The stimulation of luteinizing hormone and follicle-stimulating hormone secretion in quail with complete and skeleton photoperiods

Photostimulation of quail by long daylengths stimulates LH and FSH release, the earliest increases in these hormones being detectable after 1 long day. Reproductive maturity is complete within 1 month. Steroid feedback becomes important during the second week of photostimulation and restricts LH and FSH secretion to a fraction of the concentrations observed in gonadectomized birds. The photoperiodic response is not all-or-none, and above a certain “critical daylength” the rate of gonadal growth, primarily controlled by the levels of FSH and testosterone, is proportional to daylength. Photoperiodic responses are qualitatively identical in gonadectomized and intact quail, arguing that stimulatory daylengths act directly on the hypothalamo-pituitary axis to alter LH and FSH secretion, and do not act by altering steroid feedback sensitivity and thereby gonadotrophin release. Any changes in feedback sensitivity are a consequence not a cause of the photoperiodic drive on the system. The use of “skeleton” photoperiods to mimic complete photoperiods is discussed. Whether or not one or two peaks of photoperiodic induction appear in asymmetric skeleton experiments depends both upon the duration of the first light period and of the night break itself. The rate of induction is less when quail are photostimulated with night breaks than with “complete” daylengths. The temporal position of the circadian rhythm(s) involved in photoperiodic time measurement in quail is controlled by both “dawn” and “dusk,” and so the position of the rhythm is phase-delayed as the days lengthen, occurring later and later in the night. This arrangement might have some bearing on the seasonal shift in critical daylength that occurs in quail exposed to natural photoperiods. The situation is compared with that in insects and plants.     

Changes in gonadotrophin-releasing hormone and LH in Japanese quail during the first few days of photostimulation

Castrated Japanese quail responded to a single long day with a five- to eightfold increase in plasma LH levels. A rise in LH secretion appeared 19-24 h after dawn and LH levels were still increased 3 days later, despite the fact that the birds had been returned to a short daylength. Pituitary LH content decreased, reflecting these changes in secretion, although significant falls in content were only found 36-96 h after dawn, when LH secretion was maximal. Hypothalamic gonadotrophin-releasing hormone content was not altered. One interpretation of this is that increased synthesis of the peptide compensates fully for the increased secretion.     

A possible role for the eyes in the photoperiodic response of quail

The effects of blinding on the photoperiodic responses of male Japanese quail were investigated by measuring plasma luteinizing-hormone (LH) concentrations in intact and castrated birds. Blinded birds were still able to respond to short and long days with appropriate changes in LH levels, suggesting that the basic photoperiodic mechanisms do not require retinal photoreception. However, there were clear-cut differences between blinded and sighted birds with the LH levels being higher in blinded quail. This difference between blinded and sighted was greater in short than in long days, and was also enhanced by castration. In conclusion we propose that short day information transmitted by the eyes has an inhibitory effect for LH secretion independent from sex steroid negative feedback effects in quail.     

Episodic release of LH in gonadectomized male Japanese quail

Blood samples were taken every 15 min (for 4.75 h) from six castrated quail on three separate occasions. The birds were first bled while under short days (comprising 8 h light : 16 h darkness per 24 h; 8L : 16D) and, subsequently, after 1 and 20 days under long days of 16L : 8D. The photoperiodic alteration produced a marked increase in the mean plasma LH concentration of each bird and in four instances the rise was evident after only 1 long day. Pulsatile release patterns were not detected in the plasma LH profiles obtained during exposure to short days or after 1 long day but were pronounced in all of the birds after 20 long days. The peaks (n = 19) occurred on average every 83 +/- 14 (S.E.M.) min and had an amplitude of 12.3 +/- 1.2 micrograms/l. After 35 days under 16L : 8D three of the quail were bled more frequently (every 8 min for 2.5 h), allowing the LH pulses to be measured more precisely. Each pulse was composed of a sudden increase in secretion followed by a slower decrease which lasted for approximately 30 min. The development and functional significance of episodic LH release in the quail is discussed.     

