Distribution of gamma-aminobutyric acid in catfish (Heteropneustes fossilis) forebrain in relation to season, ovariectomy and E2 replacement, and effects of GABA administration on plasma gonadotropin-II level

In the catfish Heteropneustes fossilis, the hypothalamus and telencephalon showed seasonal variations in gamma-aminobutyric acid (GABA) with high levels in prespawning and spawning phases and low levels in preparatory and postspawning phases. Ovariectomy for 4 and 5 weeks reduced significantly the GABA contents only in the hypothalamus. Replacement with E2 (1 microgram/g BW) restored the levels to that of sham ovariectomized or parallel control group. Treatment with GABA (i.p.; 10 or 50 micrograms/g body weight (BW) alone did not produce any significant effect on plasma gonadotropin-II (GTH-II) level in any of the seasons. Injection of GABA, but not baclofen (a GABAB agonist), stimulated GTH-II secretion in pimozide or GnRH analogue-pimozide pretreated fish at both 0.5 and 2 h in early prespawning phase except at 0.5 h in the pimozide--GABA (10 micrograms) group. This stimulatory effect was not evident in other seasons. The results of the present study suggest that Estradiol-17 beta (E2) seems to stimulate GABA which may account for its high level in the recrudescent phase. GABA seems to have a permissive role in GTH-II secretion when dopamine receptor function is inhibited.     

Pituitary-gonadal Relationship in the Catfish Clarias batrachus (L): A Study Correlating Gonadotrophin-II and Sex Steroid Dynamics

A heterologous radioimmunoassay was developed for measuring gonadotrophin-II (GTH-II) in the catfish Clarias batrachus. Serum and/or pituitary levels of GTH-II showed significant annual/seasonal variations in male and female catfish, which could be correlated with both gonadosomatic index and/or serum testosterone level. GTH-II was not detected in resting phase, increased during gonadal recrudescence to peak values in late prespawning /spawning phases, and declined to low values in postspawning phase. During gonadal recrudescence, the pituitary and serum levels of GTH-II maintained positive or inverse relationships implying differential rates of hormone release and synthesis/storage. Gonadectomy resulted in increased release of GTH-II; the release pattern varied in females and hemi-castrated or completely castrated males. In females, the GTH-II increase followed a distinct biphasic pattern with the peak rise at week 4 of ovariectomy. In males, castration resulted in significant rise of serum GTH-II levels at all duration except week 5, but the magnitude of the rise was higher in completely castrated fish (weeks 1, 2 and 3). Testosterone replacement in 3-week hemi-castrated fish restored the GTH-II level to that of the sham control vehicle group. In intact fish, administration of testosterone elicited an increase in serum GTH-II levels in the low dose (0.25 and 0.5 mug / g BW) groups and no change in the high dose (1.0 mug / g BW) group. Methallibure treatment inhibited GTH-II levels in a dose-dependent manner. The reduction was greater in males. Withdrawal of the drug treatment restored the GTH-II and testosterone levels after 15 days in the low dose group (2 mug / g BW). The results indicate that there exists a dynamic positive or negative feedback relationship between gonadal steroids and GTH-II, which is essential to control the release and availability of circulating GTH-II.     

The lack of involvement of central nervous system in the antiarrhythmic effects of prostaglandins E2, F2α, and I2 in cat

The role of the central nervous system (CNS) in the antiarrhythmic effects of prostaglandins (PGs) E₂, F_2α, and I₂ was studied by administering each agent into the left lateral cerebral ventricle (i.c.v. administration) of chloralose-anesthetized cats. The cardiac arrhythmias were produced by intravenous (i.v.) infusion of ouabain (1 μg/kg/min). The PGs E₂, F_2α and I₂ on i.c.v. administration in the dose range of 1 ng to 10 μg failed to inhibit ouabain-induced cardiac arrhythmias. However, when infused i.v., PGE₂ (1 μg/kg/min), PGF_2α (5 μg/kg/min), and PGI₂ (2 μg/kg/min) effectively suppressed these arrhythmias. The standard antiarrhythmic drug propanolol (0.5–8.0 mg)oni.c.v.administration also significantly reduced the ouabain-induced cardiac arrhythmias. It is suggested that the CNS is not the site of action of PGs E₂, F_2α, and I₂ in antagonising the ouabain-induced cardiotoxicity in cats.     

