The role of arachidonic acid and its metabolites in the release of neuropeptides.
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Animals↗
Biomedical subjects
H F Urbanski
Publications and source records attributed to H F Urbanski.
Prostaglandin E2 releases luteinizing hormone-releasing hormone from the female juvenile hypothalamus through a Ca2+-dependent, calmodulin-independent mechanism.
Prostaglandin E2 (PGE2) has been implicated as a mediator of norepinephrine-induced luteinizing hormone-releasing hormone (LHRH) release from the hypothalamus. The present experiments were undertaken to examine the hypothesis that mobilization of Ca2+ from intracellular stores and cyclic AMP (cAMP) formation are involved in this effect. Incubation of median eminence (ME) nerve terminals from juvenile rats in Ca2+-free Krebs-Ringer bicarbonate buffer reduced, but failed to prevent the stimulatory effect of PGE2 on LHRH release. None of 5 calmodulin antagonists or a blocker of calmodulin-dependent kinase affected the LHRH response to PGE2. In contrast, inhibition of intracellular Ca2+ mobilization with TMB-8 or dantrolene in Ca2+-free medium prevented the LHRH releasing effect of PGE2. Similarly to PGE2, the stimulatory effect of the Ca2+ ionophore A 23187 on LHRH release was not affected by inhibition of calmodulin activity. This, however, blocked the increase in PGE2 formation induced by the ionophore. PGE2 evoked a dose-related increase in cAMP accumulation in Ca2+-containing medium and this effect was inhibited both by blockers of intracellular Ca2+ mobilization and by calmodulin antagonists. Surprisingly, removal of extracellular Ca2+ increased basal cAMP levels in the incubation medium without affecting LHRH release; PGE2 induced a further increase in cAMP which was prevented by inhibition of intracellular Ca2+ translocation. Stimulation of adenylate cyclase activity with forskolin (F) resulted in similar increases in cAMP levels both in the presence and absence of extracellular Ca2+. However, F failed to evoke LHRH release in Ca2+-free medium. The results indicate that: (a) the stimulatory effect of PGE2 on LHRH release involves mobilization of intracellular Ca2+ but not the participation of calmodulin; (b) the formation of PGE2 itself is calmodulin-dependent; (c) PGE2 stimulates cAMP formation through a calmodulin-dependent mechanism that requires translocation of intracellular (membrane?) Ca2+; (d) the cAMP system of a population of nerve terminals different from that responsive to PGE2 is normally subjected to a Ca2+-dependent inhibitory control; and (e) although PGE2 is a potent stimulator of cAMP formation in the ME and endogenously produced cAMP can induce LHRH release, in the absence of extracellular Ca2+ PGE2 stimulates LHRH release in a cAMP-independent manner.
Animals↗
N-tosyl-L-phenylalanine chloromethyl ketone inhibits LHRH-degrading activity and increases in vitro LHRH release from the immature rat median eminence.
Median eminence (ME) luteinizing-hormone-releasing hormone (LHRH)-degrading activity (LHRH-DA) may play a role in regulating the availability of releasable LHRH. Incubation of LHRH with ME tissue supernatant yields LHRH(1-5) and LHRH(6-10) degradation fragments, as detected by high-performance liquid chromatography (HPLC) analysis, suggesting a 5-6 cleavage of the decapeptide. Since these fragments are also present after incubation of LHRH with alpha-chymotrypsin (alpha-CH), we examined the possibility that the irreversible inhibitor of alpha-CH, N-tosyl-L-phenylalanine chloromethyl ketone (TPCK), might inhibit LHRH-DA and affect LHRH release. Irreversible inhibitors of trypsin-like proteases [N-alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK), and phenylmethylsulfonylfluoride (PMSF)] were used as controls. LHRH-DA was determined by HPLC estimation of the loss of synthetic LHRH incurred when the peptide was incubated with aliquots of ME supernatant in the presence or absence of the inhibitors. LHRH release from ME fragments was assessed by radioimmunoassay after incubating the tissue with the inhibitors in Krebs-Ringer bicarbonate buffer. The LHRH-DA in both the incubation medium and the ME tissue was determined at the end of the incubation. TPCK (0.5-100 microM) added to ME tissue supernatant inhibited LHRH-DA in a dose-dependent manner. In contrast, when TPCK was added to medium in which intact ME were being incubated to assess LHRH release, the LHRH-DA of these ME was inhibited only at the 25-, 50- and 100-microM doses of TPCK, suggesting a relative inability of the inhibitor to reach endopeptidase pools in intact tissue. These same doses of TPCK increased LHRH release from the incubated ME.(ABSTRACT TRUNCATED AT 250 WORDS)
Age Factors↗
Simultaneous measurement of gonadotropin-releasing hormone, luteinizing hormone, and follicle-stimulating hormone in the orchidectomized rat.