Photoperiodic differences in in vitro pituitary gonadotropin basal secretion and gonadotropin-releasing hormone responsiveness in the golden hamster

In order to examine pituitary gonadotropin secretion and responsiveness to GnRH after photic-induced changes in reproductive condition, an in vitro pituitary perifusion system was established for male golden hamster tissue. Anterior pituitaries from adult males which had been maintained on 14 h light:10 h dark (long days) or 6 h light:18 h dark (short days) for 10 weeks were perifused using an Acusyst perifusion system. Perfusates from unstimulated tissue (basal secretion) and from tissue stimulated with hourly pulses of GnRH (25, 50, or 100 ng/ml) were assayed for LH and FSH by RIA. Tissue from short-day animals had lower basal LH secretion than tissue from long day animals, but there were no significant photoperiodic differences for GnRH-stimulated LH secretion. In contrast, there were no photoperiodic differences in basal FSH secretion, but tissue from short-day animals secreted more FSH than tissue from long-day animals when stimulated with GnRH. Bioactivity of a small number of perfusate samples was assessed using in vitro rat granulosa cell and mouse Leydig cell assays for FSH and LH, respectively, and did not show any photoperiodic differences in LH or FSH bioactivity for GnRH-stimulated tissue. These studies indicate that the pituitaries of gonadally regressed hamsters are capable in vitro of responding to GnRH with similar or greater levels of gonadotropin release compared to pituitaries from animals with functional gonads. Therefore, it appears that the lowered serum gonadotropin levels seen in vivo in gonadally regressed animals are not due to a reduction in intrinsic pituitary sensitivity to GnRH.     

Sustained intermittent release of gonadotropin-releasing hormone in the prepubertal male rhesus monkey induced by N-methyl-DL-aspartic acid

The purpose of the present study was to determine whether gonadotropin-releasing hormone (GnRH) neurons in the hypothalamus of the prepubertal monkey may be prematurely provoked into producing a sustained train of intermittent GnRH release N-methyl-DL-aspartic acid (NMA), an analog of the putative excitatory neurotransmitter aspartate, was used to stimulate the hypothalamus. In order to utilize pituitary luteinizing hormone (LH) secretion as a bioassay of hypothalamic GnRH release, juvenile males were castrated and the responsiveness of their gonadotrophs to GnRH was enhanced prior to the study with a chronic intermittent intravenous infusion of the synthetic decapeptide (0.1 microgram/min for 3 min every hour). Treatment with this regimen of GnRH, which appears to provide the pituitary gonadotrophs with a hypophysiotropic stimulus similar to that produced by the hypothalamus of castrated adults, elicited a pattern of pulsatile LH secretion in prepubertal animals similar to that observed in the open-loop situation in adults. This episodic pattern of LH release was sustained without decrement following termination of GnRH priming and initiation of an intermittent intravenous infusion of NMA (4.5-6.5 mg NMA/kg body weight/pulse, administered over 1 min) delivered at a frequency of 1 pulse/1 h for 50 h. In contrast, an intermittent infusion of the vehicle employed to administer NMA (saline) failed to maintain LH secretion. Administration of the same dose of NMA at a slower frequency of 1 pulse/2 h for 52 h, while also sustaining LH secretion without decrement, resulted in an exaggeration in the LH response.(ABSTRACT TRUNCATED AT 250 WORDS)     

The general and comparative biology of gonadotropin-inhibitory hormone (GnIH)

