-induced prolactin release in estrogen- and progesterone-treated ovariectomized rats.

These experiments were conducted to test the hypothesis that the effectiveness of VIP in releasing prolactin is, like TRH, enhanced when preceded by a short period of dopamine receptor antagonism. Chronically catheterized, ovariectomized rats pretreated with estradiol benzoate and progesterone to mimic early pregnancy were used throughout these studies. In the first experiment, animals were injected either with the dopamine (DA) antagonist domperidone (DOM, 0.01 mg/rat, iv) or with vehicle (acetic acid in saline). Five minutes later, all animals were treated with the DA agonist 2-Br-alpha-ergocryptine maleate (CB-154, 0.5 mg/rat, iv) followed 60 min later by the administration of thyrotropin-releasing hormone (TRH, 1.0 micrograms/rat iv) or vasoactive intestinal peptide (VIP, 25 micrograms/rat, iv). The injection of TRH following DOM treatment increased mean plasma PRL levels 100 ng/ml above levels found in vehicle-injected rats. VIP administration, however, increased PRL levels in the blood in DOM-treated rats only 6 ng/ml above the levels in vehicle-injected animals. The same treatment protocol was used in the second experiment except that the DA antagonist, sulpiride (0.01 mg/rat, iv) was administered instead of DOM, and CB-154 was not given. In this experiment both TRH and VIP released PRL. The response to TRH, but not to VIP, was significantly greater following sulpiride than in animals treated with sulpiride vehicle. In the third experiment animals were treated with DOM, VIP, DOM plus VIP, or vehicle. Five minutes later all rats received CB-154 injections, followed 60 min later by TRH administration. The final experiment was a replicate of the third except that sulpiride was substituted for domperidone and no CB-154 was given. The resulting data revealed that (1) dopamine antagonism enhanced the effectiveness of TRH but not VIP and (2) that VIP augmented the effectiveness of DA blockade on PRL release and was additive with domperidone (but not sulpiride) on increasing the responsiveness to TRH. However, VIP administration without concurrent administration of domperidone or sulpiride did not increase the effectiveness of TRH compared to vehicle-injected animals. From these data we concluded that VIP is a PRL-releasing hormone the effect of which is not affected by interruption in dopamine tone as is observed for TRH. Second, VIP can potentiate the stimulatory actions of at least one DA receptor antagonist and TRH on PRL release. This later finding suggests that VIP may play a modulatory role in the neuroendocrine regulation of PRL secretion in the female rat.

Animals↗

PubMed1987

Ectopic prolactin secretion from a gonadoblastoma.

A 6.5-year-old girl developed isosexual, pseudoprecocious puberty secondary to a gonadoblastoma. The tumor was found to produce and secrete both immunoassayable and bioassayable prolactin based on immunohistochemical techniques and the presence of a prolactin gradient between the tumor vein and peripheral vein. The source of the prolactin was a Sertoli-like cell. Neither growth hormone nor growth hormone-releasing hormone was detected within the tumor. This case confirms the ectopic production of prolactin by neoplastic tissue.

Child↗

PubMed1987

The lack of a physiologic effect of the stress-induced decrease of the proestrous prolactin surge in the rat.

Experiments were performed to determine whether the restraint stress-induced decrease in the proestrous prolactin (PRL) surge blocked luteolysis of the corpora lutea (CL), affected ovulation, or prevented the induction of pregnancy/pseudopregnancy in the next cycle. In all experiments rats were either stressed on proestrus and estrus, administered daily sc injections of 1 mg/day of 2-Br-alpha-ergocryptine (CB-154) for 4 days starting on diestrus II or not treated. In one experiment animals were sampled on the afternoon of proestrus to determine the effect of restraint stress on plasma PRL values and sacrificed on the morning of proestrus in the next cycle. Ovaries were removed, weighed, fixed and examined for number of CL. Restraint stress resulted in a significant increase in ovarian weight when compared to controls; CB-154 resulted in significant increases in ovarian weight when compared to stress and control animals. However, only CB-154-treated animals had a significant increase in the number of CL when compared to controls. In another experiment, animals were sacrificed on estrus of the next cycle and the oviducts examined for the number of ova. There were no differences among groups. In the final experiment, animals were placed with males of proven fertility on proestrus of the next cycle and examined for evidence of sperm in the vaginal lavage and/or vaginal plugs. CB-154 prevented the induction of pregnancy or pseudopregnancy due to a carry over effect of the drug on PRL surges. Restraint stress had no significant effect on the induction of pregnancy or pseudopregnancy. We conclude that there is no physiological significance to the stress-induced decrease of the proestrous PRL surge with respect to ovarian function or fertility.