A single injection of 17β-estradiol facilitates sexual behavior in castrated male mice

Sexual behavior was assessed in castrated adult CD-1 male mice given exogenous steroids under various treatment regimens. Castrated mice maintained on 20 μg testosterone (T) daily for 1 week, but given 250 μg testosterone propionate (TP) on the day of testing showed higher levels of copulatory activity than intact mice or the males receiving an additional dose of 20 μg T on the test day, although plasma testosterone levels were not different at the time of behavioral testing. Castrated males given 50, 125, or 250 μg TP for 1 week including the day of testing showed higher levels of sexual behavior than males receiving the same doses of TP only once, on the test day. A single injection of 17β-estradiol (E₂) completely restored the male copulatory pattern, including ejaculation, in castrated mice under every condition examined. Testosterone and dihydrotestosterone (DHT) were less effective than E₂, as was the combination of E₂ and DHT. The relative efficacy of a single dose of T, DHT, and E₂ plus DHT was dependent upon factors such as the delay between steroid administration and testing, as well as whether or not the castrated mice received androgen replacement prior to testing. Estradiol benzoate (E₂B) was not capable of restoring sexual behavior in castrated mice in this study. The comparison of results obtained with TP, T, E₂, and E₂B suggests that an appreciable, but not necessarily sustained, elevation of E₂ levels in the brain may be critical in the facilitation of male copulatory behavior in mice.     

Effect of somatostatin on electrogenic ion transport in the duodenum and colon of the mouse, Mus domesticus

In this study, we have used the mouse intestine and the Ussing short circuit technique to compare the effects and mechanism of action of somatostatin (SST, 0.1 μM) on cAMP- and Ca²⁺-mediated ion secretion in the duodenum and colon of the Swiss-Webster mouse. The cAMP-dependent secretagogues, prostaglandin E₂ (1 μM) and dibutyryl-cAMP (150 μM) increased short circuit current (I_sc) in both regions, but only the colonic response was inhibited by SST. This inhibition was independent of enteric nerves, suggesting a direct action on the epithelial cells. The Ca²⁺-dependent secretagogue carbachol (10 μM) stimulated a transient increase in I_sc in both intestinal segments. In the duodenum, SST partially inhibited this increase in I_sc and both the responses to carbachol and SST were independent of enteric nerves. In the colon, while SST inhibited the carbachol induced increase in I_sc, pre-treatment with tetrodotoxin (750 nM) profoundly inhibited the carbachol induced increase in I_sc, thus markedly reducing the inhibitory effect of SST. This indicates an involvement of the enteric nervous system in the response to carbachol and the action of SST in the colon. These data indicate marked regional differences within the mouse intestine of the effects of SST on ion secretion and demonstrate different mechanisms of action of SST in the duodenum and colon.     

Vitamin B12-induced alterations in activities of α-glycerophosphate dehydrogenase and malic enzyme in brain of singi fish, Heteropneustes fossilis (Bloch)

Different doses of vitamin B₁₂ (0.25, 0.5, 1, 2 and 4 μg/g, injected intraperitoneally for three consecutive days) altered the activities of mitochondrial-α-glycerophosphate dehydrogenase (α-GPD) and NADP-dependent cytosolic malic enzyme (ME) in the brain of singi fish. The α-GPD activity increased at doses of 0.5, 1, 2 and 4 μg/g vitamin B₁₂. A dose of 0.5 μg/g vitamin B₁₂ induced less activity than higher doses. ME activity increased with 1, 2 and 4 μg/g of vitamin B₁₂/g. The mitochondrial and cytosolic protein content remained unchanged after vitamin B₁₂ administration. Cycloheximide treatment inhibited the vitamin B₁₂-induced increase in α-GPD and ME activity. Thus, vitamin B₁₂ is involved in the induction of some enzymes in fish brain.     