The decapeptide gonadotropin-releasing hormone (GnRH) is the primary factor responsible for the hypothalamic control of gonadotropin secretion. Gonadal sex steroids and inhibin inhibit gonadotropin secretion via feedback from the gonads, but a neuropeptide inhibitor of gonadotropin secretion was, until recently, unknown in vertebrates. In 2000, we identified a novel hypothalamic dodecapeptide that inhibits gonadotropin release in cultured quail pituitaries and termed it gonadotropin-inhibitory hormone (GnIH). To elucidate the mode of action of GnIH, we then identified a novel G protein-coupled receptor for GnIH in quail. The GnIH receptor possesses seven transmembrane domains and specifically binds to GnIH. The GnIH receptor is expressed in the pituitary and several brain regions including the hypothalamus. These results indicate that GnIH acts directly on the pituitary via GnIH receptor to inhibit gonadotropin release. GnIH may also act on the hypothalamus to inhibit GnRH release. To demonstrate the functional significance of GnIH and its potential role as a key regulatory neuropeptide in avian reproduction, we investigated GnIH actions on gonadal development and maintenance in quail. Chronic treatment with GnIH inhibited gonadal development and maintenance by decreasing gonadotropin synthesis and release. GnIH was also found in the hypothalamus of other avian species including sparrows and chickens and also inhibited gonadotropin synthesis and release. The pineal hormone melatonin may be a key factor controlling GnIH neural function, since quail GnIH neurons express melatonin receptor and melatonin treatment stimulates the expression of GnIH mRNA and mature GnIH peptide. Thus, GnIH is capable of transducing photoperiodic information via changes in the melatonin signal, thereby influencing the reproductive axis. It is concluded that GnIH, a newly discovered hypothalamic neuropeptide, is a key factor controlling avian reproduction. The discovery of avian GnIH opens a new research field in reproductive neuroendocrinology.     

Different effects of melatonin pretreatment on cAMP and LH responses of the neonatal rat pituitary cells

The rhythm of the pineal hormone melatonin transduces the effect of photoperiod on seasonal functions. Duration of the melatonin pulse provides information about season and the long melatonin pulse induces reproductive involution in the long day breeders such as photoperiodic rodents. The length of melatonin pulse thus carries photoperiodic information, which regulates the function of target cells. Therefore, we have studied the effects of melatonin pretreatment of various lengths on responsiveness of the neonatal rat pituitary cells cultured in vitro to GnRH or forskolin. In these cells, melatonin treatment inhibits the GnRH-induced LH release as well as the forskolin-induced cAMP accumulation. However, long preincubation with melatonin has a paradoxical stimulatory effect on the cellular responsiveness. When the cells are pretreated with melatonin for 16 hr or more, then rinsed thoroughly and treated with forskolin for 30 min, the increase of cAMP is potentiated. Moreover, in the melatonin-pretreated cells. the subsequent melatonin treatment inhibits the forskolin-induced cAMP accumulation relatively more than in the non-pretreated cells. Although melatonin pretreatment does not potentiate the GnRH-induced LH release, it protects the gonadotrophs against the GnRH-induced desensitization: pretreatment with GnRH for 12 hr or more renders the cells insensitive to subsequent GnRH stimulation, while after pretreatment with GnRH and melatonin, the subsequent GnRH treatment induces significant increase of LH release. These observations indicate that long pretreatment with melatonin improves responsiveness of the pituitary cells to the subsequent stimulation, but its effects on cAMP accumulation and LH release are different.     

Luteinizing hormone release in the anaesthetised cat following electrical stimulation of limbic structures

The release of luteinizing hormone (LH) in response to electrical stimulation of limbic centres, namely the medial preoptic region (MPO) medial basal hypothalamus (MBH) and the medial amygdala (AME) has been studied in the anaesthetised gonadectomized cat. Chronically gonadectomized cats were anaesthetised with pentobarbitone or Althesin and paired bipolar stimulating electrodes were aimed at the MPO, AME or MBH. The effect of electrical stimulation of these regions on the secretion of LH was studied by radio-immunoassay of LH in serial blood samples taken before, during and after stimulation. No change in plasma LH in response to electrical stimulation was ever recorded during pentobarbitone anaesthesia. During Althesin anaesthesia stimulation in the MPO more often than not resulted in a peak of LH release during stimulation. A peak release of LH during stimulation was also recorded when electrodes were placed in the arcuate-median eminence region of the MBH. The time-course of these peaks in LH secretion was similar to the time-course of the plasma LH responses recorded following a single intravenous injection of gonadotrophin-releasing hormone (GnRH). In contrast, electrodes placed in AME had no effect on plasma LH during electrical stimulation, but immediately after stopping it, a small LH peak was recorded. The time-course of these responses suggests a pulse release of GnRH, the rapid response to MPO and MBH stimulation possibly being the result of a direct action on GnRH neurons while the delayed AME response may be produced by AME projections to the GnRH release system. These responses could be likened to the surge of LH which in the cat occurs post-coitus.     

