Sexual dimorphism in trans-cypermethrin hydrolysis in the domestic chicken.
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Biomedical subjects
Publications and source records attributed to R T Gladwell.
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Diurnal changes of LH secretion in sexually immature hens of 9, 11, 13 and 15 weeks of age consisted of 25-40% increases in the mean concentrations of LH in plasma between 15.00 and 18.00 h, i.e. between 2 h before and 1 h after the onset of darkness. During this time there was a tendency for the mean contents of LHRH-I in the anterior hypothalamus and posterior hypothalamus to increase by 21-74% and 20-56% respectively. In hens of 9 and 15 weeks, diurnal changes in the plasma concentration of LH closely paralleled those of LHRH-I content in the posterior hypothalamus. In contrast, the diurnal rhythm of LH secretion in hens of 11 and 13 weeks was more marked and plasma concentrations of LH continued to rise steeply between 18.00 and 21.00 h, i.e. between 1 and 4 h after the onset of darkness. At 11 weeks, this was associated with a reduction (P less than 0.01) in the contents of LHRH-I and LHRH-II, particularly in the anterior hypothalamus. In laying hens, a diurnal decline (P less than 0.01) in the plasma concentration of LH between 1 and 4 h after the onset of darkness was preceded by a fall (P less than 0.05) in the content of LHRH-I in the posterior hypothalamus and in the total hypothalamic content of LHRH-II (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Changes in the hypothalamic contents of LHRH-I and LHRH-II were determined in intact and castrated cockerels injected i.m. with gonadal steroids or tamoxifen. An increase in the plasma concentration of LH after castration was accompained by a significant increase in the content of LHRH-I in the posterior hypothalamus (including the mediobasal hypothalamus and median eminence) which was reversed by oestradiol benzoate given on days 14 and 15 after castration. Under similar circumstances, testosterone propionate did not modify the hypothalamic content of LHRH-I, even though both steroids reduced the plasma concentrations of LH to levels below those of intact cockerels. Treatment of intact cockerels with oestradiol benzoate significantly increased the content of LHRH-I in the posterior hypothalamus, whilst testosterone propionate was again without effect. Tamoxifen significantly raised the plasma concentration of LH in intact cockerels and partially antagonized the suppressive effect of oestradiol benzoate and testosterone on LH secretion in castrated cockerels. However, an anti-oestrogenic effect of tamoxifen on the hypothalamic content of LHRH-I was not demonstrated. There was no evidence of any changes in the hypothalamic content of LHRH-II after castration, with or without gonadal steroid replacement. A change in the hypothalamic content of LHRH-I in response to manipulation of the steroid environment would imply an involvement of this peptide in the mechanism by which gonadal steroids regulate the release of LH. The absence of changes in the hypothalamic content of LHRH-II in the same circumstances suggest that it is not directly involved in the control of LH secretion by the gonadal steroid negative feedback loop.
The contents of LHRH-I and -II in the anterior hypothalamus and posterior hypothalamus (including the mediobasal hypothalamus and median eminence) were measured at 90, 180 and 360 min after the i.m. injection of laying hens with progesterone. Whilst no changes were observed in the content of LHRH-I in the anterior hypothalamus, LHRH-I in the posterior hypothalamus tended to fall at 90 and 180 min after injection of progesterone in hens maintained on 16 h light:8 h darkness (16L:8D) and 8L:16D respectively. Pretreatment of laying hens with tamoxifen significantly increased the hypothalamic contents of LHRH-I and -II, raised the basal plasma concentration of LH and modified the LH response to progesterone injection. In hens in which tamoxifen prevented an increase in the plasma concentration of LH after progesterone injection, the content of LHRH-I in the posterior hypothalamus remained unchanged. In contrast, in hens in which progesterone stimulated a steep increase in LH within 90 min, there was a pronounced and significant fall in LHRH-I content of the posterior hypothalamus. No change in the hypothalamic content of LHRH-II was observed during the progesterone-induced surge of LH until plasma concentrations had attained maximal values or started to decline. Then, in hens maintained on 16L:8D, a significant fall in the content of LHRH-II in the anterior hypothalamus was found at both 180 and 360 min after injection with progesterone. Tests in vitro and in vivo of the responsiveness of the pituitary gland to synthetic LHRH-I and -II revealed no change at 90 min after injection of laying hens with progesterone, when plasma concentrations of LH were increasing, but a pronounced reduction when plasma LH concentrations were maximal or falling. These results suggest that LHRH-I mediates in the progesterone-induced increase in the plasma concentration of LH. Although the subsequent decline in plasma LH was associated with a reduced responsiveness of the pituitary gland to LHRH, a significant correlation between the contents of LHRH-I and -II in the anterior hypothalamus and a fall in the hypothalamic content of LHRH-II when plasma LH was maximal or declining allows the possibility of an involvement of this peptide in the neuroendocrine events preceding ovulation.