Effects of intracerebroventricular administration of PGE1, E2 and F2α on electrically induced convulsions in mice

Intracerebroventricular administration of prostaglandins E₁ or E₂ was shown to block, while PGF_2α increased the incidence of tonic convulsion due to electroshock in mice. The Prostaglandins were administered intracerebroventricularly (i.c.v.) to conscious mice by a modification of Haley and McCormick's method (1) prior to a transcorneal maximal electroshock (MES) or a transcorneal supra-maximal electroshock (SMES). PGE₁ and PGE₂ i.c.v. blocked the tonic hindlimb extension (THE) and protected the animals from death induced by MES with ED₅₀'s for PGE₁ and PGE₂ for inhibition of the THE of 6.6 (4.3–12.0) μg/mouse i.c.v. and 13.3 (8.9–22.4) μg/mouse i.c.v. respectively. When PGE₂ was administered intraperitoneally (i.p.) in doses as high as 4.0 mg/kg it did not block the THE. However, the duration of the THE as well as the mortality were reduced by doses of 0.5–4.0 mg/kg PGE₂ i.p.. Both PGE₁ and PGE₂ were shown to cause a dose related significant (p<.001) decrease in the duration of the THE with SMES in doses of 1–10 μg/mouse i.c.v. for PGE₁ and 2–40 μg/mouse i.c.v. for PGE₂. PGF_2α, administered i.c.v. prior to a transcorneal electroshock equivalent to a current at the ED₁ level, increased the incidence of the THE as well as the mortality in doses of 20–50 μg/mouse.     

Effects of intracerebroventricular administration of prostaglandins I2, E2, F2α and indomethacin on blood pressure in the rat

The effects of intraventricularly administered prostaglandins I₂ (PGI2), E₂ (PGE2), F_2α (PGF2α) and indomethacin on systemic blood pressure were investigated in conscious rats. PGI2 (1.25 – 10 g/kg) decreased blood pressure in a dose-related manner, whereas PGE2 (100 – 1000 ng/kg) dose-dependently increased blood pressure. Both PGF2α (0.31 – 20 μg/kg) and indomethacin (0.625 – 40 μg/kg) had no effects on blood pressure. These results indicate that intraventricular injection of PGI2 or PGE2 can induce significant changes in blood pressure, while endogenous prostaglandins synthesized in the brain seem to play a minor role in direct regulation of systemic blood pressure in the rat.     

Control system for detection of the illegal use of naturally occurring steroids in calves

Within the scope of the National Plan for Hormone Control in The Netherlands, a study was performed to develop a system for control of the illegal use of three naturally occurring hormones [oestradiol-17β (E₂-17β), testosterone (T), progesterone (P)] for fattening purposes in animal production. Using a specific high-performance liquid chromatographic—radioimmunoassay method, reference values were established for concentrations of E₂-17β, T and P and some of their metabolites in blood plasma and urine from untreated male and female veal calves. E₂-17β levels of both male and female calves were <0.01 μg/l in blood plasma and <0.2 μg/l in urine. For male veal calves levels of T and epitestosterone (epiT) in blood plasma and urine varied widely. The P levels were <0.1–0.3 μg/l in blood plasma and <0.6–10 μg/l in urine from both male and female calves. To investigate the effect of anabolic treatment on the hormone levels in plasma and excreta, male veal calves were injected, subcutaneously into the dewlap, with a solution containing 20 mg of E₂-17β benzoate and 200 mg of T propionate in 5 ml of arachis oil. Only the levels of E₂-17β and E₂-17α in blood plasma and excreta were elevated until about one week after injection, compared with the untreated control calves and the reference values. T and epiT levels were similar in plasma and excreta from both untreated and treated animals.     