Seasonal morphological changes in the neuro-glial interaction between gonadotropin-releasing hormone nerve terminals and glial endfeet in Japanese quail

In a previous study we showed that photoperiodically generated T3 in the hypothalamus is critical for the photoperiodic response of gonads in Japanese quail. The expression of thyroid hormone receptors in the median eminence (ME) suggested that photoperiodically generated T3 acts on the ME. Because thyroid hormone is known to play a critical role in the development and plasticity of the central nervous system, in the present study we have examined ultrastructure of the ME in Japanese quail kept in short-day and long-day environments. Immunoelectron microscopy revealed that GnRH nerve terminals are in close proximity to the basal lamina under long-day conditions, and conventional transmission electron microscopy demonstrated the encasement of the terminals by the endfeet of glia under short-day conditions. These morphological changes may regulate photoperiodic GnRH secretion.     

Photoperiodic control of LH secretion in Japanese quail with special reference to the photoinducible phase

Repetitive blood sampling from Japanese quail showed that plasma LH concentration rose during the first dark period after the birds were transferred from 8L:16D to 16L:8D. In the second light period of long days, LH concentration decreased slightly (not significant) and maintained this lower level until the second dark period of long days. During the second dark period LH again increased. This suggests that at the first stage of LH release by long photoperiod, photoinduction can occur at least during 8 to 16 hr after lights are turned on. To test the hypothesis that LH secretion induced by long days is dependent on the photoinducible phase, 0.5-hr light pulses (0.5L) were given to quail kept under 8L:16D during the dark periods. Activity was also recorded for each bird. After 10 days of treatment, testicular growth was induced when 0.5L pulses were given at 13 or 19 hr after dawn. Testicular growth induced by 0.5L pulses given at 19 hr after dawn was less than that in birds given light 13 hr after dawn and had greater individual variation compared with other groups. The activity records of these birds revealed that some remained entrained to the primary light pulse (8 hr) while others phase shifted to the short pulse (0.5 hr). The latter were, in effect, then exposed to a 13-hr photoperiod while the former were exposed to 8L:11D: 0.5L:4.5D. LH increase by 0.5L given during the dark period was detected after 2 days of treatment when the pulses were delivered at 15 hr after dawn. These results suggest that LH release is induced when light impinges on the circadian photosensitive phase which is set by external lighting schedules.     

Diurnal variation and the episodic release of plasma gonadotrophins in Japanese quail during a photoperiodically induced gonadal cycle.

Blood samples were taken every 3 h, over a 27 h period, from (1) a group of 12 intact male quail on short days (lights on 09.00-17.00 h) and during the 2nd, 15th and 36th day of photostimulation (lights on 09.00-05.00 h); (2) 12 castrated male quail on the 2nd, 20th and 43rd long day, and (3) 12 intact male quail on the 12th long day. Plasma LH was measured in all samples and FSH in the 43rd long day castrate and 12th long day intact male samples. Although there was considerable variation in the levels of LH and FSH, both between birds and between samples taken from the same bird, statistical analyses failed to reveal any diurnal (or circadian) rhythm at any time. There was a marked correlation between the LH and FSH levels in all samples. Possible episodic LH secretion was investigated by taking blood samples every 15 min for between 3 and 6 h from six intact male quail and six laying females on long days. Samples were obtained from each bird at three time-periods which were arranged so as to overlap and cover the first 12 h of the daily photoperiod. Statistical analysis suggested that episodes of secretion occurred 6-10 times/day in males, and 4-8 times/day in females. The pulses appeared to occur at random.     