In the present study two recently developed techniques have been combined to enable the simultaneous in vivo determination of pulsatile release of GnRH, LH, and FSH in the orchidectomized rat. The first of these techniques involves the implantation of two vascular catheters and collecting serial blood samples through one while simultaneously infusing a replacement blood mixture through the other; consequently, blood samples can be collected for an extended period of time, and detailed plasma LH and FSH release profiles can be established for individual animals. The second technique involves push-pull perfusion of the pituitary gland to determine changes in GnRH concentration as might be perceived by the gonadotropes. For each animal (n = 6), blood (150 microliters) and push-pull perfusate (200 microliters) samples were collected at 5- and 10-min intervals, respectively, for approximately 6 h, and the hormone release profiles were determined by RIA. All of the rats showed a clear pulsatile release pattern for GnRH, LH, and FSH. Moreover, the interpulse interval was remarkably similar for each of these hormones (36.9, 41.5, and 43.5 min, respectively, as determined by PULSAR). The percentage of GnRH pulses associated with a gonadotropin pulse was 72% for LH and 76% for FSH; only 14% of the pulses were silent for both gonadotropins. These results demonstrate that in the orchidectomized rat the pulsatile pattern of GnRH release is reflected in the pulsatile pattern of not only LH but also FSH. They may, therefore, be construed to support the concept that the pulsatile secretion of both gonadotropins is primarily orchestrated by a single hypothalamic releasing hormone. Alternatively, if two separate hypothalamic releasing hormones do indeed exist (LHRH and FSH-releasing hormone), it would appear that in the orchidectomized rat their episodic release is tightly coupled to the same hypothalamic pulse generator.
Animals↗
Activation of luteinizing hormone-releasing hormone release advances the onset of female puberty.
The juvenile-peripubertal transition period in the female rat is associated with an ovarian-independent afternoon increase in the amplitude of plasma luteinizing hormone (LH) pulses. To determine if the immature pituitary could be activated to cause precocious puberty juvenile female rats were subjected for 4 days to a microprocessor-driven pulsatile intravenous administration of LH-releasing hormone (LHRH) at a dose that produced a peripubertal pattern of LH release. To determine if the LHRH neurons themselves could be prematurely activated to induce such a pattern of plasma LH, and hence lead to precocious puberty, the neuroexcitatory amino acid analog N-methyl-DL-aspartic acid (NMA) was similarly administered. The time of puberty (vaginal opening and first ovulation) was advanced by both the LHRH and NMA treatments, by 5 and 7 days, respectively. Ovarian weight and incidence of corpora lutea at first diestrus were similar in all animals regardless of treatment, but a juvenile body weight was retained by the animals that underwent precocious puberty. Therefore, just as the adenohypophysis can be driven by exogenous LHRH to initiate puberty, the LHRH neuronal system can be precociously activated by the episodic administration of an excitatory amino acid analog that is known to interact with specific brain receptors. It is likely, therefore, that sexual maturation is limited by factors that lie further upstream in the hypothalamo-pituitary axis (e.g., the neuronal circuits that impinge upon LHRH-producing neurons).
Animals↗
Gonadal-independent activation of enhanced afternoon luteinizing hormone release during pubertal development in the female rat.