Blood pressure and heart rate effects of prostaglandin E2 and F2α produced by intracerebroventricular injections in cats

Blood pressure and heart rate effects of prostaglandin E₂ and F_2α were examines after administrating each agent into the left lateral brain ventricle of chloralose-anesthethized cats. Administration of prostaglandin E₂ (1 μg) resulted in significant, prolonged increases in arterial pressure (25.7 ± 6.7 mm Hg) and heart rate (19.4 ± 7.7 beats/min). These responses were mimicked when the same dose of prostagland E₂ was administered into the restricted to the lateral and third ventricles via cannulation of the cerebral aqueduct, whereas no significant cardiovascular occured with administration into the fourth ventricle. Intravenous injection of prostaglandin E₂ resulted in a transient decrease in blood pressure but no change in heart rate. Administration of prostaglandin F_2α (1 and 3 μg) into the CNS produced no significant cardiovascular responses. The same was true when prostaglandin F_2α was administered by the intravenous route. These results indicate that pronounced cardiovascular effects can be produced by administering prostaglandin E₂ but not F_2α into the CNSm and that the central site of action of prostaglandin E₂ is in the forebrain.     

Motilin Stimulates Gastric Acid Secretion in Coordination with Ghrelin in Suncus murinus

Motilin and ghrelin constitute a peptide family, and these hormones are important for the regulation of gastrointestinal motility. In this study, we examined the effect of motilin and ghrelin on gastric acid secretion in anesthetized suncus (house musk shrew, Suncus murinus), a ghrelin- and motilin-producing mammal. We first established a gastric lumen-perfusion system in the suncus and confirmed that intravenous (i.v.) administration of histamine (1 mg/kg body weight) stimulated acid secretion. Motilin (0.1, 1.0, and 10 μg/kg BW) stimulated the acid output in a dose-dependent manner in suncus, whereas ghrelin (0.1, 1.0, and 10 μg/kg BW) alone did not induce acid output. Furthermore, in comparison with the vehicle administration, the co-administration of low-dose (1 μg/kg BW) motilin and ghrelin significantly stimulated gastric acid secretion, whereas either motilin (1 μg/kg BW) or ghrelin (1 μg/kg BW) alone did not significantly induce gastric acid secretion. This indicates an additive role of ghrelin in motilin-induced gastric acid secretion. We then investigated the pathways of motilin/motilin and ghrelin-stimulated acid secretion using receptor antagonists. Treatment with YM 022 (a CCK-B receptor antagonist) and atropine (a muscarinic acetylcholine receptor antagonist) had no effect on motilin or motilin-ghrelin co-administration-induced acid output. In contrast, famotidine (a histamine H₂ receptor antagonist) completely inhibited motilin-stimulated acid secretion and co-administration of motilin and ghrelin induced gastric acid output. This is the first report demonstrating that motilin stimulates gastric secretion in mammals. Our results also suggest that motilin and co-administration of motilin and ghrelin stimulate gastric acid secretion via the histamine-mediated pathway in suncus.     

The central nervous effect of prostaglandins I2, E2 and F2α on aconitine — Induced cardiac arrhythmia in rats

Intracerebroventricular administration of PGI₂ or PGE₂ reduced aconitine-induced cardiac arrhythmia in rats. PGF_2α had no antiarrhythmic effect under the same conditions. The ED₅₀ values of PGI₂ and E₂ were 0.25 μg/kg and 1.1 μg/kg, respectively. Central mechanisms may participate in the antiarrhythmic effect of these PGs.     

