Search Results
You are looking at 1 - 10 of 14 items for
- Author: R. B. JONES x
- Refine by access: All content x
Search for other papers by R. B. JONES in
Google Scholar
PubMed
Search for other papers by N. W. NOWELL in
Google Scholar
PubMed
Preputial gland activity is related to social experience (Hucklebridge, Nowell & Wouters, 1972) and these glands are thought to affect the fighting behaviour of mice through the release of an aggression-promoting pheromone (Mugford & Nowell, 1970). The coagulating glands are thought to be the source of an aggression-inhibiting pheromone (Haug, 1971). The present study provides direct evidence for the function of these glands by assessing the aggression-inducing properties of combinations of the gland secretions with bladder urine or water.
A number of 4-month-old male T.O. albino mice were killed. The preputial and coagulating glands were dissected out and the gland contents were gently squeezed into bladder urine or into the same amount of distilled water. Six test substances were used: (1) bladder urine, (2) bladder urine+preputial gland secretion, (3) bladder urine + coagulating gland secretion, (4) water, (5) water + preputial secretion, and (6) water + coagulating gland secretion.
The 15 mice used
Search for other papers by R. B. JONES in
Google Scholar
PubMed
Search for other papers by N. W. NOWELL in
Google Scholar
PubMed
SUMMARY
The aversive properties of urine of castrated male mice receiving varying doses of testosterone phenylpropionate was assayed using males housed in groups of six as subjects. The aversive efficacy of the urine was found to rise with an increase in androgen levels. There was a delay of 5 days before the exogenous androgen exerted any effect on the aversive properties of the urine. This delay indicated that the aversive factor might be a pheromonal substance released from an androgen-dependent tissue, rather than being an excreted androgen metabolite.
The results are discussed in terms of androgen levels and possible territorial functions.
Search for other papers by R. B. JONES in
Google Scholar
PubMed
Search for other papers by N. W. NOWELL in
Google Scholar
PubMed
Male mouse urine contains an androgen-dependent aversive pheromone which discourages prolonged investigation, by male conspecifics, of an area marked with such urine (Jones & Nowell, 1973a). The source of this pheromone lies in the coagulating glands, whose secretion, when combined with bladder urine, causes avoidance (Jones & Nowell 1973b). The present study describes an attempt to inhibit the release of the aversive pheromone of male mice by treatment with the potent anti-androgen cyproterone acetate. Thus the open-field responses of male mice to the urine of either oil-injected or cyproterone acetate-injected males were compared. Some confirmation of the inhibitory action of cyproterone acetate upon sex accessory organ responses to endogenous androgens was gained by recording the weights of the ventral prostate, preputial and coagulating glands.
Twenty 24-day-old male t.o. albino mice were divided into two groups of ten; the first group received s.c. injections of cyproterone acetate (2 mg/mouse)
Search for other papers by M. T. JONES in
Google Scholar
PubMed
Search for other papers by F. R. BRUSH in
Google Scholar
PubMed
Search for other papers by R. L. B. NEAME in
Google Scholar
PubMed
SUMMARY
Corticosterone was administered intraperitoneally to rats, and the consequent changes in plasma corticosterone concentration traced. Stress (sham bilateral adrenalectomy) was applied at various times when the plasma corticosterone concentration was changing at different rates, and it was shown that there was a critical rate of rise of plasma corticosterone concentration of about 1·3 μg/100 ml plasma/min in excess of which the stress response was inhibited. Rates of rise less than this did not affect the stress response. A state of ' saturation' of the control system was also demonstrated to result from high plasma corticosterone concentrations when the response to stress was not inhibited as above. A model of the system is suggested to explain these and other data.
