Search Results

You are looking at 1 - 9 of 9 items for

  • Author: A. J. S. Summerlee x
  • Refine by access: All content x
Clear All Modify Search
S. A. Jones
Search for other papers by S. A. Jones in
Google Scholar
PubMed
Close
and
A. J. S. Summerlee
Search for other papers by A. J. S. Summerlee in
Google Scholar
PubMed
Close

ABSTRACT

The effects of chronic infusion of porcine relaxin on oxytocin release were studied in lactating rats. Infusion of relaxin (4·2 μg/h for either 4 or 6 days) suppressed reflex milk ejection and reduced litter weight gain for 48 h compared with saline-infused controls. After 2 days, neither the rate of growth nor the frequency of milk ejection were significantly different from controls. For 24 h after the infusion of relaxin ended, litters gained weight more quickly than controls but there was no difference seen in the frequency of milk ejection. The effects on oxytocin release of stopping an infusion of relaxin after 3 days were investigated. There was a significant (P <0·01) rise in plasma oxytocin (up to 90 pmol/l) 30 min after the infusion was stopped, followed by a sustained rise in intramammary pressure. Treatment of relaxin-infused rats with naloxone (0·1 mg/kg) when the infusion was halted caused a more rapid release of oxytocin (within 2 min), a greater release of oxytocin (up to 140 pmol/l) and a prolonged rise in intramammary pressure.

J. Endocr. (1987) 114, 241–246

Restricted access
S. A. Jones
Search for other papers by S. A. Jones in
Google Scholar
PubMed
Close
and
A. J. S. Summerlee
Search for other papers by A. J. S. Summerlee in
Google Scholar
PubMed
Close

ABSTRACT

Experiments were carried out to investigate the effects of porcine relaxin on the course of gestation and delivery in the rat. Plasma relaxin was maintained at approximately 600 nmol/l from day 19 to day 23 of gestation by i.v. infusion from chronically implanted minipumps. Relaxin significantly (P<0·001) prolonged the length of gestation in 17 rats compared with controls, without causing dystocia or affecting the number of live births. Six rats gave birth during relaxin infusion. In these animals there was a significant (P<0·001) increase in the interval between successive deliveries compared with control animals, resulting in prolonged labour. The remaining 11 rats gave birth after the infusion was completed, when the interval between successive deliveries was significantly (P< 0·025) shorter than controls. The results are consistent with the hypothesis that relaxin has a central action suppressing the release of oxytocin as well as a peripheral action on the myometrium and cervix.

J. Endocr. (1986) 109, 85–88

Restricted access
S. A. Jones
Search for other papers by S. A. Jones in
Google Scholar
PubMed
Close
and
A. J. S. Summerlee
Search for other papers by A. J. S. Summerlee in
Google Scholar
PubMed
Close

ABSTRACT

Experiments were carried out to establish whether infusion of relaxin prolongs gestation and labour in the rat by suppressing release of oxytocin, and whether the effects of relaxin on birth could be reversed by the opioid antagonist naloxone. Female rats were implanted with subcutaneous osmotic minipumps for the infusion of purified porcine relaxin into the jugular vein for 84 h from either day 19 or day 20 of gestation. Infusion of relaxin delayed the onset of labour and in those animals which delivered during relaxin infusion, delivery was longer by approximately 45 min. Plasma oxytocin levels 40 min after delivery of the first fetus were 45·25 ± 3·6 pmol/l (mean ± s.d.) in unoperated controls and significantly (P < 0·01) depressed (23·89 ± 3·9) in rats that delivered during infusion of relaxin. Rats that delivered after the infusion of relaxin had finished, gave birth significantly (P < 0·05) faster than controls and plasma oxytocin levels were significantly (P < 0·01) raised (77·87 ±15·9 pmol/l). Naloxone treatment (1 mg/kg; i.m.) given immediately after the delivery of the first fetus reversed the inhibitory effect of relaxin and the interval between successive deliveries was slightly faster than that of controls. Plasma oxytocin levels in relaxin-infused naloxone-treated rats were significantly (P < 0·01) higher than values in unoperated control rats. The results confirm that relaxin suppresses oxytocin release possibly through an opioid system and this may be important in the control of the timing of birth.

J. Endocr. (1986) 111, 99–102

Restricted access
B C Wilson
Search for other papers by B C Wilson in
Google Scholar
PubMed
Close
and
A J S Summerlee
Search for other papers by A J S Summerlee in
Google Scholar
PubMed
Close

Abstract

Experiments were done to study the effects of porcine relaxin on osmotically evoked changes in intramammary pressure and the release of oxytocin and vasopressin in anaesthetized rats. Injections (1 μ1) of hypertonic (0·75 m) NaCl into the left lateral cerebral ventricle were used to induce consistent rises in intramammary pressure and the release of oxytocin and vasopressin. Plasma hormone concentration was determined by radioimmunoassay. Relaxin (5 μg i.v.) significantly (P<0·05) suppressed the intramammary pressure response to osmotic challenge 5 and 10 min after treatment. However, pretreatment with a specific vasopressin V1 receptor antagonist completely negated the effect of relaxin on intramammary pressure. Baseline levels of oxytocin and vasopressin in unstimulated rats were 41 ± 1·6 and 36±1·1 pmol/l respectively. Osmotic challenge induced significant (P<0·05) rises in plasma levels of both hormones (62·8 ±1·1 and 67·9 ± 1·2 pmol/l respectively) which were further augmented by relaxin (81·3±1·8 and 117·1 ±2·4 pmol/l respectively; P<0·05). The data confirm that central osmotic challenge provokes the release of oxytocin and vasopressin but the effects of oxytocin at the level of the mammary gland may be obscured by the action of vasopressin affecting blood flow to the gland.

