Abnormal Growth Hormone Release Following Luteinizing Hormone Releasing Hormone in Anorexia Nervosa

Abstract: We studied the luteinizing hormone (LH), follicle stimulating hormone (FSH) and growthhormone (GH) secretion following an i.v. injection of 0.1 nig of luteinizing hormone releasing hormone (LHRH) in patients with anorexia nervosa, who showed the GH secretion afterthyrotropin releasing hormone (TRH). Five out of 11 patients had an elevated plasma GH level in a fasting state. The administration of LHRH resulted in a significant increase in the plasma GH concentrations in 3 of the 11 patients. Three other patients also showed anelevation of the plasma GH concentration to 7.0, 18.4 and 29.6 ng/ml, which were 212, 175 and 191% of the preinjection levels, respectively. There is a positive correlation between the basal and peak plasma GH levels after LHRH. These increases, however, were related to neither the plasma gonadotropin responses to LHRH nor the plasma GH responses to TRH. The basal levels of plasma LH were reduced in 8 patients and normal responses to LHRH were observed in only one patient. Although plasma FSH was undetectable in 5 patients, the FSH response to LHRH appeared normal in 9 patients. These results indicate thatan elevation of the plasma GH level after LHRH is not confined to patients with a GH secreting pituitary tumor but observed in subjects with anorexia nervosa and further suggest that the GH responsiveness to non-specific hypothalamic releasing hormones may be due to the impaired hypothalamic control in anorexia nervosa.     

Disturbances in the hypothalamo-pituitary-adrenal and other neuroendocrine axes in bulimia

Disturbances in the hypothalamo-pituitary-adrenal (HPA) and other endocrine axes were assessed in 24 women with bulimia and healthy controls. Overnight blood samples for measuring nocturnal plasma cortisol, prolactin (PRL), growth hormone (GH), luteinizing hormone (LH), and follicle stimulating hormone (FSH) were obtained at 30-min intervals. A 1.5 mg dexamethasone suppression test (DST) and a TRH-test were performed. Patients were monitored closely while their nutritional intake was recorded over 21 days. Compared with healthy controls, nocturnal cortisol plasma levels were not elevated in the bulimics. There was a trend toward insufficient cortisol suppression in the DST in patients with bulimia, which was most pronounced in patients with signs of restricted caloric intake. Plasma dexamethasone levels were significantly reduced in bulimics compared with healthy controls. There was a trend for blunted thyrotropin stimulating hormone (TSH) responses to thyrotropin releasing hormone (TRH) in bulimia. The prolactin response to TRH was significantly reduced in bulimics with a history of anorexia nervosa. Plasma LH and plasma FSH were significantly reduced in bulimics with signs of reduced caloric intake [low T3, high levels of beta-hydroxy-butyric acid (BHBA), reduced daily caloric intake, high number of fasting days] as compared with healthy controls. Bulimics with high BHBA levels had significantly reduced nocturnal prolactin plasma levels. Results show that multiple neuroendocrine disturbances exist in bulimia in a milder form than in anorexia nervosa. Evidence for the impact of caloric intake on endocrine functions is presented. Endocrine dysfunctions in our bulimic sample did not show a positive association with the presence of depressive symptoms.     

Abnormal serum prolactin responses to luteinizing hormone-releasing hormone (LHRH) in patients with anorexia nervosa and bulimia

Abnormal responses of serum prolactin (PRL) to luteinizing hormone-releasing hormone (LHRH) stimulation have been observed in anovulatory women and in hypogonadal patients. Various endocrinological abnormalities have been demonstrated in patients with anorexia nervosa (AN). The present study was undertaken to further investigate responses of serum PRL, growth hormone (GH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) to LHRH stimulation in 65 patients with AN and in 12 patients with bulimia before therapy and in the AN patients after several months of treatment, and in comparison to 12 normal women of the same age. Serum PRL responses to LHRH were positive (peak PRL levels greater than 25 ng/ml and delta increase in PRL greater than 10 ng/ml) in 16.9% of AN and 16.6% of bulimic patients; they were negative (absent) in all controls. Following restoration of the AN patients to normal body weight, the PRL responses to LHRH became normalized in those patients whose eating disorder behavior also returned to normal. However, in those patients whose eating disorder patterns continued to be abnormal, abnormal PRL responses persisted. The bulimic patients were of normal body weight, and yet had abnormal PRL responses. Thus, the responses of PRL correlated more closely with the behavior of the underlying eating disorder rather than with body weight gain or normal body weight.     