Animals↗

PubMed1987

Restraint stress depresses prolactin surges in pseudopregnant rats and adrenalectomy does not alter the response.

Experiments were performed to determine whether restraint stress decreases the two prolactin (PRL) surges in pseudopregnant (PSP) rats in a manner similar to the stress-induced decrease of the proestrous PRL surge. Adrenal involvement as well as adaptation of the response was also investigated. Vaginal cycles were followed and animals exhibiting 2-3 normal cycles were cervically stimulated (CS) electromechanically to induce PSP. In one experiment the effect of adrenalectomy (ADX) on the nocturnal surge (NS) was investigated and was found to have no effect. In another set of experiments the effect of restraint stress was investigated. Immediately following an initial sample, the animals to be stressed had their hind legs tied together with plastic coated bell wire. Subsequent samples were taken for 3 hours. Restraint stress decreased the NS to 15% of the initial value within 30 minutes. ADX did not alter this response. Furthermore, 6-9 days of 3 hours of restraint stress did not attenuate the stress-induced decrease of the NS. Restraint stress also depressed the diurnal surge in PSP rats. These results indicate that restraint stress applied during the two PRL surges of PSP results in significant decreases in plasma PRL and that this response is not altered by ADX or by habituation to the stimulus.

Adrenalectomy↗

PubMed1987

Empty sella associated with inappropriate TSH secretion.

A child diagnosed with long-standing primary hypothyroidism at age 10 and subsequent pseudotumor cerebri after initiation of thyroid therapy developed an empty sella and inappropriate thyrotropin secretion. No other evidence of thyroid hormone resistance was evident nor was there evidence of other endocrine dysfunction. This case confirms previous reports of a relationship between autoimmune thyroid disease, pseudotumor cerebri, empty sella and inappropriate anterior pituitary function.

Adolescent↗

PubMed1987

The influence of raphe lesions, p-chlorophenylalanine, and ketanserin on the estrogen-induced afternoon prolactin surge.

Female Sprague-Dawley rats were ovariectomized and 2 weeks later injected sc with 100 micrograms polyestradiol phosphate, a long-acting estrogen, to induce the afternoon PRL surge. In one series of experiments, the dorsal raphe (DRN), median raphe (MRN), and median raphe-pontine (MRN-RPn) regions were lesioned using a radiofrequency lesion maker set at 56 degrees C for 1 min. Lesions were induced, and atrial catheters were implanted on the day of estrogen injection. Six days later, blood samples were obtained every 2 h from 1100-2100 h to monitor the afternoon PRL surge. The animals were killed, and the hypothalami were quickly frozen on dry ice and stored at -60 degrees C for determination of amine content using HPLC with electrochemical detection. The rest of the brain was fixed and sectioned to verify the location of brain lesions. Complete lesions of the DRN markedly attenuated the PRL surge (P less than 0.001) compared to the effect of sham or incomplete lesions. MRN lesions did not significantly alter the PRL surge; however, MRN lesions that included the RPn significantly (P less than 0.001) attenuated the afternoon PRL surge. Significant decreases in serotonin (5-HT) and 5-hydroxyindoleacetic acid concentrations were observed in the arcuate, ventromedial, suprachiasmatic, and medial preoptic nuclei of the hypothalamus, but not in the median eminence of the lesioned rats. DRN and MRN-RPn lesions decreased the 5-HT concentration in the ARC and MPN compared to sham lesion and DRN incomplete lesion values. Other hypothalamic areas did not show a similar effect of the lesions. The concentrations of norepinephrine, dopamine, or dihydroxyphenylacetic acid were not altered by the lesions. In a second series of experiments one group of animals was injected ip with 10 mg/kg ketanserin, a serotonergic antagonist, at 1200 h on the sampling day. A second group was given 250 mg/kg p-chlorophenylalanine (PCPA) at 1700 h for 2 days before blood sampling was initiated on the third day. Both ketanserin and PCPA completely blocked the PRL surge. In the PCPA-injected animals, the 1100 and 1300 h PRL values were significantly higher (P less than 0.01) than those in vehicle-injected controls. Animals injected with ketanserin at 1200 h had a 1300 h PRL value significantly higher (P less than 0.01) than was observed in vehicle-injected animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1987

The occurrence of pituitary prolactin depletion-transformation in lactating rats: dependence on strain of rats, homogenization conditions and method of assay.