Prostaglandin E2 opunteracts the effects of PGF2α in indomethacin treated cycling gilts

Twenty crossbred gilts with at least 2 consecutive estrous cycles of 18 to 21 days in length were used to study the effects of prostaglandins E₂ and F₂α (PGE₂ and PGF₂α) on luteal function in indomethacin (INDO) treated cycling gilts. Intrauterine and jugular vein catheters were surgically palced before day 7 of the treatment estrous cycle and gilts were randomly assigned to 1 of 5 treatment groups (4/groups). With exception of the controls (Group I) all gilts received 3.3 mg/kg INDO every 8 h, Groups III, IV and V received 2.5 mg PGF₂; 2.5 mg PGF₂α + 400 μg PGE₂ every 4 hr, or 400μg PGE₂ every 4 h, respectively. All treatments were initiated on day 7 and continued until estrus or day 23. Jugular blood for progesterone analysis was collected twice daily from day 7 to 30. Estradiol-17β (E₂-17β) concentrations were dtermined in samples collected twice daily, from 2 d before until 2 d following the day of estrus onset. When compared to pretreatment values, estrous cycle length was unaffected (P>0.05) in Group I, prolonged (P<0.05) in Groups II, IV and V; and shortened (P<0.05) in Group III. The decline in plasma progesterone concentration that normally occurs around day 15 was unaffected (P>.05) in Group I; delayed (P<0.05) in Groups II, IV and V; and occurred early (P<0.05) in Group III. Mean E₂-17β remained high (31.2 ± 4.9 to 49.3 ± 3.1 pg/ml) in Groups III and IV, while the mean concentrations in Groups III and V varied considerably (17.0 ± 2.0 to 52.2 ± 3.5 pg/ml). The results of this study have shown that PGE₂ will counteract the effects of PGF₂α in INDO treated cycling gilts. The inclusion of PGF₂α appeared to either stimulate E₂-17β secretion or maintain it at a higher level than other treatments.     

Effects of PGE1 or PGE2 on luteal function in pseudopregnant rats

Effects of PGE₁ or PGE₂ on luteal function were studied in 163 pseudopregnant rats. PGE₁ (10, 100, or 300μg) given intrauterine every 6 hr did not shorten pseudopregnancy (P < 0.05), however, the same doses of PGE₂ given intrauterine every 6 hr advanced luteolysis (P < 0.05). PGE₁ (100 or 300μg) given every 4 hr intramuscular maintained levels of progesterone in peripheral blood above controls (P < 0.05) while 100 or 300μg of PGE₂ hastened the decline in progesterone (P < 0.05). The antiluteolytic effect of PGE₁ was not via an inhibition of PGF secretion (P < 0.05) by the uterus or by induction of ovulation in treated animals. Moreover, PGE₁ (100, 200, or 500μg) given intramuscular every 4 hr from day 4 of pseudopregnancy until the next proestrus delayed luteal regression around 3 days (P < 0.05). PGE₂ at doses of 100, 200, or 500μg every 4 hr given intramuscular consistently shortened pseudopregnancy (P < 0.05). Lower doses were without effect (P < 0.05). Based on the above data it is concluded that PGE₂ is consistently luteolytic whereas PGE₁ is not luteolytic in pseudopregnant rats and that PGE₁ may be an antiluteolysin.     

Failure of LH and/or prolactin to prevent PGF2α-induced luteolysis of ovine corpora lutea

Infusions of phosphate buffered saline, LH (4 μg/min or 14 μg/min), prolactin (42 μg/min) or LH (4 μg/min) plus prolactin (42 μg/min) for 12 hr did not prevent luteolysis following intramuscular injections of prostaglandin F₂α-tham salt two and six hr after beginning the infusion. Likewise, these treatments did not delay luteolysis since a similar rate of decline in peripheral plasma progesterone occurred in all groups. It was concluded that elevation of serum concentrations of LH and prolactin to high levels had no effect on PGF₂α-induced luteolysis on day 8 following induced ovulation.     