Journalof Endocrinology (1994) 141, 75–80

Restricted access
A. J. S. SUMMERLEE
Search for other papers by A. J. S. SUMMERLEE in
Google Scholar
PubMed
Close
and
D. W. LINCOLN
Search for other papers by D. W. LINCOLN in
Google Scholar
PubMed
Close

A method is described for making extracellular recordings of the spontaneous activity of single hypothalamic neurones in unanaesthetized, freely moving, lactating rats using chronically implanted micro-wire electrodes. Extracellular recordings taken from individual neurones were maintained for periods of between 1 and 12 days. These records were not affected by any normal movement of the animal. As several micro-wires were implanted into each animal it was possible to make simultaneous recordings from several different hypothalamic sites in the same animal. Some recordings were identified as those from magnocellular neurones in the paraventricular nucleus on the basis of antidromic invasion after electrical stimulation of the neurohypophysis.

Milk ejection in response to the prolonged sucking of ten or more pups was intermittent, and individual milk ejections recurred at intervals of 2–10 min throughout each period of nursing. The rise in intramammary pressure at milk ejection was associated with a vigorous extensor response from the pups. This was monitored by radar to provide an index of milk ejection in the unanaesthetized rat.

Eleven antidromically identified neurones were recorded through 321 milk ejections. Eight of these neurones displayed a transient (2–6 s) and very substantial acceleration in discharge at the time predicted for oxytocin release, i.e. 10–12 s before milk ejection. The background discharge of these cells was 0·1–2·6 action potentials/s; this increased to 16–50 action potentials/s during the brief period of accelerated activity. Twenty-five neurones were studied during 365 milk ejections in rats which did not have a stimulating electrode implanted in the neurohypophysis. Thirteen of these neurones displayed a burst of high frequency discharge before each milk ejection, similar to that described for the antidromically identified neurones. Two of the non-responsive cells displayed a phasic pattern of discharge, characteristic of vasopressinergic neurone discharge recorded in anaesthetized rats.

These observations of putative oxytocinergic neurones in unanaesthetized, freely moving rats are identical with those previously made on anaesthetized rats, and establish that the high frequency burst of electrical activity displayed by magnocellular neurones some 10–12 s before milk ejection is responsible for oxytocin release under normal physiological circumstances.

Restricted access
A. D. Mumford
Search for other papers by A. D. Mumford in
Google Scholar
PubMed
Close
,
L. J. Parry
Search for other papers by L. J. Parry in
Google Scholar
PubMed
Close
, and
A. J. S. Summerlee
Search for other papers by A. J. S. Summerlee in
Google Scholar
PubMed
Close

ABSTRACT

Experiments were performed on anaesthetized, lactating rats to investigate the acute central actions of relaxin on blood pressure and vasopressin release. When compared with saline and control injections of isotonic protein extract, administration of relaxin into either the lateral or dorsal portion of the third ventricle caused a significant and sustained rise in arterial blood pressure. In contrast, relaxin administered to the ventral portion of the third ventricle caused only a short-term rise in blood pressure. Injections of relaxin into the fourth ventricle were without significant effect, suggesting that the central actions of relaxin on blood pressure are mediated by receptors restricted to the diencephalon or mesencephalon. A similar ventricular specificity was noted for the central relaxin-induced stimulation of vasopressin release as judged by concentrations of the hormone in the peripheral plasma. It is unlikely that the stimulation of vasopressin release is wholly responsible for the observed pressor effect observed.

Lesion of the subfornical organ negated the pressor effect to relaxin injected into the dorsal region of the third ventricle, but did not affect the pressor response observed after injection of relaxin into the ventral portion of the third ventricle. These results demonstrate a biphasic action of centrally administered relaxin, with the response to dorsally placed third ventricle relaxin being mediated by the subfornical organ, and the response to ventral injections associated with an unknown structure of the ventral third ventricle wall.