The objectives of this study were to determine whether pre-release transformation (depletion) of pituitary prolactin occurs as the result of suckling to the same extent in several strains of lactating rats, the molecular nature of the transformed hormone, whether the quantity of transformed (depleted) prolactin recovered is dependent upon the type of homogenization buffer used and whether the method of assay influences the extent to which transformed prolactin is detected. During the course of these experiments other factors such as the methods of handling and storing pituitaries and homogenates were also found to influence the amount of prolactin recovered. The results indicated that transformation of prolactin is a very labile event which is affected by many factors. Strain and supplier of rats was critical to the observation of suckling-induced depletion of prolactin, with Spartan- and Holtzman-derived Sprague-Dawley strains exhibiting the most consistent responses. When transformation was observed, it mattered little which buffer was used for homogenization; however, alkaline or acidic buffers extracted more prolactin than did neutral buffers. Triton X-100 also significantly enhanced the efficiency of extraction by neutral buffers. Maintaining pituitaries on dry ice immediately upon removal from the animal increased the amount of prolactin recovered, as did freezing the homogenate for 1-5 weeks before assay. The addition of the protease inhibitor, benzamidine hydrochloride, did not affect the pituitary content of prolactin. Assay of prolactin by polyacrylamide electrophoresis and densitometry yielded more prolactin than either radioimmunoassay or the Nb2 lymphoma bioassay. The molecular nature of pituitary prolactin, extracted at neutral pH, as judged by gel filtration was altered slightly but consistently by suckling, such that large molecular forms increased at the expense of the smallest molecular form. We conclude from these studies that great care must be exercised when attempting to characterize dynamic changes in pituitary prolactin content in lactating rats. Strain and supplier of rats, methods of handling and storing pituitaries, types of buffers used for homogenization and methods of assay all influence the amount of prolactin recovered and can influence the extent to which rapid changes in pituitary prolactin are detected.

Animals↗

PubMed1986

A comparison of the effects of suckling or transient dopamine antagonism on thyrotropin-releasing hormone and suckling induced prolactin release in lactating rats.

Prolactin (PRL) release was studied in mid-lactational female rats by comparing the stimulatory influence of suckling to a drug protocol that mimics the effect of suckling on the anterior pituitary (AP). Animals that nursed pups for 15 minutes and were allowed to suckle again 60 minutes later for 10 minutes, released PRL effectively during both nursing episodes; however, in animals that received the dopamine (DA) agonist 2-Br-alpha-ergocryptine maleate (CB-154, 0.5 mg/rat i.v.) at the end of the first nursing period did not show an increase in plasma PRL to a second suckling stimulation by the pups. When thyrotropin releasing hormone (TRH) was substituted for the second suckling period in CB-154 treated rats, a slight increase in plasma PRL occurred 5 minutes after the injection. In a third study we transiently blocked the action of DA at the AP by injecting the DA antagonist domperidone (0.01 mg/rat i.v.), followed 5 minutes later by the administration of CB-154. One hour later animals were either allowed to suckle pups for 10 minutes or were injected with TRH. Treatment with TRH resulted in an 11 fold increase in plasma PRL but suckling was completely ineffective in inducing PRL release. These data suggest that the lack of PRL release to suckling in CB-154 treated rats was due to inhibitory effects of CB-154 on neural mechanisms which link nursing to PRL release. In addition, the data show that pharmacologic DA antagonism affects TRH releasable PRL more than does suckling. This may be due to a reduction, by suckling, of the pool of PRL that is available to be released by TRH administration.

Animals↗

PubMed1986

Restraint stress decreases afternoon plasma prolactin levels in female rats. Influence of neural antagonists and agonists on restraint-induced changes in plasma prolactin and corticosterone.