In the present study we investigated the extent to which expression of the diurnal pattern of LH secretion in prepubertal female rats is driven by an ovarian-independent neuroendocrine mechanism. To remove gonadal influences, rats were ovariectomized (OVX) during early juvenile, late juvenile, or peripubertal phases of development (20-22, 26-27, and 32-33 days of age, respectively), and blood samples were collected throughout the day (every 30-60 min) 2 or 4 days after surgery. Morning plasma LH levels were relatively low 2 days after ovariectomy (30-120 ng/ml), but rose during the afternoon to reach levels ranging from 180-300 ng/ml. This afternoon elevation was sustained both in late juvenile and peripubertal rats, but not in early juvenile rats. The predominant change observed 4 days after ovariectomy was an overall 3- to 6-fold increase in plasma LH levels, which masked the afternoon elevation. Analysis of plasma LH profiles from individual rats, however, revealed that at each of the three ages studied the peak plasma LH levels occurred in the afternoon, and these were most pronounced in the peripubertal animals. To further clarify the existence of such a diurnal pattern of LH release in the 4-day OVX animals pulsatile LH release profiles were obtained from individual animals, using a 5-min bleeding paradigm, at either 24 days (in the morning) or 36 days of age (in either the morning or the afternoon). LH release was episodic in all of the animals studied, with pulses occurring on average of about once every 30 min. Analysis of the plasma LH profiles using the PULSAR algorithm revealed that the overall mean plasma LH levels of the peripubertal animals was enhanced during the afternoon, compared to that in the morning or to the afternoon LH levels in the early juvenile rats. Mean nadir and mean peak LH levels were also greater. No differences in LH pulse amplitude and only marginal differences in LH pulse frequency were detected among the three groups studied. The enhancement of afternoon LH secretion in the OVX rats could not be attributed to age-related or diurnal changes in adenohypophyseal responsiveness to LHRH. The results suggest that the initiation of enhanced afternoon LH secretion, previously shown to occur in intact female rats during the juvenile-peripubertal transition period, results primarily from the activation of a central neuroendocrine mechanism. Although the ovaries might play a role in the development of this diurnal pattern, it is clear that its activation is ovarian independent.
Animals↗
The onset of female puberty: studies in the rat.
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Aging↗
Activation of two different but complementary biochemical pathways stimulates release of hypothalamic luteinizing hormone-releasing hormone.
Evidence exists that a norepinephrine/prostaglandin E2 (PGE2)/cAMP pathway is involved in the regulation of luteinizing hormone-releasing hormone (LHRH) secretion. The aim of the present experiments was to determine if release of LHRH from the immature rat hypothalamus could also be stimulated by activation of protein kinase C. Median eminences from 28-day-old female rats were incubated in vitro with either dioctanoylglycerol (a synthetic diacylglycerol that selectively activates protein kinase C in intact cells) or 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (another protein kinase C activator). Both agents increased LHRH release, the response to dioctanoylglycerol being more pronounced than that to the phorbol ester. This direct activation of protein kinase C was not accompanied by changes in PGE2 formation. Activation of the PGE2/cAMP pathway by either norepinephrine, PGE2, or forskolin (a stimulator of adenylate cyclase) increased LHRH release. Dioctanoylglycerol or phorbol ester in conjunction with either norepinephrine, PGE2 or forskolin resulted in an additive effect on LHRH release suggesting coexistence of both pathways. Phospholipase C, which activates protein kinase C via formation of diacylglycerol, increased the release of both LHRH and PGE2. This suggests that an increase in endogenous phospholipase C activity caused by neurotransmitter inputs may lead to both activation of protein kinase C and PGE2 formation. Blockade of cyclooxygenase activity by indomethacin obliterated phospholipase C-induced PGE2 release. The same treatment reduced the LHRH response by only 50% indicating that protein kinase C activation can cause LHRH release in the absence of PGE2 synthesis. It is suggested that the median eminence of the rat possesses a protein kinase C-dependent pathway that is coupled positively to LHRH release and complements PGE2/cAMP-dependent mechanisms. Norepinephrine, however, does not appear to be the neurotransmitter responsible for activating the protein kinase C pathway. Simultaneous activation of both pathways may provide a mechanism by which a large increase in LHRH secretion occurs, such as in the afternoon of first proestrus.
Animals↗
Activation of estradiol-positive feedback at puberty: estradiol sensitizes the LHRH-releasing system at two different biochemical steps.
Experiments were performed to examine whether estradiol (E2) can influence some of the intraneuronal mechanisms involved in luteinizing hormone-releasing hormone (LHRH) release during the onset of puberty in the female rat. The capacity of median eminence (ME) nerve terminals to secrete LHRH, as determined by both their basal release of LHRH and by their response to prostaglandin E2 (PGE2) in vitro, increased significantly during the juvenile-early peripubertal periods of development (postnatal days 22-34). Ovariectomy (OVX) on day 22 led to a striking reduction in LHRH response to PGE2 on day 34. E2 administered via s.c. Silastic capsules, at a dose that reproduces juvenile serum E2 levels, restored the response. Simulation of first proestrous serum E2 levels in late juvenile (28-day-old) female rats enhanced both the sensitivity and the responsiveness of LHRH-containing terminals to PGE2. Furthermore, E2 enhanced the sensitivity and the responsiveness of LHRH terminals to norepinephrine (NE). This effect appeared to be related to both the increased LHRH response to PGE2 and an enhanced sensitivity of the PGE2-synthesizing pathway to NE. This is because MEs from E2-treated rats showed a marked increase in PGE2 release in response to a NE concentration which was barely effective in untreated controls. It is suggested that one of the mechanisms by which E2 activates the first preovulatory discharge of LHRH release in the female rat is by facilitating the occurrence of two different but sequentially related biochemical events: the stimulation of PGE2 formation by NE and the enhancement of LHRH release by PGE2.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
The development of afternoon minisurges of luteinizing hormone secretion in prepubertal female rats is ovary dependent.