Thyrotropin, prolactin, and growth hormone responses to thyrotropin-releasing hormone in anorexia nervosa and bulimia

Serum thyrotropin (TSH), prolactin (PRL), and growth hormone (GH) levels were measured before and after stimulation with thyrotropin-releasing hormone (TRH) in 10 patients with bulimia, 7 with features of the restricting subtype of anorexia nervosa, and 6 with bulimic subtype of anorexia nervosa. The mean basal levels of TSH, PRL, and GH did not differ among the three groups. A delayed TSH response was found in 86% of the restricting anorectics, 80% of the bulimic anorectics, and 22% of the bulimics. The PRL response was normal in all patients, with no significant difference among the three groups. Elevated basal GH levels were found in 29% of the restricting anorectics, 33% of the bulimic anorectics, and 33% of the bulimics. An abnormal GH increase after TRH stimulation was observed in 50% of the restricting anorectics, 20% of the bulimic anorectics, and 13% of the bulimics. These results suggest that some patients with bulimia, and some with anorexia nervosa, have a hypothalamic dysfunction. These neuroendocrine abnormalities do not appear to be due solely to low weight or to metabolic changes resulting from binge eating and are not associated with depressive symptoms.     

The endocrine status in anorexia nervosa (author's transl)

Alterations in the secretion of iodothyronines, cortisol, testosterone and growth hormone have previously been described in anorexia nervosa. We have studied prolactin and gonadotropins secretion in 23 cases of anorexia nervosa. Prolactin secretion was normal. Modifications in gonadotropins release were observed. However they could not be always related to weight loss since amenorrhea could either precede weight loss or still be present after return of the weight to normal. In all cases, FSH release after LHRH stimulation was normal. No increase in LH levels was observed after LHRH injection when the weight was 70% below the ideal weight. With increasing weight, LH release progressively recovered and normal LHRH-induced LH release was obtained when the weight was above 90% of the ideal weight. At normal weight, the ratio of LH/FSH was normal in patients menstruating less than 3 months after the test, while the ratio was low in non-menstruating females. In conclusion, when the weight was insufficient basal levels of FSH and LH and responses after LHRH stimulation corresponded to a prepuberal stage. An increase in the LH/FSH ratio and a normal LH/FSH ratio preceeded the recovery of menstruations. In about 1/3 of the cases, such an evolution was not observed without any satisfactory explanation. Other factors than weight may be involved, especially when the amenorrhea persists after weight recovery.     

Deranged anterior pituitary responsiveness to hypothalamic hormones in depressed patients.

Abnormal anterior pituitary (AP) responsiveness to acute administration of thyrotropin-releasing hormone (TRH) and luteinizing hormone-follicle stimulating hormone-releasing hormone (LH-RH) was investigated in 14 patients (two men and 12 women) suffering from primary affective disorders. In ten, TRH, 500 microgram given intravenously, induced a rise in plasma growth hormone (GH) level, while in eight patients it induced a rise in plasma levels of FSH or LH or both. When LH-RH, 150 microgram was administered intravenously to ten patients, it induced a rise in plasma GH level in one patient and increased plasma prolactin level in three patients. Collectively, in only three of 14 patients was conventional AP responsiveness to hypothalamic neurohormones present. These findings demonstrate the existence of a profound derangement of AP responsiveness to hypothalamic neurohormones in depressed patients and suggest that a primary alteration in the physiologic links between the central nervous system and the AP may be at the origin of the neuroendocrine disturbance.     

Serum leptin and gonadotropin levels in patients with anorexia nervosa during weight gain

Leptin plays an important role in reproductive function. In patients with acute anorexia nervosa, serum leptin levels have repeatedly been shown to be lower than in age-matched controls. We have previously hypothesized that the amenorrhea characteristic of anorexia nervosa is related to this low leptin secretion. In an attempt to address this hypothesis, serum levels of leptin and follicle stimulating hormone (FSH) and luteinizing hormone (LH) of 16 female inpatients with anorexia nervosa or an eating disorder not otherwise specified (atypical anorexia nervosa) were measured on a biweekly basis during weight gain. We hypothesized that a serum leptin level of 1.85 microg L(-1) would be associated with gonadotropin levels at or above the minimal level observed during the menstrual cycle in healthy adult fertile females. Our results revealed that increments of LH levels generally tracked increments of leptin levels during the first weeks of treatment. Similarly, in those patients with low referral leptin levels, FSH initially also tracked leptin levels. In contrast, a relationship between gonadotropin levels and leptin secretion was no longer discernible after LH and FSH levels had peaked. Those patients with exceedingly low leptin levels upon admission revealed a slow increase of gonadotropin levels. Our hypothesis of a threshold leptin level of 1.85 microg L(-1) was supported for LH only.     