Treatment of chickens at different stages of sexual development with a single i.v. injection of synthetic chicken LHRH (cLHRH)-I or -II stimulated a rise in the plasma concentration of LH within 1 min. The activity of cLHRH-II was 1.3- to 2.7-fold greater than that of cLHRH-I in sexually immature cockerels and hens as determined by the changes in the plasma concentration of LH during the 5 or 10 min after injection. This could be attributed to both a greater effectiveness of cLHRH-II to stimulate LH release and to a more prolonged action. Thus, LH concentrations in plasma were maximal within 1-2 min of injection of all doses of cLHRH-I but within 2-5 min of injection at the higher doses of cLHRH-II. The responsiveness of the pituitary gland to cLHRH-I and -II was substantially greater in the sexually immature cockerel than in the hen and diminished during sexual development of the hen. Coincident with the onset of egg laying, the characteristics of the LH response to cLHRH-II changed to consist of an initial rise during the first 2 min, followed by a more sustained increase with LH concentrations still rising 10 min after injection. In contrast, after injection with cLHRH-I, plasma concentrations of LH rose to a peak at 2 min and thereafter declined gradually. Treatment of the sexually immature hen with oestradiol, progesterone or a combination of both steroids did not enable the expression of a laying hen-type response to the injection of cLHRH-II.(ABSTRACT TRUNCATED AT 250 WORDS)
An in-vitro superfusion technique was used to study basal and depolarization-induced (32 mmol K+/l) release of LHRH from the mediobasal hypothalamus (MBH) of pullets at 8-25 weeks of age. Plasma LH concentrations and the incremental change (delta LH) after an i.v. injection of 1 or 15 micrograms synthetic ovine LHRH/kg body weight were also determined. Between 8 and 25 weeks of age, significant (P less than 0.01) increases in basal and depolarization-induced release of LHRH (93 and 330%, respectively) were accompanied by a significant (P less than 0.01) rise in the residual LHRH content of MBH tissue (152%), observations which suggest that the ability of the hypothalamus to synthesize and secrete LHRH increases as sexual maturation proceeds. However, plasma LH, which reached a maximum concentration of 2.05 +/- 0.43 micrograms/l at 15 weeks, fell significantly (P less than 0.05) to 1.14 +/- 0.05 micrograms/l at 25 weeks. Since delta LH in response to exogenous LHRH showed a marked and progressive decline between 12 and 20 weeks of age, the low plasma concentration of LH typical of the mature hen is probably attributable to a direct negative-feedback action of ovarian steroids on the anterior pituitary gland rather than to an impaired secretion of LHRH from the median eminence. It is suggested that a dramatic increase in the responsiveness of LHRH nerve terminals in the MBH to depolarization by 32 mmol K+/l between 20 and 25 weeks of age (mean age at onset of lay 21.9 weeks; range 19-25 weeks) may reflect the development of hypothalamic responsiveness to the positive feedback action of progesterone.
Castration of immature cockerels caused a significant rise in plasma luteinizing hormone concentrations. This effect was prevented by testosterone (T) replacement therapy. In vivo T replacement therapy reduced the release of endogenous catecholamines from hypothalamic tissue following in vitro incubation with high K+ artificial avian cerebrospinal fluid (ACSF). In vitro incubation with 500 nM T significantly reduced the release of endogenous catecholamines from hypothalamic tissue following incubation with high K+ ACSF. These results suggest that T can reduce the functional activities of catecholaminergic neurones in the hypothalamus and that these neurones may play a facilitatory role in the control of gonadotrophin secretion in the cockerel.
Concentrations of LHRH, dopamine, noradrenaline and adrenaline in the anterior hypothalamus-preoptic region (AH-POR) and posterior hypothalamus-median eminence (PH-me) were determined in hens killed at different times in relation to the first ovulation of a sequence. The occurrence of a preovulatory rise in plasma LH concentration 4-6 h before the expected time of ovulation was confirmed. This rise in plasma LH was accompanied by a significant (P less than 0.01) 50% reduction in the LHRH content of the AH-POR and PH-me while the subsequent fall in plasma LH was accompanied by a restoration of the LHRH content of both regions to their former levels. Although no significant fluctuations in the hypothalamic content of either dopamine, noradrenaline or adrenaline were detected during the ovulatory cycle, significant correlations between LHRH content and catecholamine content were observed in the AH-POR (P less than 0.05) and PH-me (P less than 0.01). Thus mean levels of each amine followed the same temporal pattern as LHRH content with minimum values being observed shortly before the peak of the preovulatory surge of LH. These findings support the conclusion that an enhanced secretion of LHRH from the median eminence, possibly associated with an increased activity of catecholaminergic neurones, is a prerequisite for the preovulatory release of LH in the hen.