We have recently disclosed sustained episodes of LH release (minisurges) during the afternoons of the juvenile-peripubertal transition period in the female rat. To determine if these LH minisurges are gonad independent, i.e. develop in the absence of the ovaries, animals were ovariectomized when neonates, and the mode of LH release was examined using a 5-min blood-sampling regimen at one of three ages corresponding to the juvenile, peripubertal, or adult phase of development. In no instance was a minisurge of LH secretion detected. We were concerned, however, that LH minisurges may have been obscured by the exceedingly high level of LH secretion in these long term ovariectomized rats and, therefore, decided to pursue the study employing a short term (48-h) ovariectomy paradigm. Late juvenile rats which had been ovariectomized for 48 h exhibited conspicuous LH pulses, but, again, LH minisurges were not detected, further suggesting that these sustained secretory episodes do not occur in the absence of the ovaries. Next, plasma estradiol (E2) levels were differentially raised in 48-h ovariectomized juvenile rats via sc implantation of Silastic capsules containing the steroid (dissolved in corn oil at various concentrations), and plasma LH was measured at 1-h intervals. The highest E2 concentration elicited a midafternoon LH increase of preovulatory magnitude in all cases, whereas the lowest E2 concentrations consistently suppressed plasma LH. However, intermediate E2 concentrations (producing plasma E2 levels 20-30% greater than those found in intact controls) elicited, in several instances, an increase in LH release of intermediate magnitude. To clarify the nature of these LH responses, we examined, using a 5-min blood-sampling regimen, the afternoon pulsatile pattern of LH release after treatment with appropriate doses of E2. As expected from the results of the infrequent blood-sampling paradigm, the highest E2 dose induced proestrus-like surges of LH secretion, while the lowest dose suppressed pulsatile LH release. Moreover, an intermediate E2 dose which raised plasma E2 levels just above those of intact animals, was again able to cause suppression of LH pulses, a proestrus-like surges of LH secretion, while the lowest dose suppressed pulsatile LH release. Moreover, an intermediate E2 dose which raised plasma E2 levels just above those of intact animals, was again able to cause suppression of LH pulses, a proestrus-like increase in LH output, or, more importantly, a minisurge of LH secretion.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Development and amplification of mid-afternoon surges of prolactin secretion in ovariectomized immature rats.
The immature female rat shows a mid-afternoon surge of prolactin secretion which reaches a maximum on the day of first pro-oestrus. The present experiments were undertaken to elucidate the mechanisms which underly the development of this prolactin discharge. Detailed plasma prolactin profiles were obtained from short-term (48 h) ovariectomized rats at 23, 28 or 37 days of age. In the two older groups, but not the youngest, a mid-afternoon surge of prolactin secretion occurred in spite of the absence of the ovaries. To exclude the possibility that such an apparent ovarian-independent discharge of prolactin was due to an oestradiol effect which persisted for 2 days following ovariectomy, another study was conducted using long-term ovariectomized animals. Plasma profiles were obtained from neonatally ovariectomized rats at ages equivalent to juvenile (26-28 days), peripubertal (38-41 days) or adult (46-49 days) phases of development. A mid-afternoon surge of prolactin secretion was observed in the majority of animals (eight out of twelve) irrespective of the interval after ovariectomy; this finding further indicates that in the female rat there is a centrally originated mid-afternoon episode of prolactin secretion which is expressed during juvenile development even in the absence of the ovaries. The relatively small magnitude of these ovarian-independent prolactin discharges (c.f. the preovulatory prolactin surge) suggested that in the intact animal they are amplified by ovarian secretions. To test this hypothesis, oestradiol-containing silicone elastomer capsules were implanted s.c. into juvenile rats, immediately after ovariectomy, and plasma prolactin profiles examined 2 days later (28 days of age).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
In vitro simulation of prepubertal changes in pulsatile luteinizing hormone release enhances progesterone and 17 beta-estradiol secretion from immature rat ovaries.
