EFFECTS OF PINEALECTOMY ON THE RAT OESTROUS CYCLE AND PITUITARY GONADOTROPHIN RELEASE

1976 ◽  
Vol 69 (1) ◽  
pp. 67-75 ◽  
Author(s):  
C. A. BLAKE
Keyword(s):  
Pineal Gland ◽  
Oestrous Cycle ◽  
Ovariectomized Rats ◽  
Prolactin Release ◽  
Medial Basal Hypothalamus ◽  
Blood Samples ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Permissive Role

SUMMARY In 4-day cyclic rats kept in a room with the lights on from 05.00 to 19.00 h, sham pinealectomy or pinealectomy on the morning of pro-oestrus did not alter the length of the oestrous cycle for 44 days or the time and magnitude of the rises in LH, FSH and prolactin in the circulation in the afternoon on pro-oestrous days 0, 20 or 44. On day 45, the light schedule was set forward 4 h to run from 09.00 to 23.00 h. The rats continued to have seven additional consecutive 4-day oestrous cycles. On day 27 after the resetting of the light schedule, the pro-oestrous rises in serum LH, FSH and prolactin were delayed 4 h in all rats and a normal quota of eggs was ovulated that night. Other 4- and 5-day cyclic rats which had been made persistently oestrous by anterior deafferentation of the medial basal hypothalamus (AC) underwent pinealectomy. These AC-pinealectomized rats were ovariectomized 60 days later and histological examination of the ovaries revealed no evidence of recent ovulation. Five to six weeks after ovariectomy, sequential blood samples were withdrawn through indwelling atrial cannulas in the AC-pinealectomized-ovariectomized rats and in ovariectomized, pinealectomized-ovariectomized and AC-ovariectomized rats. Regular pulsatile rhythms in plasma LH were measured in all rats. Subcutaneous injection of 50 μg oestradiol benzoate in oil lowered plasma LH levels in all four groups but caused an LH surge in the afternoon 2 days later only in the ovariectomized and pinealectomized-ovariectomized rats. The results indicate that the pineal gland in rats kept on a 14 h light: 10 h darkness schedule does not play an active or permissive role in the timing or magnitude of LH, FSH or prolactin release at pro-oestrus, the length of the oestrous cycle, or LH release in ovariectomized rats.

EFFECT OF NOREPINEPHRINE SYNTHESIS INHIBITORS AND A DOPAMINE AGONIST ON HYPOTHALAMIC LH-RH, SERUM GONADOTROPHIN AND PROLACTIN LEVELS IN GONADAL STEROID TREATED RATS

1978 ◽  
Vol 89 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Satya P. Kalra ◽  
Pushpa S. Kalra ◽  
C. L. Chen ◽  
James A. Clemens
Keyword(s):  
Dopamine Agonist ◽  
Ovariectomized Rats ◽  
Prolactin Release ◽  
Feedback Effects ◽  
Medial Basal Hypothalamus ◽  
Serum Lh ◽  
Lh Release ◽  
Low Levels ◽  
Lh Rh ◽  
The Relationship

ABSTRACT The relationship between the medial basal hypothalamus (MBH) LH-RH activity and LH release was studied following progesterone (P) treatment of oestrogen-primed ovariectomized rats (day 0). Following P administration at 10.00 h (day 2) serum LH levels increased rapidly after 13.00 h to peak levels attained at 15.00 h and maintained until 18.00 h. Coincident with the onset of augmented release and peak serum LH concentrations at 15.00 h there was a significant enhancement in the MBH LH-RH activity. Thereafter, the MBH LH-RH stores promptly fell and remained at morning low levels through the rest of the LH surge period. P treatment also stimulated release of FSH and prolactin in the afternoon. Administration of norepinephrine (NE) synthesis inhibitors, diethyldithiocarbamate (DDC) and U-14,624 before P blocked the afternoon increments in serum gonadotrophins and the MBH LH-RH levels; prolactin release was also suppressed in DDC treated rats. In contrast, lergotrile mesylate (dopamine agonist) treatment prior to P administration suppressed only the afternoon increase in prolactin release. These studies show that (1) P can stimulate MBH LH-RH activity in oestrogen-primed rats and these effects are transmitted to the LH-RH peptidergic neurons via NE synapses in the preoptic area and (2) a common central NE system may mediate the stimulatory feedback effects of P on gonadotrophin and prolactin release.