Role of the thyroid gland in seasonal reproduction. III. Thyroidectomy blocks seasonal suppression of gonadotropin-releasing hormone secretion in sheep

Previous studies demonstrated that the thyroid gland is required for the changes in LH secretion that lead to the end of the breeding season of female sheep, a reproductive transition generated within the ewe by an endogenous annual rhythm. The present study tested the hypothesis that this role of the thyroid is mediated via the GnRH neurosecretory system. The pulsatile secretion of GnRH into hypophyseal portal blood and LH into peripheral blood, as well as the neuroanatomical distribution of GnRH neurons and their light microscopic morphology, were compared among anestrous ewes and thyroidectomized (THX) ewes that failed to make the transition to the anestrous season. The study was conducted under photoperiodic conditions in which the transition to anestrus was generated by the endogenous rhythm. Each animal was ovariectomized and treated sc with a constant release implant of estradiol to normalize gonadal steroid status among thyroid-intact and THX ewes. High frequency pulses of GnRH and LH were evident in THX ewes that failed to make the transition to anestrus, whereas pulsatile secretion of GnRH and LH was generally not observed in thyroid-intact controls that had entered anestrus. This marked effect of thyroidectomy on GnRH secretion was not associated with widespread changes in the total number, distribution, or light microscopic morphology of GnRH neurons in the hypothalamus and preoptic area. Our finding that pulsatile secretion of GnRH is elevated in THX ewes that fail to make the transition to anestrus supports the hypothesis that the thyroid gland is required for the endogenously generated switch in function of the GnRH neurosecretory system that leads to the end of the breeding season of the ewe.     

Cellular mechanisms and integrative timing of neuroendocrine control of GnRH secretion by kisspeptin

The hypothalamus integrates endogenous and exogenous inputs to control the pituitary–gonadal axis. The ultimate hypothalamic influence on reproductive activity is mediated through timely secretion of GnRH in the portal blood, which modulates the release of gonadotropins from the pituitary. In this context neurons expressing the RF-amide neuropeptide kisspeptin present required features to fulfill the role of the long sought-after hypothalamic integrative centre governing the stimulation of GnRH neurons. Here we focus on the intracellular signaling pathways triggered by kisspeptin through its cognate receptor KISS1R and on the potential role of proteins interacting with this receptor. We then review evidence implicating both kisspeptin and RFRP3 – another RF-amide neuropeptide – in the temporal orchestration of both the pre-ovulatory LH surge in female rodents and the organization of seasonal breeding in photoperiodic species.     

Changes in the pulsatile pattern of luteinizing hormone secretion during the rat estrous cycle

To ascertain whether changes in the pattern of GnRH release from the hypothalmus occur during the 4-day rat estrous cycle, the pattern of LH release was characterized on each day of the estrous cycle, and the results were interpreted in light of the changes in pituitary responsiveness to GnRH previously described by this laboratory to occur during this time. Blood samples were taken from intact, freely moving rats via venous catheters at 6- to 10-min intervals for 3-4 h. LH pulse height and LH interpulse interval were quantified on each day of the cycle, and the transition on the afternoon of proestrus from tonic LH release to the preovulatory LH surge was detailed. The effects on the pattern of LH release during estrus of small doses of GnRH (0.4 ng) and the continuous infusion of the opioid antagonist naloxone were also examined. Plasma LH concentrations (NIAMDD rat LH-RP-1) were determined with a highly sensitive LH RIA. LH pulses were identified using the PULSAR algorithim. The LH interpulse intervals of 46 +/- 2 min on diestrous-1 day, 49 +/- 4 min on diestrous day 2, and 60 +/- 8 min on proestrus immediately before the LH surge were not significantly different. There were no changes immediately preceding the preovulatory LH surge on the afternoon of proestrus in either the LH interpulse interval or the LH pulse height. Instead, the transition from tonic LH secretion to the preovulatory LH surge was found to occur abruptly. These data suggest that an abrupt increase in GnRH secretion during the afternoon of proestrus initiates the dramatic rise in LH concentrations. The pattern of LH secretion during the day of estrus differed significantly from that on the other days of the cycle in that no LH pulses were observed. However, the administration of small pulses of GnRH elicited physiological elevations in LH release. Furthermore, the continuous infusion of naloxone to estrous rats immediately stimulated a pulsatile pattern of LH secretion, with a LH interpulse of 56 +/- 4 min. These data indicate that the absence of LH pulses during estrus may result from a deficit in GnRH release. Similar modifications in GnRH release during the other days of the cycle were inferred from the observed changes in LH pulse heights. The LH pulse height of 21 +/- 3 ng/ml on diestrous day 2 was significantly less than the LH pulse height of 41 +/- 4 ng/ml on diestrous day 1 or 35 +/- 4 ng/ml on proestrus before the surge.(ABSTRACT TRUNCATED AT 400 WORDS)     

Evidence for the dependence of serum luteinizing hormone surge on a transient, enhanced secretion of gonadotropin-releasing hormone from the hypothalamus.