The validity of using a radioimmunoassay employing an antiserum raised against synthetic luteinizing hormone releasing hormone (LH-RH) for the quantification of luteinizing hormone releasing factor (LH-RF) in birds was investigated. Extracts of avian hypothalamus yielded displacement curves which were parallel to that of the synthetic LH-RH standard and the immunoreactive potencies of a number of extracts assayed concurrently using two different anti-LH-RH sera were found to be similar. Moreover, after chromatography of cockerel hypothalamic extract on carboxymethyl-cellulose, immunoreactive and biologically active LH-RF were found in the same eluate fractions. Immunoreactive LH-RH was shown to be widely distributed in cockerel hypothalamus with the highest concentrations present in the mediobasal hypothalamus (MBH; 6.55 +/- 1.86 pg/microgram protein, n = 6) and medial preoptic region (POR; 0.95 +/- 0.07 pg/microgram protein, n = 6). The postcastration rise in plasma LH in the cockerel was accompanied by significant (P less than 0.05) increases in the concentration of LH-RH in five hypothalamic areas including the POR; testosterone replacement therapy completely reversed these effects. Although castration raised the mean concentration of LH-RH in four other hypothalamic areas including the MBH, these differences were not significant. However, testosterone replacement therapy depressed LH-RH in all four regions to levels significantly (P less than 0.05) less than those in castrated cockerels. These findings constitute the first direct evidence that the negative feedback action of testosterone on LH secretion in the cockerel is mediated, at least in part, by an action on hypothalamic LH-RF-producing neurones.
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The effects of various pharmacological treatments, designed to perturb central catecholaminergic neurotransmission, on the pattern of LH release during the preovulatory period in the domestic hen were studied. Treatment of hens with either L-dihydroxyphenylalanine or diethyldithiocarbamate which raised the concentration of dopamine in the hypothalamus by 42 and 110% respectively, or with apomorphine, attenuated the preovulatory surge of LH. In contrast, treatment with either alpha-methyl-p-tyrosine which produced a 65% decline in the concentration of dopamine in the hypothalamus without affecting the concentrations of noradrenaline or adrenaline or treatment with pimozide did not affect the LH surge. While treatment with propranolol was similarly ineffective, phenoxybenzamine attenuated the LH surge to a marked extent. These observations suggest that the preovulatory surge of LH in the hen is influenced by facilitatory alpha-adrenergic and inhibitory dopaminergic mechanisms. Evidence to corroborate these findings was sought by determining the steady-state concentrations of dopamine, noradrenaline and adrenaline in five discrete diencephalic regions of the hen throughout the ovulatory cycle.
Concentrations of dopamine, noradrenaline and adrenaline in discrete areas of the diencephalon in male and female domestic fowl were correlated with changes in the plasma concentrations of LH induced by gonadectomy. Gonadectomized birds of both sexes exhibited raised plasma concentrations of LH and in castrated cockerels the daily administration of testosterone propionate was completely effective in preventing the postcastration rise in LH. Although no significant alterations in the brain concentrations of noradrenaline or adrenaline were observed in cockerels, the concentration of dopamine in the paraventricular nucleus (PVM), dorsomedial thalamic nucleus and mediobasal hypothalamus (MBH) were significantly raised in castrated compared with sham-operated birds by 136, 182 and 52% respectively. In each case the increase was partially suppressed by testosterone replacement therapy. In pullets, ovariectomy resulted in significant increases in the concentrations of dopamine (83%) and noradrenaline (78%) in the MBH and noradrenaline (35%) and adrenaline (34%) in the PVM. These findings suggest that in the fowl at least part of the negative feedback effect of gonadal steroids on LH secretion may be mediated by catecholaminergic mechanisms at the level of the hypothalamus.
1. The p.d. of rat seminiferous tubules was 5.86 +/- 0.15 mV, lumen negative, at 33 degrees C and varied linearly with temperature between 24 and 37 degrees C, exhibiting an apparent Q(10) (25-35 degrees C) of 2.0 with a slope of 0.43 mV/ degrees C. Exposing testes to a temperature of 37-43 degrees C resulted in an initial hyperpolarization followed by depolarization of the tubules. These changes were more rapid in testes exposed to 41-43 degrees C than in testes exposed to 37-39 degrees C.2. The R(in) of seminiferous tubules was 198 +/- 7.8 kOmega at a testis temperature of 33 degrees C. The R(in) decreased when testes were maintained at 37 and 41 degrees C, the rate of decrease being similar to the rate of depolarization.3. Exposing testes to deep body temperature by unilateral surgical cryptorchidism caused a reduction of 30 and 64% in tubular p.d. and R(in) respectively when measured 24 hr after surgery. Exposure to deep body temperature for up to 4 days did not cause any further change in either parameter.4. There was no evidence that lanthanum penetrated through the Sertoli cell tight junctions after exposing testes to 41 degrees C for up to 30 min.5. The results indicate that the seminiferous tubule p.d. is maintained by a temperature-sensitive, cellular mechanism. Exposing testes to deep body temperature or above depolarized the tubules and increased their permeability.
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