Effects of 2-buten-4-olide, an endogenous feeding suppressant, on the pulsatile secretion of luteinizing hormone in ovariectomized rats

1993 ◽  
Vol 129 (5) ◽  
pp. 467-472 ◽  
Author(s):  
Seiichiro Saito ◽  
Keiji Shitsukawa ◽  
Minoru Irahara ◽  
Toshiya Matsuzaki ◽  
Toshihiro Aono

The effects of 2-buten-4-olide (2-B40), an endogenous feeding suppressant, on the secretion of luteinizing hormone (LH) were studied in ovariectomized rats. Intraperitoneal (ip) administration of 2-B40: adult female ovariectomized Wistar rats were given daily ip injections of solution containing 2-B40 at 0, 50 or 100 mg/kg body wt for 14 days. This ip treatment with 2-B40 significantly decreased the mean LH concentration and pulse frequency of LH. Intravenous (iv) administration of 2-B40: a solution of 2-B40 (50 or 100 mg/kg body wt) was slowly injected through an intra-atrium catheter and blood samples were taken every 6 min for 2 h. This iv treatment significantly suppressed the LH pulse frequency but had no significant effect on the LH amplitude or mean LH. Injection of 2-B40 into the third cerebroventricle: the injection of 2-B40 into the third cerebroventricle of freely moving rats decreased the mean LH concentration and the frequency and amplitude of LH pulses. Third cerebroventricle injection of a corticotropin-releasing factor (CRF) receptor antagonist before third cerebroventricle injection of 2-B40: the specific CRF receptor antagonist α-helical-CRF (9–41) was injected into the third cerebroventricle of ovariectomized rats before injection of 2-B40. Administration of 2-B40 into the third cerebroventricle significantly decreased the mean LH, concentration and pulse frequency. Third cerebroventricle injection of the CRF antagonist at 50 μg/rat and then 2-B40 also resulted in significant suppression of the mean LH concentration and pulse frequency. These findings suggest that 2-B40 may suppress gonadotropin-releasing hormone secretion in ovariectomized rats and that its effect in decreasing LH pulses may not be caused through the CRF pathway.

1986 ◽  
Vol 111 (1) ◽  
pp. 51-59 ◽  
Author(s):  
C. W. Coen ◽  
R. V. Gallo

ABSTRACT This study was undertaken to investigate whether hypothalamic adrenaline is involved in pulsatile LH release in rats. Various inhibitors of phenylethanolamine N-methyltransferase (PNMT), the enzyme which catalyses the conversion of noradrenaline to adrenaline, were administered to freely moving ovariectomized rats bearing an atrial cannula. Blood samples were taken continuously from 09.00 to 11.00 h and from 14.30 to 17.00 h. The drugs were administered either at 11.00 h only or at both 11.00 and 14.00 h. The various treatments with the vehicle or an inhibitor of peripheral PNMT, SKF 29661, produced no decrease in any parameter of pulsatile LH release. A single injection of one of the central PNMT inhibitors, SKF 64139 or LY 134046, at 11.00 h had no effect on LH release, but when given at both times the drugs suppressed the mean LH level, pulse frequency and amplitude. The effect of these drugs on the level of dopamine, noradrenaline and adrenaline in the hypothalamus (including preoptic area) was assessed. There was no effect on the concentration of the catecholamines after SKF 29661. None of the treatments with SKF 64139 or LY 134046 resulted in a change in the level of dopamine or noradrenaline; the double dose did, however, produce a significantly greater depletion of adrenaline than that which was achieved with the single injection. These results suggest that the maintenance of normal LH pulses is dependent upon the presence of a sufficient level of hypothalamic adrenaline. The presence of at least 41% of the control level of hypothalamic adrenaline was compatible with the maintenance of LH pulses, but 30% or less of that level was insufficient for their normal occurrence. The effects of LY 134046 are particularly significant since this drug, unlike some of the other PNMT inhibitors, lacks α-adrenergic antagonist properties. J. Endocr. (1986) 111, 51–59


1997 ◽  
Vol 65 (2) ◽  
pp. 217-224 ◽  
Author(s):  
F. Forcada ◽  
J. M. Lozano ◽  
J. A. Abecia ◽  
L. Zarazaga

AbstractThe role of endogenous opioids and the dopaminergic system on the inhibition of luteinizing hormone (LH) secretion during early and late anoestrus, together with its modulation by the plane of nutrition were investigated in ewes with a short anoestrous season. In early anoestrus (22 March; day 0), two groups of ovariectomized, oestradiol-treated adult Rasa Aragonesa ewes, maintained under natural photoperiod at 41°N, were given enough food to provide 1·4 × (high; H; no. = 6) or 0·5 × (low; L; no. = 6) energy requirements for maintenance. The effects of administration of the opiate receptor antagonist naloxone (1 mg/kg at four 1-h intervals) (day 15) and of the dopaminergic2 receptor antagonist pimozide (0·08 mg/kg) (day 21) on LH secretion were assessed. A second experiment was carried out in late anoestrus (21 June) using the same protocol. A significant increase in LH pulse frequency after naloxone treatment for both H and L groups was detected in late anoestrus. Number ofLH pulses after naloxone injections in early anoestrus also increased in H (P < 0·05) and L ewes (P = 0·08). The effect of pimozide injection on mean LH pulse frequency was greater in early than in late anoestrus, especially in ewes receiving a high plane of nutrition (P < 0·05 and P = 0·07 for H and L ewes, respectively in April and P = 0·07 for H ewes in July). A significant increase of LH pulse amplitude was also detected in early anoestrus in H ewes (P < 0·01). These results provide evidence that endogenous opioid mechanisms are involved in the inhibition ofLH pulsatile release both in early and late anoestrus in ewes with a short seasonal anoestrus. The ability of pimozide to increase LH pulse frequency in early anoestrus could be enhanced by a high plane of nutrition in the breed studied.