Female Sprague-Dawley rats were ovariectomized, given estrogen, and blood samples were obtained via an atrial catheter in the afternoon during the prolactin (PRL) surge. Restraint stress applied at 16.00 h and continued for 3 h resulted in marked decrease in plasma prolactin (PRL) and an increase in plasma corticosterone (B). The neural mechanism(s) involved in the plasma PRL decrease to restraint stress in the afternoon were examined using neural agonists and antagonists. The administration of pimozide, a dopamine antagonist, increased plasma PRL and completely prevented the restraint-induced decrease in PRL. This result suggested that an increase in dopamine secretion mediated the stress-induced decrease of PRL in the afternoon. In unrestrained animals, the intravenous administration of atropine (a muscarinic cholinergic antagonist), arecoline (a muscarinic cholinergic agonist), propranolol (a beta-adrenergic antagonist) and morphine (a beta-endorphin agonist) at 16.00 h decreased plasma PRL from that of vehicle-injected animals. Bicuculline (a GABAergic antagonist) had no effect while phentolamine (an alpha-adrenergic antagonist) and phenoxybenzamine (an alpha-adrenergic antagonist) initially increased and then decreased plasma PRL. Naloxone (a beta-endorphin antagonist) initially decreased and then increased plasma PRL in unrestrained animals. In restrained animals, the intravenous administration of atropine and naloxone had no effect on the decrease in plasma PRL. Bicuculline and propranolol decreased plasma PRL below that observed for restrained animals alone, while phentolamine and morphine slightly retarded the course of the decrease. Arecoline did not alter the PRL decrease to restraint in the early sample periods but was followed by a rebound increase at later times.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

The effect of transient dopamine antagonism on thyrotropin-releasing hormone-induced prolactin release in pregnant rats.

The effect of transient dopamine (DA) antagonism on the sensitivity of pituitary lactotrophs to the PRL-releasing effect of TRH was investigated in rats on days 3, 9, 15, and 21 of pregnancy. Each animal, bearing an indwelling intraatrial catheter, received injections of either the DA antagonist domperidone (0.01 mg/rat, iv) or saline at 0930 h on the day of the experiment. Five minutes later, all animals were given the DA agonist 2-bromo-alpha-ergocryptine maleate (CB-154; 0.5 mg/rat, iv), followed 60 min later by the administration of TRH (1.0 microgram/rat iv). Plasma samples obtained during the experiment were assayed by RIA for PRL and progesterone (P). The results showed that transient DA antagonism increased the sensitivity to TRH as a PRL-releasing stimulus on the morning of day 3 of pregnancy, but not on days 9 and 15. However, the response was present on day 9 in animals that were hysterectomized (HS) on day 6 of pregnancy. The increase in sensitivity of lactotrophs to TRH after DA blockade was observed on day 21 of pregnancy. Plasma levels of P were high on days 3, 9, and 15, but decreased markedly by day 21. In a second experiment, the anterior pituitary (AP) PRL content was determined on days 3, 9, 15, and 21 of pregnancy. The results demonstrated that AP PRL significantly decreased between days 3 and 9 of pregnancy in both intact and HS animals. However, AP PRL concentrations in animals killed on days 15 and 21 were significantly greater than that on day 9 but were not different from that observed on day 3 of pregnancy. We conclude that the ability to transform AP PRL to a TRH-releasable pool by the transient blockade of DA is present in early and late pregnancy, but is absent in midpregnancy. Since this secretory mechanism is retained on day 9 after hysterectomy on day 6 of pregnancy, it appears that the secretory products of the uterine-placental unit are inhibitory to transformation. Further, this inhibitory effect at midpregnancy cannot simply be the result of decreased AP PRL content or changes in plasma P. Finally, the return of the transformation mechanism on the day before parturition (day 21) may be due to the increase in estrogen secretion that occurs in late pregnancy, since we have previously shown that estrogen can induce this AP secretory mechanism.

Animals↗

PubMed1986

The effects of transient dopamine antagonism on thyrotropin-releasing hormone-induced prolactin release in pseudopregnant rats.