Triiodothyronine administration reduces serum growth hormone levels and growth hormone responses to thyrotropin-releasing hormone in patients with anorexia nervosa

The aim of this study was to test the hypothesis that low serum T3 concentrations may promote an abnormal growth hormone (GH) response to thyrotropin-releasing hormone (TRH) in patients with anorexia nervosa. Eight anorexic women and two anorexic men, ages 15-25 years, with low free T3 circulating levels (mean +/- SEM = 2.8 +/- 0.3 pmol/l) were studied. A TRH test (200 micrograms IV) was carried out under basal conditions and repeated following treatment with oral T3 (1.5 micrograms/kg BW/day) for eight days. Following T3 administration, GH levels dropped significantly from a baseline of 7.1 +/- 1.3 micrograms/l to 3.1 +/- 0.7 micrograms/l (p less than 0.02), as did GH peak responses to TRH (9.0 +/- 1.0 micrograms/l vs 4.4 +/- 0.8 micrograms/l, p less than 0.01). ANOVA and analysis of area under the curve (AUC) confirmed that after T3 treatment there was a significant reduction in TRH-induced GH release in these patients (GH AUC: 902 +/- 132 micrograms/l vs. 456 +/- 91 micrograms/l, p less than 0.02). TSH responses to TRH, which were normal prior to T3 treatment, completely disappeared following it, and PRL responses to TRH also were diminished. Although our experimental approach does not permit a conclusion that low T3 levels were the primary reason for these changes, the data support the theory that low T3 circulating levels may facilitate abnormal GH secretion and the GH-releasing activity of intravenous TRH.     

In vivo and in vitro effects of cholecystokinin on gonadotropin, prolactin, growth hormone and thyrotropin release in the rat

Varying doses of cholecystokinin (CCK) dissolved in 2 μl of 0.9% NaCl or 2 μl of saline alone were injected into the third ventricle of conscious ovariactomized (OVX) rats bearing 3rd ventricular cannulae. Plasma luteinizing hormone (LH), prolactin (PRL), growth hormone (GH), thyrotropin (TSH) and follicle stimulating hormone (FSH) levels were measured by RIA in jugular blood samples drawn through an indwelling silastic cannula. Control injections of saline i.v. or into the 3rd ventricle did not modify plasma hormone levels. Intraventricular injections of 4, 40 and 500 ng CCK produced a significant suppression of plasma LH within 5 min of injection. Injection of 4 or 500 ng doses of CCK has no effect on plasma PRL levels, but injection of the 40 ng dose produced a significant elevation of plasma PRL within 15 min. Plasma GH levels increased significantly within 15 min of the 3rd ventricular injection of each dose of CCK. The 40 ng dose of CCK caused a progressive reduction of plasma TSH which was significant by 15 min and lasted through the 60 min of experimentation. The highest dose of 500 ng reduced plasma TSH levels within 5 min. Plasma FSH was not altered by any dose of CCK. Intravenous injection of CCK caused a dose-related increase in plasma prolactin levels within 5 min, but only the highest dose of 1000 ng produced a significant decrease in plasma LH. No significant changes in GH, TSH or FSH levels were observed after i.v. injection of CCK. In vitro incubation of hemipituitaries from male rats with doses of CCK ranging from 10 ng to 5 μg had no effect on pituitary hormone release into the medium. The results indicate that CCK can alter pituitary hormone release via a hypothalamic action and suggest that it may act as t transmitter or modulator of neuronal activity controlling the release of hypothalamic releasing and/or inhibiting hormones.     

Pituitary hyperplasia after goserelin (LHRH–analogue) therapy

A 78-year-old male was treated with goserelin (Zoladex) for 16 months for metastasizing prostate carcinoma. This therapy is clinically equivalent to orchidectomy, as the application of the luteinizing hormone-releasing hormone (LHRH)-analogue Zoladex causes suppression of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) by down-regulation of pituitary receptors. Consequently, testicular androgen production is inhibited and testosterone levels are decreased to castration levels. In the present case we found diffuse, partially nodular hyperplasia of growth hormone (GH) and adrenocorticotropin (ACTH) producing cells in the anterior pituitary gland at autopsy. As Zoladex reduces pituitary receptors for releasing hormones (RH), a globally increased hypothalamic secretion of RH might be responsible for the ACTH- and the GH-cell hyperplasia. We cannot exclude that Zoladex may cause not only adenomas in rat pituitary glands as reported previously, but also a (nodular) hyperplasia of the pituitary gland in man.     