Changes in the characteristics of pulsatile luteinizing hormone secretion during the oestrous cycle and after ovariectomy and oestrogen treatment in female rats

1982 ◽  
Vol 94 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Takashi Higuchi ◽  
Masazumi Kawakami
Keyword(s):  
Hormone Secretion ◽  
Pulse Amplitude ◽  
Pulse Frequency ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Luteinizing Hormone Secretion ◽  
Oestrogen Treatment ◽  
Serum Lh ◽  
Lh Release

Changes in the characteristics of LH secretory pulses in female rats were determined in different hormonal conditions; during the oestrous cycle and after ovariectomy and oestrogen treatment. The frequency and amplitude of the LH pulses were stable during the oestrous cycle except at oestrus when a pattern could not be discerned because of low LH concentrations. These were significantly lower than those measured during other stages of the cycle. Mean LH concentrations and LH pulse amplitudes increased with time up to 30 days after ovariectomy. The frequency of the LH pulse was unchanged 4 days after ovariectomy when mean LH levels had already increased. The frequency increased 10 days after ovariectomy and then remained stable in spite of a further increase in mean serum LH concentrations. Oestradiol-17β injected into ovariectomized rats caused a decrease in LH pulse amplitude but no change in pulse frequency. One day after treatment with oestradiol benzoate no LH pulse was detectable, probably because the amplitude was too small. A generator of pulsatile LH release is postulated and an oestrogen effect on its function is discussed.

Adrenal progesterone facilitates the negative feedback of oestrogen on LH release in ovariectomized rats

1993 ◽  
Vol 139 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A. M. Salicioni ◽  
R. W. Carón ◽  
R. P. Deis
Keyword(s):  
Ovariectomized Rats ◽  
Adrenal Steroids ◽  
Serum Progesterone ◽  
Oestrogen Treatment ◽  
Ovx Rats ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

ABSTRACT There is evidence that the adrenals play a role in the regulation of the synthesis and release of gonadotrophins in various vertebrates. The aim of this study was to determine the part played by adrenal steroids, with special reference to progesterone, on the concentration of LH in ovariectomized (OVX) and oestrogen-primed rats. OVX rats received a single s.c. injection of vehicle or oestradiol benzoate (OB, 20 μg/rat). This day was designated as day 0. Three or four days later (day 3–day 4), the rats were treated with mifepristone (10 mg/kg) or with two doses of progesterone antiserum and blood samples were obtained at 13.00 and 18.00 h. OB treatment of OVX rats reduced serum LH at 13.00 h and 18.00 h on day 3 but only at 13.00 h on day 4. The administration of mifepristone at 08.00 h to OVX and oestrogen-treated rats induced a significant increase in serum LH at 18.00 h on days 3 and 4, without modifying the values at 13.00 h. When mifepristone was given at 13.00 h a much larger increase in serum LH was obtained at 18.00 h. In OVX and oestrogen-treated rats, adrenalectomy on day 2 (08.00–09.00 h) induced an increase in serum LH at 18.00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone treatment. In order to determine the specificity of the effect of mifepristone, a group of OVX and oestrogentreated rats was injected with progesterone antiserum at 08.00 and 13.00 h on day 3. Serum LH concentrations at 13.00 and 18.00 h on day 3 were similar to values obtained in OVX rats treated with oestrogen and mifepristone. Serum progesterone was measured at 08.00 and 13.00 h in OVX and OVX and oestrogenprimed rats. At both times, values were similar in OVX rats but oestrogen treatment significantly increased serum progesterone levels. The important role of adrenal progesterone on the regulation of LH secretion in OVX and oestrogen-primed rats is evident from these results. Blocking progesterone action at the receptor level, we showed that OB significantly increased LH values at 18.00 h. On the basis of these studies it is tempting to speculate on the possibility of an inhibitory or stimulatory effect of oestrogen on serum LH concentration in OVX rats, according to the presence or absence of adrenal progesterone action. Journal of Endocrinology (1993) 139, 253–258

Plasma LH levels following electrochemical stimulation of the deafferented medial basal hypothalamus

1980 ◽  
Vol 94 (1) ◽  
pp. 11-17
Author(s):  
A. J. Carrillo ◽  
N. Hagino ◽  
G. Setalo
Keyword(s):  
Median Eminence ◽  
Jugular Vein ◽  
External Jugular Vein ◽  
Female Rats ◽  
Medial Basal Hypothalamus ◽  
Blood Samples ◽  
Ether Anaesthesia ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Stimulation Of