Search for other papers by T. H. Jones in
Google Scholar
PubMed
Search for other papers by B. L. Brown in
Google Scholar
PubMed
Search for other papers by P. R. M. Dobson in
Google Scholar
PubMed
Introduction
Intercellular communication is effected through the release and action of substances known as paracrine agents. Recent studies are providing increasing evidence that pituitary hormone secretion is under the control of paracrine as well as hypothalamic factors. The individual cell types within the rat anterior pituitary gland appear to be arranged in specific groups and juxtapositions, and this precise organization of cells provides an anatomical basis for an intercellular control system in the pituitary gland. There is good circumstantial evidence for a variety of paracrine interactions within the anterior pituitary gland, although the exact physiological functions of different proposed paracrine agents have yet to be fully elucidated. Many substances have been shown to affect the release of each of the pituitary hormones directly, and there is evidence that some of these are synthesized and released within the anterior pituitary and may therefore act as paracrine agents. Established and
Search for other papers by T. H. Jones in
Google Scholar
PubMed
Search for other papers by B. L. Brown in
Google Scholar
PubMed
Search for other papers by P. R. M. Dobson in
Google Scholar
PubMed
ABSTRACT
Gonadotrophin-releasing hormone (GnRH) stimulated the accumulation of inositol phosphates and prolactin secretion in anterior pituitary cells from young male rats. Saralasin ([Sar1,Ala8]-angiotensin II; a competitive antagonist of angiotensin II) inhibited the increase in both inositol phosphates and prolactin in a dose-dependent manner. Since angiotensin II has been shown to be a potent stimulus for inositol phosphate accumulation and prolactin secretion in the lactotroph, these findings suggest that angiotensin II acts as a paracrine agent, being released from the gonadotroph in response to GnRH and causing the lactotroph to release prolactin through an effect on phosphoinositide metabolism. The ability of GnRH to promote prolactin release was lost in pituitaries from older rats, and the increase in total inositol phosphate accumulation was less. These findings provide evidence of a physiological role for the presence of the renin–angiotensin system within the pituitary gland.
J. Endocr. (1988) 116, 367–371
Search for other papers by D. B. Jones in
Google Scholar
PubMed
Search for other papers by D. Marante in
Google Scholar
PubMed
Search for other papers by B. C. Williams in
Google Scholar
PubMed
Search for other papers by C. R. W. Edwards in
Google Scholar
PubMed
ABSTRACT
The possible involvement of the lipoxygenase pathway of arachidonic acid metabolism in the events which take place during ACTH-induced stimulation of corticosterone secretion has been studied using an isolated rat adrenal cell system. Incubation with arachidonic acid resulted in an inhibition of ACTH-stimulated corticosterone production. The lipoxygenase pathway inhibitors nordihydroguaretic acid (NDGA), eicosatetraynoic acid (ETYA) and compound BW755C also produced inhibition of ACTH-stimulated corticosterone synthesis. The concentrations of the inhibitors at which 50% inhibition occurred were 15, 34 and 37 μmol/l respectively. The inhibitions produced by NDGA and ETYA were independent of cyclic AMP output. NDGA also inhibited corticosterone production induced by dibutyryl cyclic AMP but had no effect on corticosterone synthesis induced by pregnenolone.
Preincubation of adrenal cells with the lipoxygenase products 5, 12 and 15 hydroxyeicosatetraenoic acid (HETE) and with leukotrienes A4, B4, C4, D4 and E4 resulted in significant inhibitions of corticosterone production in response to ACTH with leukotriene A4 (LTA4) and with 15HETE and 5HETE. Conversely, incubation with glutathione (GSH), which is known to reduce intracellular LTA4 levels, produced stimulation (at 5 mmol GSH/1) and inhibition (at 50 mmol GSH/1) of corticosterone output. These studies suggest that the lipoxygenase pathway may be involved in ACTH-stimulated corticosterone synthesis.
J. Endocr. (1987) 112, 253–258
Search for other papers by D. B. Dunger in
Google Scholar
PubMed
Search for other papers by D. R. Matthews in
Google Scholar
PubMed
Search for other papers by J. A. Edge in
Google Scholar
PubMed
Search for other papers by J. Jones in
Google Scholar
PubMed
Search for other papers by M. A. Preece in
Google Scholar
PubMed
ABSTRACT
The patterns of secretion of GH, LH, FSH and prolactin were determined over a single night (20.00–08.00 h; 15-min sampling) in 34 normal subjects (17 male, 17 female, aged 9·1–20·9 years). Plasma GH was measured by an immunoradiometric assay and LH, FSH and prolactin by radioimmunoassay in all samples. Data were analysed by Fourier transformation and cross-correlation after stationarization.
The highest mean GH levels were noted in girls at Tanner stage 2/3 and in boys at stages 4/5. Prolactin levels were highest in girls at stage 4/5 and in boys at stage 2/3. LH and FSH showed a progressive rise by puberty stage in both sexes. The dominant pulse periodicities of GH and prolactin were 150–180 min in girls and 180 min in boys. LH and FSH pulse periodicity was around 90 min in early puberty and 180 min in later puberty in both sexes. LH and prolactin pulses showed a phase relationship with GH with a lag of 30–75 min (r = 0·32; P < 0·001) and 30 min (r = 0·47; P < 0·0001) respectively. Generally, LH and prolactin pulses were in phase (r = 0·42; P < 0·0001) and there was a highly significant correlation (r = 0·64; P < 0·0001) between FSH and LH pulsatility.