The effectiveness of TRH in releasing PRL after transient dopamine (DA) blockade was investigated in female rats between days 3 and 11 of pseudopregnancy (PSP). At 0930 h on the morning of the experiment, each animal was injected with the DA antagonist domperidone (0.01 mg/rat, iv) or vehicle (acetic acid in saline); 5 min later, the DA agonist 2-bromo-alpha-ergocryptine maleate (CB-154; 0.5 mg/rat, iv) was administered. Sixty minutes later, TRH (1.0 micrograms/rat, iv) was administered. Blood samples were withdrawn via indwelling catheters before, 5, 20, 40, and 70 min after domperidone or vehicle administration, and 5 and 10 min after TRH administration. On day 3 of PSP, TRH-induced PRL release was significantly enhanced by the domperidone-CB154 treatment compared to that in vehicle-treated control rats. By day 9 of PSP, the effectiveness of TRH in stimulating PRL release after domperidone treatment was decreased by 50% compared to that on day 3 of PSP. This reduction in PRL response to TRH was not due to decreased progesterone levels, as no difference was observed in plasma progesterone between days 3 and 9. Rats that were given domperidone on day 11 of PSP did not exhibit a significant increase in sensitivity to TRH; however, the effectiveness of TRH was enhanced by domperidone on day 11 of PSP in animals that were hysterectomized on day 2 of PSP. Since DA receptor blockage increased the sensitivity to a putative PRL-releasing factor (TRH) and this mechanism was eliminated around the time that the PRL surges of PSP disappear, we suggest that this pituitary mechanism is a critical component of the PRL release mechanism during the surges of PSP. Further, the observed loss of the mechanism between days 9 and 11 of PSP may be due to the direct influence at the anterior pituitary of a uterine PRL inhibitory factor which has been recently described.

Animals↗

PubMed1986

The effect of transient dopamine antagonism on thyrotropin-releasing hormone-induced prolactin release in ovariectomized rats treated with estradiol and/or progesterone.

PRL release was studied in ovariectomized (OVX) rats pretreated with estradiol benzoate (EB), progesterone (P), or a combination of both steroids using a protocol that was selected to mimic ovarian steroid changes that have been observed during the female rat 4-day estrous cycle and early pregnancy. On the morning of the experiment, the animals received injections of either the dopamine (DA) antagonist domperidone (0.01 mg/rat iv) or vehicle (acetic acid in saline). Five minutes later, all animals received injections of the DA agonist 2-bromo-alpha-ergocryptine (CB-154; 0.5 mg/rat, iv) followed 60 min later by the administration of TRH (1.0 microgram/rat, iv). Plasma obtained from blood samples taken during the experiment was assayed for PRL by RIA. In OVX or P-treated OVX rats, a transient blockade of DA by domperidone did not alter the sensitivity of the pituitary to TRH administration, as measured by an increase in plasma PRL. However, such an effect of DA blockade was induced by 2 days of EB treatment and was maintained and amplified by P administration after EB injections. We conclude that enhancement of the PRL-releasing effect of TRH by DA antagonism, a mechanism we previously observed in female rats during midlactation, proestrus, estrus, and metestrus using the present drug protocol, can be induced by estrogen and maintained by P. Further, our data suggest that the previously observed loss of this secretory mechanism on the morning of diestrus may be due to the decrease in plasma P that takes place between metestrus and diestrus.

Animals↗

PubMed1985

The influence of blinding, olfactory bulbectomy and pinealectomy on plasma and anterior pituitary prolactin levels and on uterine and anterior pituitary weights in normal and neonatally androgenized rats.

Lactating Sprague-Dawley rats had their litters adjusted to 8-10 pups on day 3 of lactation favoring females and some litters were injected with 1.25 mg of testosterone propionate to neonatally androgenize (NA) them. At 22-25 days of age both normal and NA animals were ovariectomized (OVX) and subjected to either sham olfactory bulbectomy (ANOS) + sham pinealectomy (PX), blinding (BLD) + ANOS or BLD + ANOS + pinealectomy (PX). At 13 weeks of age all animals were injected with 0.5 mg of polyestradiol phosphate. At 15 weeks of age the animals were fitted with atrial catheters and at 16 weeks of age blood samples (0.3 ml) were obtained every 3 hours over a 24 hour period. Uterine and anterior pituitary (AP) weights were recorded at sacrifice. Plasma and AP were assayed for prolactin (PRL) by RIA and AP were also assayed for PRL using the Nb2 lymphoma cell PRL bioassay. In both normal and NA animals, BLD + ANOS suppressed plasma PRL levels and PX partially prevented this response. Uterine weights were similar among groups while AP weights were significantly lower for sensory deprived animals. Anterior pituitaries extracted at pH 7.6 had a PRL concentration that was higher for the BLD + ANOS groups when estimated by either RIA or BA, a result that was not observed when the AP were extracted at pH 10.6. The amount of PRL extracted at pH 10.6 was twice that obtained at pH 7.6. Sensory deprived animals that were OVX prepubertally and administered estrogen as adults had a small but significant increase in mean plasma prolactin at 1700 hr. Both normal and NA animals responded in a similar manner to experimental manipulation.