The effect of locally administered PGE2 on the contractility of the nonpregnant human uterus in vivo

The effect of locally administered prostaglandin E₂ on the sensitivity and reactivity of the nonpregnant human uterus during the menstrual cycle was studied in seven women. An increase in uterine contractility in response to as little as 0.25 μg PGE₂ could be observed during both the mid-proliferative and mid-secretory phases of the menstrual cycle, but around ovulation a marked decrease in sensitivity to PGE₂ was noted. An inhibition of uterine motility was observed during menstruation in response to 30–40 μg PGE₂. Endogenous E prostaglandin normally occurs in the secretory endometrium in levels comparable to the amount of exogenous PGE₂ which elicited increased or decreased uterine activity in this study. These findings suggest that PGE₂ may play an important role in the cyclical regulation of uterine motility during the menstrual cycle.     

Stimulation by melittin of adrenocorticotropin and beta-endorphin release from rat adenohypophysis in vitro

The effect of melittin on the release of adrenocorticotropin (ACTH) and β-endorphin from the corticotropic cells of the rat adenohypophysis was examined in vitro. Anterior pituitary quarters were perifused or incubated in vitro and ACTH- (ACTH-IR) or β-endorphin-like immunoreactivity (β-End-IR) in the medium was measured by radioimmunoassays. Melittin stimulated ACTH-IR and β-End-IR release. This effect was rapid in onset, reversible, and concentration-related (50–5000 ng/ml) and dependend on the presence of calcium ions in the incubation medium. Melittin also elevated the tissue content of unesterified ³H-arachidonic acid that had previously been incorporated into lipids. Purported phospholipase A₂ inhibitors, mepacrine (up to 1 mM), dexamethasone (0.5 mg/kg in vivo, 50 nM in vitro), or p-bromophenacylbromide (100 μM), did not decrease the Melittin (500 ng/ml) — induced β-End-IR release, although mepacrine and dexamethasone may have inhibited phospholipase A₂ activity as indicated by an inhibition of melittin-evoked prostaglandin E₂ formation. After stimulation by melittin (500 ng/ml), β-End-IR release was not affected by the cyclooxygenase inhibitor inddomethacin (up to 140 μM), whereas nordihydroguaiaretic acid (100 μM), a lipoxygenase inhibitor, or BW755C (250 μM), an inhibitor of both cyclooxygenase and lipoxygenase, abolished melittin-induced hormone secretion. We conclude that melittin generates a signal in the corticotropic cells of the rat adenohypophysis which induces hormone secretion by exocytosis. This signal may be unrelated to the activation by melittin of phospholipase A₂.     

Dose response relation of the renal effects of PGA1, PGE2, and PGF2α in dogs

The effects of the three prostaglandins A₁, E₂, and F_2α on renal blood flow, glomerular filtration rate (GFR), fluid excretion, and urinary output of Na, K, Ca, Cl, and solutes were evaluated at a dose range of 0.01 – 10 μg/min. The prostaglandins were infused into the renal artery of dogs. GFR was not significantly altered by the PGs. PGA₁ increased renal blood flow by approximately of the control at 0.01 μg/min without dose dependence at higher infusion rates. It had only little effects which were not dose dependent on fluid and electrolyte output. The effects of PGE₂ on renal blood flow, fluid, sodium, and chloride excretion were dose dependent with a steep slope of the dose response curve between 0.1 and 1.0 μg/min. Blood flow was increased maximally by 80 %, urine volume by more than 400 %. PGF_2α had no effect on renal blood flow, whereas urinary output was increased to approximately the same maximal level as by E₂ although ten times higher doses were needed. Potassium excretion was less influenced than the excretion of Na and Cl and osmolar clearance was less increased than urine volume by all three prostaglandins.It is concluded that if a PG is involved in the regulation of the renal fluid or electrolyte excretion it is likely to be of the PGE-type. A PGA could only be involved in regulation of renal hemodynamics, whereas PGF although effective in the kidney exerts its effects at doses too high to have physiological significance.     