Journal of Endocrinology (1989) 122, 747–755

Restricted access
A. J. S. Summerlee
Search for other papers by A. J. S. Summerlee in
Google Scholar
PubMed
Close
,
K. T. O'Byrne
Search for other papers by K. T. O'Byrne in
Google Scholar
PubMed
Close
,
S. A. Jones
Search for other papers by S. A. Jones in
Google Scholar
PubMed
Close
, and
L. Eltringham
Search for other papers by L. Eltringham in
Google Scholar
PubMed
Close

ABSTRACT

Experiments were carried out on anaesthetized, lactating rats to investigate the possible role of the subfornical organ in mediating relaxin-induced inhibition of reflex milk ejection. Milk ejection was judged by the behavioural response of the sucklings and by transient rises in intramammary pressure. Radiofrequency lesions of the subfornical organ, or control lesions in adjacent areas of the cerebrum, did not affect the pattern or the magnitude of intramammary pressure changes at reflex milk ejection. Purified porcine relaxin given by either i.v. (5 μg) or intracerebroventricular (50 ng) injection suppressed reflex milk ejection in intact, sham-lesioned and control-lesioned rats, but had no effect on either the pattern or magnitude of reflex milk ejection in rats with lesions of the subfornical organ. The subfornical organ, which is situated at the interface between the blood, brain and the cerebrospinal fluid appears to mediate, at least in part, the relaxin-induced inhibition of reflex milk ejection in the rat.

J. Endocr. (1987) 115, 347–353

Restricted access
K. T. O'Byrne
Search for other papers by K. T. O'Byrne in
Google Scholar
PubMed
Close
,
L. Eltringham
Search for other papers by L. Eltringham in
Google Scholar
PubMed
Close
,
G. Clarke
Search for other papers by G. Clarke in
Google Scholar
PubMed
Close
, and
A. J. S. Summerlee
Search for other papers by A. J. S. Summerlee in
Google Scholar
PubMed
Close

ABSTRACT

The effect of relaxin on electrically evoked release of oxytocin from the posterior pituitary was examined by monitoring changes in intramammary pressure in the anaesthetized lactating rat.

The amount of oxytocin released by electrical stimulation of the neurohypophysis in vivo was dramatically reduced following i.v. injection of highly purified porcine relaxin (2·5–10 μg/rat). Relaxin inhibited oxytocin release in a dose-dependent manner and the onset of inhibition occurred within 6–10 min and lasted for 10–60 min. No effect on the sensitivity of the mammary gland to exogenous oxytocin was observed after relaxin treatment. During the period of inhibition, i.v. injection of the opioid antagonist naloxone chloride (1 mg/kg) completely and immediately restored electrically evoked oxytocin release. The neurohypophysis is known to contain endogenous opioid peptides, therefore the effect of relaxin on electrically stimulated release of oxytocin from the rat isolated neural lobe in vitro was examined. Relaxin (500–2000 ng/ml) failed to inhibit oxytocin release in vitro.

The results suggest that relaxin can inhibit the release of oxytocin from terminals in the neurohypophysis, but by an indirect mechanism. This action appears to be mediated through endogenous opioid peptides whose source is not clear. They are unlikely to be of neurohypophysial origin and may probably come from the adrenal medulla, since acute adrenalectomy negated the inhibitory effect of relaxin on oxytocin release.

J. Endocr. (1986) 109, 393–397

Restricted access
A. J. S. Summerlee
Search for other papers by A. J. S. Summerlee in
Google Scholar
PubMed
Close
,
A. C. Paisley
Search for other papers by A. C. Paisley in
Google Scholar
PubMed
Close
,
K. T. O'Byrne
Search for other papers by K. T. O'Byrne in
Google Scholar
PubMed
Close
,
K. M. Fairhall
Search for other papers by K. M. Fairhall in
Google Scholar
PubMed
Close
,
I. C. A. F. Robinson
Search for other papers by I. C. A. F. Robinson in
Google Scholar
PubMed
Close
, and
J. Fletcher
Search for other papers by J. Fletcher in
Google Scholar
PubMed
Close

ABSTRACT

Nursing behaviour and reflex milk ejection were studied over 257 suckling periods in 26 Californian rabbits. Detailed plasma profiles of oxytocin were obtained for 161 suckling periods in 16 animals. Plasma oxytocin was detected by radioimmunoassay in serial samples of 0·2 ml blood collected during nursing. Oxytocin titres were below the lower limit of the assay (5 pmol/l) before suckling, and started to rise at a rate of 2·8 ± 0·8 (s.d.) pmol/l per s 10–30 s after the onset of suckling. Peak levels of hormone were 345 ± 113 pmol/l and were attained towards the end of nursing. In 33 of these experiments simultaneous records of activity from oxytocin neurones were taken whilst chronically sampling the blood. Each neurone gave an average of seven bursts of neurosecretory activity in suckling. Onset of this bursting pattern of discharge began 5–24 s before the rise in plasma oxytocin was detected. Oxytocin neurone activity alone was monitored in a further 55 suckling periods in eight rabbits. A marked relationship between the duration of suckling period, milk yield, peak oxytocin levels and the length of neurosecretory bursts was demonstrated over the course of lactation. All four parameters increased in parallel from day 1 to reach maximal values on days 15–20 of lactation then started to wane until the doe ceased nursing her litter on days 25–27 of lactation.

J. Endocr. (1986) 108, 143–149

Restricted access