Postmortem stability and characterization of immunoreactive luteinizing hormone releasing hormone and thyrotropin releasing hormone in human brain tissue

PARKER, C. R., JR. AND J. C. PORTER. Postmortem stability and characterization of immunoreactive luteinizinghormone releasing hormone and thyrotropin releasing hormone in human brain tissue. BRAIN RES. BULL. 8(6) 623–630, 1982.—The content and concentration of immunoreactive luteinizing hormone releasing hormone (LHRH) and of thyrotropin releasing hormone (TRH) were evaluated in hypothalamic tissue of 52 cadavers of adult humans (33 males, 18 to 70 years of age, and 19 females, 17 to 74 years of age). Autopsy was performed between 2.5 and 21 hr after death. When the data were subjected to linear regression analysis, it was found that neither the concentration nor content of LHRH or TRH varied significantly between 2.5 and 21 hr postmortem. The stability of LHRH or TRH in hypothalamic fragments that included the pituitary stalk was similar to the stability of these peptides in hypothalamic fragments that did not include the pituitary stalk. The concentration as well as content of LHRH and TRH in specimens analyzed 2.5 to 12 hr postmortem was similar to that in specimens analyzed 13 to 21 hr postmortem. When aliquots of a homogenate or a synaptosomal fraction of hypothalamic tissue were incubated at 4° or 37°C prior to the analysis of endogenous LHRH and TRH, it was found that the concentration of each peptide remained constant for several hours. However, when synthetic LHRH or TRH was mixed with aliquots of homogenates or subcellular fractions of hypothalamic tissue and incubated at 37°C, each exogenous peptide was rapidly degraded. Based upon the results of gel filtration chromatography, high performance liquid chromatography, biological activity (LHRH), and susceptibility to degradation by serum (TRH), immunoreactive LHRH and TRH in extracts of human brain tissue appeared to be similar to synthetic LHRH and TRH. These findings support the view that, although human brain tissue has the capacity to degrade LHRH and TRH, the endogenous pools of these peptides are sequestered in such a manner that they are stable for several hours in the postmortem human brain. These data are suggestive that brain tissues obtained at autopsy may be useful in the study of peptidergic systems in the human.     

Acute ethanol treatment lowers hypophyseal portal plasma luteinizing hormone-releasing hormone (LH-RH) and systemic plasma LH levels in orchidectomized rats

Acute ethanol (EtOH) treatment resulted in a significant decline in hypophyseal portal plasma levels of luteinizing hormone-releasing hormone (LH-RH) in orchidectomized rats. This was accompanied by a similar decrement in circulating luteinizing hormone (LH) without, however, modifying plasma follicle-stimulating hormone (FSH) levels at time when peak blood alcohol concentrations occurred. Thus, acute alcohol intoxication lowers circulating LH levels primarily by impairing hypothalamic neuronal secretion of LH-RH into the portal blood.     

Studies of growth hormone (GH), thyrotropin (TSH) and prolactin (PRL) secretion in anorexia nervosa.

(1) Studies of serum thyrotropin (TSH), growth hormone (GH) and prolactin (PRL) responses following TRH administration were performed in 7 subjects with anorexia nervosa (AN). (2) Five patients demonstratod significant increases in circulating GH from a mean of 15.6 ng/ml to a peak of 31.8 ng/ml 30 min after TRH. (3) Basal TSH concentrations were undetectable (< 2μU/ml) in all patients prior to stimulation but following TRH, significant elevations (ΔTSH > 6 μU/ml) in TSH were identified in 3/7 patients. (4) The largest elevations in TSH occurred in the two subjects in whom no GH rises were found, whereas blunted TSH rises were noted in 4/5 subjects who showed substantial GH secretory responses to TRH. (5) Basal PRL concentrations were normal and rose appropriately after TRH in all subjects. (6) These studies demonstrate that GH secretion can be provoked in AN by TRH similar to patterns in other states (acromegaly, uremia, protein-calorie malnutrition), characterized by elevated basal GH concentrations. (7) It is hypothesized that activated GH secretion may favor TRH responsivity of somatotrophs. (8) Obtundation of TSH secretion in AN, moreover, may be related to the augmented secretion of GH, since TSH secretion can be lowered by exogenous GH administration in man.     