1982 ◽  
Vol 94 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Takashi Higuchi ◽  
Masazumi Kawakami

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.


Endocrinology ◽  
2020 ◽  
Vol 161 (2) ◽  
Author(s):  
Su Young Han ◽  
Isaiah Cheong ◽  
Tim McLennan ◽  
Allan E Herbison

Abstract The gonadotrophin-releasing hormone (GnRH) pulse generator drives pulsatile luteinizing hormone (LH) secretion essential for fertility. However, the constraints within which the pulse generator operates to drive efficient LH pulsatility remain unclear. We used optogenetic activation of the arcuate nucleus kisspeptin neurons, recently identified as the GnRH pulse generator, to assess the efficiency of different pulse generator frequencies in driving pulsatile LH secretion in intact freely behaving male mice. Activating the pulse generator at 45-minute intervals generated LH pulses similar to those observed in intact male mice while 9-minute interval stimulation generated LH profiles indistinguishable from gonadectomized (GDX) male mice. However, more frequent activation of the pulse generator resulted in disordered LH secretion. Optogenetic experiments directly activating the distal projections of the GnRH neuron gave the exact same results, indicating the pituitary to be the locus of the high frequency decoding. To evaluate the state-dependent behavior of the pulse generator, the effects of high-frequency activation of the arcuate kisspeptin neurons were compared in GDX and intact mice. The same stimulus resulted in an overall inhibition of LH release in GDX mice but stimulation in intact males. These studies demonstrate that the GnRH pulse generator is the primary determinant of LH pulse profile and that a nonlinear relationship exists between pulse generator frequency and LH pulse frequency. This may underlie the ability of stimulatory inputs to the pulse generator to have opposite effects on LH secretion in intact and GDX animals.


1989 ◽  
Vol 257 (6) ◽  
pp. R1359-R1364 ◽  
Author(s):  
J. M. Manning ◽  
F. H. Bronson

Immature female rats were required to run for prolonged periods of time to obtain food. The amount of food they earned was adequate for full pubertal development and moderate growth under nonworking conditions, but both processes were blocked by the exercise requirement. Prolonged exercise also blocked the pulsatile release of luteinizing hormone (LH); only two LH pulses were seen in seven exercising females during a total of 24 h of monitoring at 8 wk of age. By comparison, almost 1 pulse/h was seen in postpubertal, normally growing females of this same age during metestrus. When the exercising females' running requirement was relaxed at 8 wk of age they experienced rapid catch-up growth and reproductive development. Both basal secretion and LH pulse frequency increased markedly within 48 h, and most of these females ovulated during the third dark period after relaxation. Altogether, the experimental paradigm and techniques employed here yield highly predictable results, and they should prove useful for exploring other neuroendocrine pathways through which excessive exercise antagonizes reproduction.


1989 ◽  
Vol 256 (3) ◽  
pp. R751-R756 ◽  
Author(s):  
K. Arase ◽  
N. S. Shargill ◽  
G. A. Bray

Corticotropin-releasing factor (CRF) has been administered into the third ventricle of sham-operated and ventromedial hypothalamic (VMH)-lesioned rats in acute and chronic experiments. After a single 5-microgram injection of CRF, there was an acute reduction of food intake in both sham-operated and VMH-lesioned rats that persisted for 3 h. The effect was still present in the VMH-lesioned rats between 3 and 6 h but had dissipated in the sham-operated controls. Guanosine 5'-diphosphate (GDP) binding to mitochondria from interscapular brown adipose tissue was used as an index of thermogenic activity in this tissue. In 21-h food-deprived rats, GDP binding was significantly lower in VMH-lesioned than in sham-operated animals. Although the mean increase in sham-operated animals was increased, this was not significantly different from saline-injected controls. In the VMH-lesioned rats, however, CRF acutely increased GDP binding to values not different than those of the sham-operated controls. Serum corticosterone was significantly lower in the VMH-lesioned rats, but both groups showed a significant stimulation by CRF during a 7-day infusion of CRF (4.8 micrograms/day) into the third ventricle. Food intake was significantly depressed in the VMH-lesioned animals that received CRF, from values of 35 g/day to approximately 25 g/day. Body weight showed a slow steady decrease, having fallen by nearly 15 g at the end of the 7-day infusion period. In contrast the mean value in the VMH-lesioned controls had significantly higher in CRF-infused animals.(ABSTRACT TRUNCATED AT 250 WORDS)


Sign in / Sign up

Export Citation Format

Share Document