We have previously demonstrated changes in the episodic pattern of LH secretion in female rats as they approach first ovulation. In the present study, ovaries were taken from peripubertal rats and perifused in vitro with a medium containing FSH and LH. The concentration of FSH in the medium was kept constantly low, whereas the concentration of LH was modulated, simulating as closely as possible the various episodic secretory profiles previously observed in vivo. Medium from the perifusion chambers was collected every 10 min for 5 h and assayed for progesterone (P) and 17 beta-estradiol (E2). Exposure of the ovaries to low amplitude LH pulses (20 ng/ml; comparable to those found in the plasma of peripubertal rats during the morning) did not elicit a significant steroidogenic response. On the other hand, exposure to large amplitude LH pulses (80 ng/ml; as seen during the afternoon) led to a marked increase in the output of both P and E2. Similarly, increased steroid secretion occurred when ovaries were exposed to a 2-h minisurge of LH (160 ng/ml) or to a minisurge preceded by three large amplitude pulses (as seen in some animals during the afternoons of the peripubertal period). Continuous exposure to LH at concentrations similar to either the large amplitude pulses or the LH minisurge increased P and E2 release. However, the increase was not significantly larger than that produced by the discontinuous LH perifusion patterns, even though the total amount of LH reaching the ovaries during the 5-h perifusion period was considerably greater. The results show that episodic LH secretion is functionally much more efficient at eliciting release of P and E2 from immature ovaries than is continuous LH secretion. Furthermore, they strongly suggest that changes in the LH secretory pulse patterns, as seen in vivo close to the time of puberty, are fundamental for the activation of ovarian steroidogenesis that leads to the first preovulatory surge of gonadotropins.
Animals↗
The juvenile-peripubertal transition period in the female rat: establishment of a diurnal pattern of pulsatile luteinizing hormone secretion.
Previous descriptions of pulsatile LH release in immature female rats have been mostly inaccurate because of infrequent blood sampling, discontinuous and unbalanced blood replacement procedures, and possibly because of the use of a heterologous RIA. The present study was undertaken to circumvent these problems and to characterize more precisely the changes in episodic LH secretion previously observed during the juvenile-peripubertal transitional period (27-38 days of age). Changes in LH levels were measured in plasma samples obtained every 5 min from unrestrained conscious animals using a recently developed technique that permitted continuous withdrawal of blood for 4-5 h and simultaneous replacement with an artificial blood mixture. In virtually all of the rats, LH release was pulsatile. In both the juvenile (27-29 days old) and peripubertal (30-38 days old) animals, mean plasma LH levels and LH pulse amplitude were low in the mornings. A similar pattern of LH secretion was found in the afternoon during the juvenile period. In contrast, most of the peripubertal animals exhibited an afternoon increase in LH pulse amplitude. A change in pulse frequency was not detected at this time, but a 1.8-fold increase in mean LH levels suggests that large amplitude pulses may be accompanied by low amplitude, high frequency pulses not revealed by the 5-min sampling paradigm. Some of the peripubertal rats (5 of 12) had plasma LH profiles in which the large amplitude pulses were accompanied by a midafternoon minisurge of secretion which lasted for up to 2 h and reached peak levels of 174 +/- 19 ng/ml; the LH surge at first proestrus was greater than 1000 ng/ml. The results demonstrate the prepubertal development of an afternoon increase in LH pulse amplitude and the appearance of a more prolonged and larger secretory episode of LH secretion (minisurge). Disclosure of a concomitant increase in pulse frequency may necessitate blood sampling at more frequent intervals. It is suggested that the changes in the mode of LH release described here may enhance peripubertal ovarian steroidogenesis and provide an appropriate stimulus for initiating the final stages of ovarian development.
Aging↗
Stimulation of cyclic adenosine 3',5'-monophosphate production enhances hypothalamic luteinizing hormone-releasing hormone release without increasing prostaglandin E2 synthesis: studies in prepubertal female rats.