Abstract. We have investigated the capability of a completely deafferented medial basal hypothalamus (MBH) pituitary complex to support LH release following electrochemical stimulation (ECS) of the arcuate-median eminence (ARC-ME) region. In adult female rats the MBH was completely deafferented (CD) on the morning of pro-oestrus (08.00-10.00 h of day 0). In the first experiment the animals were divided into 5 groups depending on the day of ECS (14.00–16.00 h) and oestradiol benzoate (Oe) treatment (08.00–10.00 h): group No. 1) ECS on day 0; 2) no ECS; 3) ECS on day 1; 4) Oe on day 0 and ECS on day 1; 5) Oe on day 4 and ECS on day 5. Blood samples were collected from the external jugular vein under ether anaesthesia for LH determinations just before and 1 and 2 h after ECS. ECS on day 0 resulted in a significant (P<0.01) rise in plasma LH at 1 and 2 h, while the rats subjected to CD, but not ECS failed to show any changes in plasma LH levels. ECS on days I and 5 (groups 3 and 5) failed to alter plasma LH levels, however, ECS on day 1 in Oe treated rats produced a significant (P < 0.01) elevation in plasma LH that was comparable to that of day 0. In a second experiment Oe was injected on days 1–5 and ECS of the ARC-ME was done bilaterally. ECS on day 5 resulted in a significant (P < 0.05) rise in plasma LH levels in rats with a completely deafferented MBH. In animals with an incomplete deafferentation ECS resulted in a much greater (P < 0.005) rise in plasma LH at l and 2 h. Since LH was released several days after complete hypothalamic deafferentation, these data suggest that LRH secreting cells may be present within the MBH of the rat. In a third experiment injection of LRH (400 ng) on days 0, 1 and 5 with Oe on days 0, 4 or 1–5 resulted in a significant (P < 0.001) rise of plasma LH at 30 and 60 min in all groups. Rats injected on day 0 showed the greatest elevation at 60 min in all groups. Saline injected rats did not show any changes in plasma LH levels.

DYNAMIC CHANGES IN HYPOTHALAMIC LH-RH LEVELS ASSOCIATED WITH THE OVARIAN STEROID-INDUCED GONADOTROPHIN SURGE

1979 ◽  
Vol 92 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Satya P. Kalra ◽  
Pushpa S. Kalra
Keyword(s):  
Temporal Changes ◽  
Ovariectomized Rats ◽  
Ovarian Steroid ◽  
Dynamic Changes ◽  
Medial Basal Hypothalamus ◽  
Lh Surge ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Definite Pattern ◽  
Lh Rh

ABSTRACT Pro-oestrous-type LH surges were induced by treating ovariectomized rats (day 0) with either oestradiol benzoate (OeB, 40 μg/rat) or oestrogen (10 μg/rat followed by progesterone (4 mg/rat, day 2, OeBP). To characterize the temporal changes associated with the LH surge on day 2, LH-RH levels in the medial basal hypothalamus (MBH) and the pre-optic area (POA) were analyzed by RIA in rats sacrified at hourly intervals between 10.00–19.00 h. Following these treatments the LH-RH content of POA fluctuated somewhat but no definite pattern was observed. In OeB rats, the MBH LH-RH levels were unchanged through the initial LH surge period (13.00–15.00 h) declining significantly, as in the OeBP group, near the end of the surge period (19.00 h). However, in OeBP rats, the MBH LH-RH contents decreased at 14.00 h and these were followed by markedly elevated levels between 15.00–17.00 h coincident with maximal increments in serum LH. The OeBP group alone showed a surge of serum FSH.

PROSTAGLANDIN-STIMULATED LH RELEASE IN CYCLIC AND OVARIECTOMIZED RATS

1979 ◽  
Vol 92 (1) ◽  
pp. 20-27 ◽  
Author(s):  
J. C. Carlson ◽  
S. J. Kehl
Keyword(s):  
Luteinizing Hormone ◽  
Differential Response ◽  
Oestrous Cycle ◽  
Ovariectomized Rats ◽  
Regulatory Activity ◽  
Ovarian Steroid ◽  
Similar Treatment ◽  
Blood Samples ◽  
Lh Release