Whereas mean overnight concentrations and pulse periodicity of the principal pituitary hormones varied between the sexes during early puberty, by the end of puberty a dominant pulse periodicity of around 150–180 min was established and there was remarkable temporal coupling of pulsatility.
Journal of Endocrinology (1991) 130, 141–149
Search for other papers by M. Saffran in
Google Scholar
PubMed
Search for other papers by J. B. Field in
Google Scholar
PubMed
Search for other papers by J. Peña in
Google Scholar
PubMed
Search for other papers by R. H. Jones in
Google Scholar
PubMed
Search for other papers by Y. Okuda in
Google Scholar
PubMed
ABSTRACT
Bovine crystalline insulin, mixed with an absorption enhancer, was loaded by hand into gelatin capsules, which were then coated with an azopolymer designed to deliver the insulin in the upper colon. In 34 experiments with 14 pancreatectomized mongrel dogs of both sexes, the coated capsules were administered orally after a pre-dose period of 1 h. The dogs had cannulae in the portal vein, hepatic vein and femoral artery and Doppler flow probes on the portal vein and hepatic artery. Insulin and food were withdrawn the day before an experiment. Responses measured were plasma glucose, plasma insulin, hepatic glucose production rate, hepatic plasma flow rate and plasma glucagon-like immunoactivity (GLI). Control experiments, with capsules without insulin, produced small changes from 'pre-dose' values. Insulin-containing capsules, without the azopolymer coating, resulted in some early changes consistent with upper gastrointestinal absorption. Single oral doses (66 to 400 nmol/kg) of insulin in completely coated capsules produced peaks of portal plasma insulin and transient decreases in plasma glucose, hepatic glucose production, hepatic plasma flow and plasma GLI. The changes usually began 1·5–2 h after administration of a single dose, and lasted for up to 3 h, but were not significantly related to the dose of insulin. Multiple oral doses of insulin, given at 1·5-h intervals, resulted in multiple peaks of plasma insulin, a continuing dose-dependent fall in plasma glucose to near-euglycaemia with the highest dose, and profound decreases in hepatic glucose production and plasma GLI. These data demonstrate that insulin absorbed from the gastrointestinal tract causes changes in glucose metabolism in the diabetic dog that are consistent with the action of insulin primarily on the liver and that repeated oral doses are necessary to correct the hyperglycaemia.
Journal of Endocrinology (1991) 131, 267–278
Search for other papers by S. A. Nicholson in
Google Scholar
PubMed
Search for other papers by T. E. Adrian in
Google Scholar
PubMed
Search for other papers by B. Gillham in
Google Scholar
PubMed
Search for other papers by M. T. Jones in
Google Scholar
PubMed
Search for other papers by S. R. Bloom in
Google Scholar
PubMed
ABSTRACT
The effect of six hypothalamic peptides on the basal release of ACTH and that induced by arginine vasopressin (AVP) or by ovine corticotrophin releasing factor (oCRF) from fragments of the rat anterior pituitary gland incubated in vitro was investigated. Dose–response curves to AVP and to oCRF were obtained, and the response to a low dose of oCRF was potentiated by a low dose of AVP. Basal release of ACTH was not affected by any of the peptides in concentrations in the range 10−12 to 10−6 mol/l, and only substance P (SP) and somatostatin (SRIF) inhibited significantly the response to oCRF in a dose-related manner. The responses to a range of doses of oCRF or AVP were reduced by 10−8 and 10 − 6 mol SP or SRIF/1, and to a greater extent by the higher dose. Except in the case of 10−6 mol SRIF/1 on the response to AVP, the response was not further diminished by preincubation of the tissue with the peptide before the stimulating agent was added. The inhibition of the responses to AVP or oCRF by 10−9 mol SP/1 was not potentiated by its combination with either 5 × 10−10 or 10−8 mol SRIF/1; the inhibitory effects were merely additive. The results suggest that although SRIF and SP are able to modulate the release of ACTH from the anterior pituitary gland, they do so only at a high concentration. In the case of SRIF these concentrations are several orders of magnitude higher than those reported to be present in the hypophysial portal blood and therefore a physiological role for this peptide in the control of ACTH secretion is unlikely.
J. Endocr. (1984) 100, 219–226