A role for cAMP in the process of LHRH release was suggested several years ago, but only recently has the validity of this notion come under close scrutiny. In the present experiments we have used three probes, which stimulate adenylate cyclase activity via different mechanisms, to determine whether an increase in endogenous cAMP results in LHRH release from the hypothalamus of prepubertal female rats. Median eminences from juvenile, 28-day-old animals were incubated in vitro with either forskolin (F), cholera toxin (CT), or pertussis toxin (PT). All three substances enhanced LHRH release. The estimated ED50 values were 28.7 microM and 20.0 ng/ml, for F and PT, respectively. The effect of CT appeared biphasic and thus no ED50 could be calculated. None of these agents increased the release of prostaglandin E2 (PGE2), an obligatory component in the process of norepinephrine-induced LHRH secretion. Doses of PGE2 and F, which were maximally effective in stimulating LHRH release when administered separately, did not produce any further response when administered concomitantly, thus suggesting that PGE2 and F act along a common pathway. Blockade of phosphodiesterase activity with 1-methyl-3-isobutylxanthine increased LHRH secretion without enhancing PGE2 release, implying that cAMP metabolism was elevated in the median eminence nerve terminals in vitro. Addition of 1-methyl-3-isobutylxanthine augmented the LHRH response to CT and PT, but it did not increase further the already marked LHRH response to PGE2 or F. The results indicate that both an increase in adenylate cyclase activity and a decrease in phosphodiesterase activity lead to LHRH release from the median eminence. They also suggest that, upon proper (neurotransmitter?) stimulation, cAMP production increases subsequent to the activation in PGE2 synthesis, which itself causes LHRH release. Furthermore, the capacity of PT to induce LHRH release suggests the involvement of an inhibitory guanine nucleotide-binding regulatory protein in transducing inhibitory inputs impinging on LHRH-secreting neurons.
1-Methyl-3-isobutylxanthine↗
An automated system for the study of pulsatile hormone secretion in the immature rat.
A procedure is described for prolonged sampling of blood from unrestrained immature rats which overcomes some of the problems associated with contemporary techniques. 1 or 2 days before sampling, the animal is fitted with two indwelling catheters, one inserted into the right jugular vein and the other into a femoral vein. On the day of the experiment blood is continuously withdrawn from the jugular vein (30 microliter/min) using a peristaltic pump and is dispensed into sample tubes every 5 min by means of an automatic fraction collector. A second channel of the same pump continuously infuses a blood replacement mixture (at 37 degrees C) into the femoral vein thereby keeping the animal's blood volume constant. In the present study this technique was used to sample blood from both ovariectomized and immature, intact female rats for as long as 5-7 h. The procedure did not appear to disturb the normal locomotion, feeding, drinking and sleeping behavior of the animals. Plasma luteinizing hormone (LH) profiles obtained from the ovariectomized rats showed a normal pulsatile pattern of LH secretion. The frequency and amplitude of the pulses was not affected, even when the animals were bled on 2 consecutive days. Moreover, the procedure permitted accurate detection and characterization of pulsatile LH release in intact, immature rats although the episodes of LH secretion were more variable and much less pronounced. It is believed that this novel sampling technique could prove to be a valuable tool in the study of pulsatile hormone secretion in small laboratory rodents.
Animals↗
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.
Animals↗
Effects of short-term treatment with testosterone on the secretion of FSH and LH in castrated golden hamsters exposed to short days.
Castrated hamsters which were transferred from long (14L:10D) to short (9L:15D) days and received testosterone-filled capsules for 1 week after transfer failed to show a significant suppression in the plasma levels of FSH and LH after capsule removal. In contrast, gonadotrophin concentrations were suppressed in hamsters in which the long-day castration response had been blocked with exogenous testosterone. After castration on long days and exposure to 10 weeks of short days pituitary gland weight and gonadotrophin content, as well as plasma FSH titres, were higher in control animals than in those that had received testosterone implants for 7 weeks of short days. The results suggest that failure of castrated hamsters to respond to the suppressive effects of short days reflects castration-induced changes in hypothalamo-pituitary physiology rather than a neuroendocrine mechanism by which photoperiod modulates gonadotrophin secretion.
Animals↗
The pineal gland and the photoperiodic control of luteinizing hormone secretion in intact and castrated Japanese quail.
The effects of pinealectomy on a range of photoperiodic responses were investigated in male Japanese quail by measuring plasma LH concentrations in intact, sham-operated and pinealectomized birds in the following four experiments: (1) transfer of sexually quiescent birds from a short photoperiod of 8 h light: 16 h darkness (8L:16D) to a photostimulatory daylength of 16L:8D; (2) transfer of sexually mature birds from 16L:8D to 8L:16D; (3) castration in 16L:8D and exposure to 13L:11D; (4) castration in 8L:16D and exposure to 13L:11D. There was no evidence of effects of the pineal gland on the photoperiodically induced changes in LH secretion, the quantitative relationship between LH secretion and photoperiod in intact and castrated birds, or the induction of relative photorefractoriness by prolonged exposure to 16L:8D. This suggests that there is no pineal influence on the photoperiodic clock or its effectors in this bird.
Animals↗