ABSTRACT The ability of prostaglandin (PG) E2 treatment to stimulate luteinizing hormone (LH) release was compared in cyclic (4-day) and ovariectomized rats. PGE2 (500 μg) was injected sc and plasma LH concentration was determined in serial jugular blood samples. Administration of PGE2 at 13.30 h on each day of the oestrous cycle resulted in a significantly greater increase in plasma LH levels at pro-oestrus and oestrus than at dioestrus 1 and 2. This differential response by the hypothalamo-hypophyseal axis during the oestrous cycle implicates regulatory activity by ovarian steroid feedback. In oestrogen-primed ovariectomized rats, PGE2 administration stimulated a significant increase in plasma LH, but similar treatment in non-primed castrates decreased plasma LH levels. This finding suggests a major role for oestrogen in regulating this response.

Effects of pentobarbital on hypothalamic catecholamines and LRH activities

1980 ◽  
Vol 95 (1) ◽  
pp. 1-6 ◽  
Author(s):  
S. P. Kalra ◽  
J. W. Simpkins ◽  
P. S. Kalra
Keyword(s):  
Preoptic Area ◽  
Ovariectomized Rats ◽  
Medial Basal Hypothalamus ◽  
Significant Fall ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Apparent Decrease ◽  
Lrh Neurons

Abstract. Pentobarbital (Pnt) injection at 12.30 h to ovariectomized rats suppressed the LRH contents of the medial basal hypothalamus (MBH) in association with a significant fall in serum LH 60–90 min later. The LRH contents in the preoptic area (POA) were unchanged in Pnt treated rats. A similar effect on LRH levels in the MBH was also evident in ovariectomized rats pre-treated with oestradiol benzoate. Pnt administration rapidly reduced the noradrenergic (NE) turnover in the MBH and POA, whereas dopamine (DA) turnover was unaltered. These studies show that: (i) the apparent decrease in LRH secretion (release + contents) following Pnt treatment was associated with a fall in the hypothalamic NE neurotransmission, and (ii) LRH neurons and fibres in the MBH alone respond to Pnt treatment.

Antioestrogen inhibition of oestradiol-induced alterations in hypothalamic noradrenaline turnover

1985 ◽  
Vol 106 (1) ◽  
pp. 37-42 ◽  
Author(s):  
C. Hiemke ◽  
B. Poetz ◽  
R. Ghraf
Keyword(s):  
Brain Area ◽  
Serum Levels ◽  
Ovariectomized Rats ◽  
Noradrenaline Turnover ◽  
Stimulatory Action ◽  
Enhanced Sensitivity ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Secretory System

ABSTRACT Long-term (4–6 weeks) ovariectomized rats were injected with either oestradiol benzoate (OB; 20 μg s.c.) or monohydroxytamoxifen (MTAM; 0·2 mg i.p.) plus OB. Oestradiol benzoate was administered at 12.00 h on day 0 and MTAM was given immediately before OB, followed by further injections twice daily to maintain sufficiently high antioestrogen levels. When given alone, OB reduced the serum levels of LH during the morning (08.00–09.00 h) and afternoon (17.30–18.30 h) hours of day 3 after priming. The feedback actions of OB on LH release were accompanied by time-dependent alterations of noradrenaline turnover in the preoptic–anterior hypothalamic brain area (POAH). On day 3 after priming the noradrenaline turnover rate was reduced in the morning and increased in the afternoon. The increase correlated with an enhanced sensitivity of the LH secretory system to progesterone. The antioestrogen MTAM blocked the OB-induced sensitization of LH release to the stimulatory action of progesterone and interfered with the stimulatory long-term effect of oestradiol on hypothalamic noradrenaline turnover. The data strongly support the view that the oestrogen-induced afternoon increase of noradrenaline turnover in the POAH represents a pre-requisite for the induction of LH surges. The stimulatory effect of oestradiol on hypothalamic noradrenaline turnover seems to be mediated by a classical oestrogen receptor mechanism. J. Endocr. (1985) 106, 37–42

RESTORATION BY OESTRADIOL BENZOATE OF A NEURAL AND HORMONAL RHYTHM IN THE OVARIECTOMIZED RAT

1975 ◽  
Vol 64 (1) ◽  
pp. 27-35 ◽  
Author(s):  
F. R. BURNET ◽  
P. C. B. MACKINNON
Keyword(s):  
Single Injection ◽  
Time Of Day ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Functional Link ◽  
Initial Injection ◽  
Oestradiol Benzoate ◽  
Before And After ◽  
Lh Release ◽  
The Brain