Effect of indomethacin and 7-oxa-13-prostynoic acid on luteinization of transplanted rat ovarian follicles induced by luteinizing hormone and prostaglandin E2

The ability of prostaglandin E₂ (PGE₂) to initiate luteinization was demonstrated using a system of in vitro incubation of ovarian follicles followed by transplantation. Follicles from diestrous rats were incubated with 0.05 to 50 μg/ml PGE₂, 10 μg/ml luteinizing hormone (LH), or alone in Krebs-Ringer bicarbonate buffer plus glucose for 2 hr. Then follicles were transplanted under the kidney capsules of hypophysectomized recipients, with follicles exposed to PGE₂ on one side and those exposed to LH or buffer only on the other side. As determined at autopsy 4 days later and confirmed by histological examination, follicles exposed to PGE₂ at concentrations of 0.5 μg/ml or greater, or to LH, transformed into corpora lutea, but control follicles regressed. Incubation of follicles with LH in the presence of indomethacin, an inhibitor of prostaglandin synthesis, significantly reduced the incidence of luteinization. Prostaglandin E₂ (10 μg/ml) was able to override the inhibition of luteinization by indomethacin (150 μg/ml). The prostaglandin analogue 7-oxa-13-prostynoic acid (100 μg/ml) failed to prevent luteinization in response to either 5 μg/ml LH or 1 μg/ml PGE₂. Results with PGE₂ and with indomethacin suggest a role for prostaglandins in the luteinizing action of LH.We have reported previously that in vitro exposure of diestrous rat follicles to luteinizing hormone (LH) will result in transformation of the follicles to corpora lutea following transplantation under the kidney capsules of hypophysectomized rats. Dibutyryl cyclic AMP (DBC) mimics this effect of LH, and transplants produce progesterone in measurable amounts after both LH and DBC exposure when prolactin is administered in vivo to recipients.Kuehl et al. have suggested that prostaglandins may act as obligatory intermediates in the effect of LH on the ovary, acting between LH and adenylate cyclase. Preliminary results indicated that prostaglandin E₂ (PGE₂) could induce luteinization in our system. The extent of prostaglandin involvement in luteinization was further investigated in this work, using two reported antagonists of prostaglandin action, indomethacin and 7-oxa-13-prostynoic acid. Indomethacin has been found to inhibit synthesis of prostaglandins E₂ and F_2α; 7-oxa-13-prostynoic acid, which acts as a competitive antagonist of prostaglandins, prevented the effect of LH and prostaglandins E₁ and E₂ on cyclic AMP production in mouse ovaries.     

Follicle stimulating hormone and prolactin release induced by prostaglandins in rat

Ten to 60 minutes following a single i.v. injection of PGE₂ (500 μg/rat) into male rats of 30 to 35 days of age FSH concentration in the serum was raised significantly. The rise in FSH was maintained from 10 to 60 minutes after treatment, then at 90 minutes FSH had declined and was not significantly different from that of the control before treatment. Prostaglandin E₁, E₂ or F_2α (670μg/rat) significantly increased the serum prolactin level 10 to 60 minutes after a single i.v. injection in spayed rats primed with estrogen and progesterone. And, rats primed with estrogen and progesterone. And, increases in prolactin in the serum were observed with as little as 2μg of PGE₁ or E₂, and 20μg of PGF_2α. Twenty μg of PGE₂, and 200μg of PGE₁ or F_2α gave the maximum stimulation. These results indicate that release of pituitary hormones is affected by prostaglandins.Prostaglandins (PGs) are widely distributed in mammalian tissues, and they have been reported to have an almost equally wide variety of endocrine and metabolic effects. It was recently postulated that PGs may be involved in the process of ovulation because ovulation was blocked by inhibitors of PG synthesis (1–5).