Episodic hormone secretion during sleep in Kleine-Levin syndrome: evidence for hypothalamic dysfunction

"Acute" hypothalamic-pituitary function tests including insulin tolerance test, LRH, ACTH and TRH stimulation tests and nocturnal secretory pattern of human growth hormone, 11-OHCS, prolactin, FSH, LH and TSH were studied in a 23-year-old male with Kleine-Levin syndrome during the course of a typical hypersomnic attack. The "acute" tests revealed paradoxical growth-hormone response to TRH stimulation, borderline high basal plasma prolactin levels with normal response to TRH. The hormonal secretory pattern during sleep revealed abnormalities in LH, 11-OHCS and prolactin secretion. These together with the results of the "acute" tests are indicative of an abnormality in the hypothalamic regulation of various pituitary hormones. This observation may indeed be the first laboratory demonstration confirming a long-standing hypothesis that Kleine-Levin syndrome is related to hypothalamic dysfunction.     

Neuroendocrine aspects of primary endogenous depression. X: Serum growth hormone measures in patients and matched control subjects

To determine the extent of dysregulation of growth hormone (GH) secretion in endogenous depression, we measured nocturnal serum GH concentrations and GH responses to thyrotropin-releasing hormone (TRH, gonadotropin-releasing hormone (LHRH), and dexamethasone administration in 40 Research Diagnostic Criteria primary, definite endogenous depressives and 40 individually matched normal control subjects. Compared with their controls, the patients showed no difference in basal nocturnal GH concentrations or in GH responses to TRH or LHRH. The GH measures were not significantly related to the other endocrine measures reported previously, including dexamethasone suppression test status. None of the diagnostic schemes for endogenous/melancholic depression which we studied was significantly related to the GH measures in the patients. Of the other subject and symptom variables, the mood depression factor of the Hamilton depression scale and the performance difficulty factor of the Beck depression inventory were moderately negatively correlated with the nocturnal GH measures. These findings suggest that, in contrast to the previously reported hypothalamopituitary-adrenal cortical and thyroid axis abnormalities in our patients, GH secretion was relatively normal. Patients with more severe depressed mood and greater difficulty accomplishing tasks did have moderately lower nocturnal GH values.     

L-tryptophan and neuroendocrine regulation in neurologic patients: hormone responses to L-tryptophan loading in patients with hypothalamic lesions

1. Oral administration of 2 g of l-tryptophan induced a marked plasma elevation of total and free tryptophan during the 2 hr of sampling in both normal subjects and in neurologic patients. Plasma free trytophan concentration showed a peak about 60 min after loading with l-tryptophan. 2. Plasma immunoreactive follitrophin (FSH) and lutrophin (LH) levels were not altered after l-tryptophan treatment. 3. Plasma immunoreactive somatotrophin (growth hormone, GH) levels showed a statistically significant elevation after l-tryptophan loading in both normal subjects and in neurologic control patients. In two acromegalic patients there was a very marked elevation of plasma somatotrophin levels 90 min after loading. No responses of plasma somatotrophin to l-tryptophan were observed in patients with hypothalamic lesion or with hypopituitarism. 4. Plasma cortisol levels showed significant morning decline during loading either with l-tryptophan or with l-leucine as placebo in normal subjects and in neurologic control patients. In patients with hypothalamic lesion the monitoring of plasma cortisol concentrations during l-tryptophan loading revealed a primary elevation with a subsequent slight decline. No variation of plasma cortisol was found in patients with hypopituitarism. 5. It was concluded that the brain serotoninergic system can be activated by l-tryptophan treatment which results in alterations of the hypothalamic regulation of somatotrophin secretion. When neuroendocrine dysfunction is due to structural lesions in the hypothalamus or in related regions, l-tryptophan loading is unable to modify somatotrophin secretion. The normal morning decline of plasma cortisol levels is lacking in such patients.     