Data that a substantial, transient release of gonadotropin-releasing hormone (GnRH) from the hypothalamus is a prerequisite for the serum luteinizing hormone (LH) surge are presented. Ovariectomized rats, in which daily afternoon LH peaks can be induced by estradiol benzoate (EB), were used as the experimental model. These rats present a homogenous, synchronized population having low hypothalamic stores of GnRH, thus facilitating detection of small physiological fluctuations in the levels of hypothalamic GnRH. Blockade, by Nembutal administration, of the serum LH surge on 2 consecutive afternoons results in elevated GnRH levels in the hypothalamus (1.79 ng in blocked rats vs 0.94 ng in controls). Abolition of LH secretion by administration of antiserum to GnRH, unlike the Nembutal blockade, does not affect GnRH levels. These results indicate that the afternoon LH surge is dependent on a transitory, enhanced release of GnRH from the hypothalamus, reflected by a depletion of GnRH stores.     

Effect of pulsatile gonadotropin-releasing hormone on the release of luteinizing hormone and follicle-stimulating hormone in vitro by anterior pituitaries from lactating and cycling rats

The ability of pituitaries from lactating animals to secrete LH and FSH in response to gonadotropin-releasing hormone (GnRH) was studied in vitro using a pituitary incubation system. Hemipituitaries were exposed to GnRH for 6 min during each hour of incubation. LH release by anterior pituitaries (APs) from day 5 postpartum rats nursing eight pups, in response to pulsatile exposure to GnRH, was significantly less than that released by APs from diestrous cycling females. Even though the amount of LH released by APs increased as lactation progressed, LH release by APs from day 15 postpartum rats nursing eight pups was still less than LH release by APs from diestrous females. In contrast pituitaries from lactating females nursing two pups released amounts of LH similar to that released by pituitaries from diestrous females, whereas females deprived of their litters for 48 h showed a greater response than diestrous females. Generally, there was a good quantitative relationship between the amount of LH released in vitro and plasma LH concentrations for all the intact groups studied. The ability of lactation to suppress the postcastration rise in serum LH also was demonstrated in vitro as pituitaries from ovariectomized or intact females nursing eight pups released similar amounts of LH on days 5 and 10 postpartum. However, by day 15 postpartum, even though serum LH concentrations were still very low, pituitaries from ovariectomized lactating females released LH in vitro at a rate similar to pituitaries from nonlactating rats. Serum FSH concentrations were not suppressed but similar in intact and cycling females. Also, the total amount of FSH released in vitro in response to GnRH by pituitaries from lactating and cycling females did not differ significantly, even though LH release differed greatly among these groups of animals. However, the patterns of GnRH-stimulating FSH secretion differed among intact lactating, ovariectomized lactating, and nonlactating females. Pituitary LH concentrations were similar on day 5 postpartum and diestrus and on day 15 postpartum and proestrus. Pituitary FSH concentrations on day 5 postpartum were similar to those during diestrus and proestrus and had increased 2-3 times by day 15 postpartum. Generally, there was no correlation between the amount of LH or FSH released by pituitaries in response to GnRH and pituitary gonadotropin content. In summary, the inability of pituitaries from lactating rats to respond adequately to large doses of GnRH in vitro suggests that the suckling stimulus indirectly suppresses pituitary responsiveness to GnRH. This suppression differentially affects basal LH secretion, but not basal FSH secretion, and may be the direct result of inadequate GnRH stimulation in vivo.     