Animals↗

PubMed1985

Effect of lesions of the corticomedial amygdala on the nocturnal prolactin surge.

It has been reported that the corticomedial amygdala (CMA) is involved in regulating various hypothalamic and neuroendocrine events. This study examined the role of the CMA in the regulation of the nocturnal surge of prolactin (PRL) induced by cervical stimulation (CS). Female Sprague-Dawley rats were ovariectomized, received CMA or sham lesions, and were placed on a reversed lighting schedule of 14 h light:10 h dark. 3 weeks later, all rats were cervically stimulated. 5 days after CS (CS + 5) rats were fitted with chronic, intraatrial catheters, and daily progesterone (P) injections (10 mg s.c.) were initiated. On CS + 8, CS + 12, and CS + 15, sequential blood samples were taken from unrestrained rats at 00.00, 02.00, 04.00, 06.00, 08.00, and 10.00 h (animal time). CMA lesions significantly reduced peak PRL levels on CS + 12 and CS + 15, but not on CS + 8. When ovariectomized CS rats received either 1 or 10 mg P/day and were sampled on CS + 12, CS + 15, and CS + 19, CMA lesions reduced the magnitude of the surge on CS + 12 and CS + 15, a time when P amplification of the surge was apparent. On CS + 19, when P amplification of the surge was absent, CMA lesions had no effect. CMA lesions greatly reduced peak PRL levels on CS + 12, but not on CS + 8, when rats were lesioned, catheterized, and injected daily with 1 or 10 mg P/day on CS + 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗

PubMed1985

Central nervous system regions involved in the estrogen-induced afternoon prolactin surge. I. Lesion studies.

Central nervous system regions were examined in long term ovariectomized rats to determine if they are involved in the estrogen-induced afternoon surge in plasma PRL. Adult female rats were ovariectomized 2-3 weeks before bilateral radiofrequency or electrolytic lesions of the brain were placed on day 0. In short term lesion studies, catheterizations and sc injections of polyestradiol phosphate (PEP) were done after the lesion was made; blood sampling was performed on day 2, 3, 4, or 6. In long term lesion studies, the catheterization and PEP injection were done on day 21; blood was collected on day 28. In short term experiments, extensive lesions in the medial preoptic area/suprachiasmatic nuclei (MPO/SCN) completely blocked the PEP-induced afternoon PRL surges sampled on days 2, 3, 4, and 6, while bilateral lesions in the corticomedial amygdala (CMA) had no effect. Discrete bilateral lesions of either MPO or SCN eliminated the afternoon PRL surge on day 6. Discrete, yet complete, lesions of the ventromedial nuclei of the hypothalamus also blocked the PRL surge; however, lesions in the dorsomedial nuclei of the hypothalamus increased, the magnitude of the afternoon PRL surge. In long term studies, lesions of the CMA delayed and attenuated the PEP-induced PRL surge, and lesions of the stria terminalis for 4 weeks had a similar effect. As in the short term lesion studies, long term lesions of the MPO/SCN eliminated the daily rhythm of PRL secretion, although small sporadic rises in plasma PRL levels could be observed throughout the sampling period. It can be concluded that structural integrity of the MPO/SCN and ventromedial hypothalamic nuclei is essential for the estrogen-induced afternoon PRL surge; destruction of the dorsomedial hypothalamic nuclei can increase the magnitude of the afternoon PRL surge; and the CMA is not essential for induction of the PRL surge even though removing its neural input to the hypothalamus for an extended period can delay the onset of and suppress the magnitude of hormone release.

Amygdala↗