Gonadotropin response to LH-RH in anorexia nervosa and bulimia

Serum LH and FSH levels before and after stimulation with LH-RH were measured in 9 patients with bulimia, 7 with a restricting subtype and 6 with a bulimic subtype of anorexia nervosa. All patients with anorexia nervosa and 5 (56%) patients with bulimia showed amenorrhea for at least 5 months, while 4 (44%) of the bulimic patients showed oligomenorrhea. Mean basal levels of LH and FSH were low in patients with restricting and bulimic anorexia nervosa, but were normal in patients with bulimia. The response of LH and FSH to LH-RH was impaired in approximately half of the patients with the two subtypes of anorexia nervosa, whereas it was normal in all but one patient with bulimia. These results suggest that bulimic patients with amenorrhea or oligomenorrhea have hypothalamic dysfunctions, which do not appear to be due solely to low weight or to metabolic changes resulting from binge eating, vomiting or purgative use.     

The in vitro role of tumour necrosis factor-alpha and interleukin-6 in the hypothalamic-pituitary gonadal axis

The adipocyte derived hormone leptin has been implicated as an important nutritional signal to the reproductive system, but the role of other adipocyte related cytokines is not clear. Tumour necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 are present in adipose tissue and released into the circulation where plasma levels correlate positively with body mass index and body fat mass. These cytokines could play a role in signalling nutritional status to the hypothalamic-pituitary-gonadal axis. We investigated the effects of TNF-alpha and IL-6 on basal and luteinizing hormone releasing hormone (LHRH) stimulated luteineizing hormone (LH) release from cultured anterior pituitary cells, harvested from either proestrus female or male Wistar rats. We examined the effects of TNF-alpha and IL-6 on LHRH release from hypothalamic explants harvested from proestrus female and male rats in vitro. IL-6 significantly suppressed LHRH stimulated LH release from male dispersed pituitaries throughout the dose range, but did not influence basal LH release. IL-6 had no effect on basal or LHRH stimulated LH release in dispersed pituitaries from proestrus females. By contrast, TNF-alpha significantly suppressed LHRH stimulated LH release in dispersed pituitaries from proestrus female rats in a dose responsive manner, but did not influence basal LH release. TNF-alpha had no effect on basal or LHRH stimulated LH release in dispersed pituitaries from male rats. TNF-alpha and IL-6 had no effect on LHRH release from male hypothalamic explants in vitro. TNF-alpha and IL-6 had no effect on LHRH release from proestrus female hypothalamic explants in vitro. TNF-alpha and IL-6 have differential effects in dispersed pituitaries harvested from males and proestrus female rats. TNF-alpha and IL-6 may be important in mediating some of the nutritional effects on the reproductive axis by acting at the level of the anterior pituitary rather than the hypothalamus.     

Luteinizing hormone and luteinizing hormone-releasing hormone secretion is under locus coeruleus control in female rats

It has been suggested that norepinephrine (NE) from the locus coeruleus (LC) plays an important role in triggering the preovulatory surge of gonadotropins. This work intended to study the role of LC in luteinizing hormone (LH) secretion during the estrous cycle and in ovariectomized rats treated with estradiol and progesterone (OVXE(2)P) and to correlate it with LH releasing hormone (LHRH) content in the medial preoptic area (MPOA) and median eminence (ME). Female rats on each day of the estrous cycle and OVXE(2)P were submitted to jugular cannulation and LC electrolytic lesion or sham-operation, at 09:00 h. Blood samples were collected hourly from 11:00 to 18:00 h, when animals were decapitated and their brains removed to analyze LC lesion and punch out the MPOA and ME. Plasma LH levels and LHRH content of MPOA and ME were determined by radioimmunoassay. During metestrus, diestrus and estrus, LC lesion did not modify either LH plasma concentrations or LHRH content, but completely abolished the preovulatory LH surge during proestrus and the surge of OVXE(2)P. These blockades were accompanied by an increased content of LHRH in the MPOA and ME. The results suggest that: (1). LC does not participate in the control of basal LH secretion but its activation is essential to trigger spontaneous or induced LH surges, and (2). the increased content of LHRH in the MPOA and ME may be due to a decreased NE input to these areas. Thus, LC activation may be required for depolarization of LHRH neurons and consequent LH surges.     

Changes in specialized cognitive function following changes in hormone levels

Increase of follicle stimulating hormone (FSH) and luteinizing hormone (LH) in men by injection of luteinizing hormone releasing hormone (LHRH) prevented improvement in a spatial orientation test relative to a placebo condition. By contrast, performance on a fluency task was significantly increased after LHRH injection relative to the placebo condition. These data support between-subject results where FSH was negatively correlated with visuospatial skills and positively correlated with fluency. There was no change in cognitive function in males following injection of testosterone. There were also no fluctuations in cognitive function that coincided with hormonal fluctuations of the menstrual cycle in women.