Release of gonadotropin-releasing hormone from the Japanese quail hypothalamus in vitro

The regulation of GnRH (gonadotropin-releasing hormone) secretion in Japanese quail was studied by maintaining excised hypothalamic slices containing the median eminence region in a continuous flow superfusion system. GnRH released into the superfusate was measured by radioimmunoassay using an antibody generated against synthetic GnRH. GnRH secretion increased in a dose-response manner when hypothalamic slices from female quail were exposed to superfusion medium containing elevated potassium ion concentrations. The potassium-induced GnRH release was found to be calcium dependent. GnRH was also increased when either 1 × 10^?6M norepinephrine, epinephrine, or 1 × 10^?5M of the β-adrenergic agonist, isoproterenol was added to the superfusion medium. GnRH secretion from hypothalami of castrate and intact male quail was measured on Days 1, 10, and 21 of photostimulation and was elevated on Day 21. No differences were observed between the castrate and intact groups. It is concluded that GnRH is released from the quail hypothalamus in a manner analogous to mammals and that its release is subject to adrenergic stimulation.     

Neuroendocrine regulation of gonadotrophin-releasing hormone secretion in the Japanese quail

Following the transfer of quail to long days, an increase in plasma and pituitary levels of LH and FSH is observed. The integrity of both the preoptic region (POR) and the posterodorsal part of the infundibular nuclear complex (PD-INC) appears to be essential for mediating this photoperiodic response. The INC may, however, operate autonomously in being able to regulate the low levels of LH-RH release of nonphotostimulated immature birds. By combining the techniques of electrical stimulation and electrolytic lesioning it can be demonstrated that stimulation of the POR can increase LH-RH secretion in quail where the photoinduced release has been blocked by a PD-INC lesion. Electrical stimulation of the preoptic region in immature birds similarly stimulates the secretion of LH-RH. These results suggest a direct link, perhaps neurosecretory, between the preoptic region and the median eminence.     

The suppression of pulsatile luteinizing hormone secretion during lactation in the rat

The inhibition of LH secretion during lactation may be the consequence of a pituitary insensitivity to GnRH stimulation and/or an inhibition of GnRH release from the hypothalamus. To assess the contribution that these mechanisms may make to the suppression of LH secretion during lactation, we described the pattern of LH secretion in lactating rats and the magnitude of LH secretion in response to a GnRH stimulus. We assessed the effect of the strength of the suckling stimulus (two and eight pups), the length of lactation (5 and 10 days), and the presence of the ovaries on the pattern of LH secretion. We also examined the pattern of LH secretion after removal of a large suckling stimulus. In the intact rat, the pattern of LH secretion during lactation was uniformly nonpulsatile, despite significant differences between animals suckling two and eight pups in pituitary responsiveness to GnRH. In intact rats suckling two pups during day 10 of lactation, significant LH secretion was stimulated by 0.4-ng pulses of GnRH every 50 min, while animals with eight pups secreted little LH in response to the same stimulus. It was concluded that a two-pup suckling stimulus was sufficient to completely suppress pulsatile GnRH release without affecting pituitary function, whereas an eight-pup suckling stimulus also depressed pituitary sensitivity to GnRH. In ovariectomized (ovx) rats suckling two pups, seven of nine animals showed no postcastration rise in LH secretion or evidence of pulsatile LH secretion during day 5 of lactation. In the remaining two animals, a castrate pattern of pulsatile LH secretion was observed, with a LH interpulse interval of 31 +/- 6 min. By day 10 of lactation, all animals suckling two pups had castration patterns of LH secretion, with a LH interpulse interval of 35 +/- 2 min, which was significantly different from the LH interpulse interval of 26 +/- 1 min observed in ovx animals without pups. Therefore, a two-pup suckling stimulus is capable of retarding the increase in LH pulse frequency characteristically seen in the rat after castration. In ovx rats suckling eight pups, the postcastration rise in LH secretion was completely inhibited in all animals examined on days 5 and 10 of lactation, and the pattern of LH secretion was uniformly nonpulsatile. A consistent pattern of pulsatile LH secretion was not reinitiated until 72 h after removal of the suckling stimulus (LH interpulse interval, 31 +/- 2 min).(ABSTRACT TRUNCATED AT 400 WORDS)