SUMMARY The rate of [35S]methionine incorporation into protein in discrete cerebral areas was measured before and after the administration of oestradiol benzoate (OB) to chronically ovariectomized rats. The circadian rhythm of incorporation which is normally seen in the intact cyclic female rat was deleted by ovariectomy. A daily rhythm of incorporation reappeared, however, in all the brain areas studied 30 h after a single injection of OB (20 μg), and was still present 12 days later. The release of luteinizing hormone (LH) after administration of 20 μg OB was measured in chronically ovariectomized animals and was found to be biphasic. High levels of LH after ovariectomy were initially reduced by negative feedback, but this phase was followed 52 h later by a facilitation of LH release between 15.00 and 18.00 h. The facilitation of LH release at this time of day was still detectable 12 days after the initial injection. The evidence for a functional link between the rhythm of neural activity which is reflected by [35S]methionine incorporation, and the ability to 'time' the facilitation of LH release is discussed.

Influence of melatonin and oestradiol on the opioidergic regulation of LH and prolactin release in pony mares

1997 ◽  
Vol 154 (2) ◽  
pp. 241-248 ◽  
Author(s):  
C Aurich ◽  
J Lange ◽  
H-O Hoppen ◽  
J E Aurich
Keyword(s):  
Prolactin Secretion ◽  
Opioid Antagonist ◽  
Short Term ◽  
Melatonin Treatment ◽  
Prolactin Release ◽  
Oestradiol Treatment ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

Abstract The aim of this study was to investigate the influence of oestradiol, melatonin and season on the opioid regulation of LH and prolactin release. Effects of the opioid antagonist naloxone (0·5 mg/kg) on LH and prolactin secretion were determined in ovariectomized pony mares. In experiment 1, mares in January (n=6) were pretreated with oestradiol benzoate (5 μg/kg) for 20 days. In experiment 2, beginning in May, mares (n=7) received melatonin (15 mg) for 15 days and subsequently a combination of melatonin plus oestradiol for 20 days. In experiment 3, beginning in May, mares (n=6) were pretreated with oestradiol for 30 days, left untreated for 12 days and then given melatonin for 35 days. In all experiments the animals were injected with the opioid antagonist naloxone and saline on 2 consecutive days prior to treatment. In experiment 1, animals received naloxone and saline on days 10 and 11 and 20 and 21 following oestradiol treatment. In experiment 2, naloxone and saline were administered on days 15 and 16 following melatonin treatment and on days 10 and 11 and 20 and 21 of melatonin plus oestradiol treatment. In experiment 3, the animals received naloxone and saline on days 10 and 11, 20 and 21 and 30 and 31 of oestradiol treatment, prior to melatonin treatment and on days 15 and 16, 25 and 26 and 35 and 36 following melatonin. In January (experiment 1), naloxone evoked a significant (P<0·05) LH release at all times, however the LH increment in response to naloxone increased during oestradiol pretreatment (P<0·05) During the breeding season (experiments 2 and 3), naloxone induced a significant (P<0·05) increase in plasma LH concentrations when mares had not been pretreated with oestradiol or melatonin and after oestradiol pretreatment. Basal LH concentrations and the LH increment in response to naloxone increased significantly (P<0·05) during the 30-day oestradiol pretreatment. Melatonin decreased the naloxone-induced LH release and the LH release in response to naloxone and saline no longer differed after 25 and 35 days of melatonin pretreatment. When melatonin was given together with oestradiol for 20 days, again a significant (P<0·05) LH release in response to naloxone occurred. Prolactin release was significantly (P<0·05) increased by naloxone when mares had been pretreated with only melatonin. The opioid antagonist did not affect prolactin release in mares that had not been pretreated or received oestradiol either alone or in combination with melatonin. In conclusion, in long-term ovariectomized mares, opioids inhibit LH secretion independent from ovarian factors. This opioid inhibition of LH secretion is enhanced by oestradiol and reduced by melatonin. Although short-term melatonin treatment in-activates the opioid regulation of LH release, a prolonged influence of melatonin as occurs in winter does not prevent activation of the opioid system. This indicates that effects of melatonin on the opioid regulation of LH release change with time. An opioid inhibition of prolactin secretion is activated by melatonin given for 15–35 days but is lost under the prolonged influence of a short-day melatonin signal in winter. Journal of Endocrinology (1997) 154, 241–248

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