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R F Parrott

Publications and source records attributed to R F Parrott.

At least 55 records · Page 3Linked to original sources
PubMed1993

Peripheral and central effects of CCK receptor agonists on operant feeding in pigs.

Operant feeding was recorded in 18 h deprived pigs after peripheral (IV) or central (ICV) administration of saline, the CCK A agonist A-71378, the CCK B agonist pentagastrin, or pentagastrin vehicle. In Experiment 1 (n = 10), A-71378 (0.5, 1.0, and 2.0 micrograms/kg) given IV produced a sustained dose-related reduction in food intake (p < 0.02), whereas the same doses of pentagastrin were without effect. In Experiment 2 (n = 10), neither agonist given ICV (1 microgram) had consistent effects on operant responding. A higher ICV dose of A-71378 (5 micrograms) was also ineffective, whereas 1 microgram CCK octapeptide given ICV inhibited feeding (p < 0.03). These findings suggest that A receptors outside the blood-brain barrier mediate the suppressant effect of IV CCK on feeding in the pig and that neither peripheral nor central B receptors influence food intake in this species.

Animals↗
PubMed1993

Distribution and cellular localization of vasopressin mRNA in the ovine brain, pituitary and pineal glands.

In this study, in situ hybridization histochemistry was used to determine the regional and cellular localization of vasopressin-neurophysin II (AVP) mRNA in the sheep brain and pituitary with an 35S-labelled synthetic 45-mer oligonucleotide probe complementary to the bovine AVP gene. The highest densities of labelled cell bodies were found in the paraventricular nucleus (PVN), supraoptic nucleus (SON) and suprachiasmatic nucleus (SCN) of the hypothalamus, though such cells were also found in other regions of the diencephalon, including the accessory magnocellular nuclei. Labelled cells were also observed sparsely distributed in every major cortical field as well as in choroid plexus and the pineal gland. No AVP mRNA-expressing cells were found in the bed nucleus of the stria terminalis, the amygdala, or in the medulla and brainstem. In the pituitary, a dense AVP mRNA signal was observed in the intermediate lobe whereas, cells in the anterior or neural lobe did not express AVP mRNA. The dense population of AVP-expressing neurons in both magnocellular and parvocellular fields of the hypothalamus support major roles of AVP in both posterior and anterior pituitary function. Finally, the extrahypothalamic distribution of AVP mRNA transcripts suggest that vasopressinergic neurons may be involved in diverse physiological functions, including the regulation of pineal function and cognition.

Animals↗
PubMed1993

Central effects of naloxone and selected opioid agonists on cortisol and prolactin secretion in non-stressed sheep.

1. Intravenous morphine decreases cortisol and increases prolactin concentrations in male sheep whereas naloxone has the opposite effect. 2. In this investigation, the effects of intracerebroventricular injections of naloxone, morphine (mu agonist), dynorphin (kappa agonist) and DADLE (delta/mu agonist) on cortisol and prolactin release were investigated. 3. None of the drugs affected cortisol secretion. 4. Naloxone transiently decreased prolactin levels (P < 0.05). 5. All the opioids tended to enhance prolactin secretion and the highest dose (300 micrograms) of DADLE produced a significant (P < 0.007) sustained increase. 6. These results are consistent with the view that exogenous and endogenous opioids affect the pituitary to influence cortisol release in sheep but act also at the hypothalamic level to influence prolactin secretion.

Animals↗
PubMed1993

A70104 and food intake in pigs: implication for the CCK 'satiety' hypothesis.

The aim of the present study was to determine whether CCK released from the small intestine during a meal acts as a satiety factor. The effects of the novel CCKA antagonist A70104 (50-200 micrograms kg-1, i.v.) were investigated on operant food intake in 4 h food-deprived pigs. None of the doses used had any significant effects on the amount of food consumed by the animals over the 2 h measurement period. However, pretreatment of the pigs with A70104 (100 micrograms kg-1) did block the inhibitory effect of exogenous CCK (1 microgram kg-1, i.v.) on operant feeding. These results thus question the validity of the hypothesis that endogenous peripheral CCK acts as a satiety factor.

Animals↗
PubMed1993

Isolation- and dehydration-induced changes in neuropeptide gene expression in the sheep hypothalamus.

Changes in neuropeptide gene expression in the hypothalami of sheep subjected to psychological stress (isolation, 1 h; n = 3) or dehydration (48 h; n = 3) were examined using in-situ hybridization histochemistry. Compared with non-stressed euhydrated control animals (n = 3), isolation induced significant accumulation of mRNA for corticotrophin-releasing hormone, pro-enkephalin and pro-dynorphin (DYN) in the paraventricular nucleus (PVN), but no change in mRNA content within the supraoptic nucleus (SON). By contrast, dehydration significantly increased DYN mRNA in the magnocellular neurones of the PVN and SON. However, neither isolation nor dehydration altered the expression of mRNA for vasopressin (AVP) in either the PVN or the SON. These results indicate that in the ovine hypothalamus (1) stress represents a powerful stimulus to co-ordinated neuropeptide synthesis and (2) expression of DYN mRNA and AVP mRNA may be independently regulated during changes in plasma osmolality.

Animals↗
PubMed1992

The effects of intravenous administration of cholecystokinin on feeding behaviour and release of pituitary hormones in pigs are not mediated by serotonergic (5-HT3) receptors.

Two experiments were carried out using the serotonergic (5-HT3) antagonist ondansetron (GR 38032F) to investigate whether the actions of peripherally-administered cholecystokinin octapeptide (CCK) in the prepubertal pig might involve 5-HT3 receptors. In Experiment 1, it was shown that ondansetron (10 or 30 mg, i.v.) did not affect the initial feeding response and did not modify the behavioural inhibition induced by a subsequent injection of CCK (1.3 microgram/kg, i.v.). In Experiment 2, it was demonstrated that the nauseogenic action of CCK, indicated by its stimulatory effect on release of vasopressin and cortisol, was not markedly altered by ondansetron (30 mg, i.v.). These results suggest that 5-HT3 receptors play a negligible part in mediating the behavioural and endocrine responses induced by bolus intravenous injections of CCK in this species.

Animals↗
PubMed1992

Effects of intracerebroventricular corticotropin-releasing hormone and intravenous morphine on cortisol, prolactin and growth hormone secretion in sheep.

It has previously been demonstrated that naloxone and morphine modify the adrenocortical and pituitary responses of sheep to stress. Since CRH acts within the brain to co-ordinate the stress response, the present experiment was conducted to determine whether morphine has similar effects in sheep given oCRH centrally. Plasma concentrations of cortisol, prolactin and growth hormone were measured in blood samples collected at 10 min intervals from sheep (N = 5) over a 3-hr period. Intravenous injections of saline vehicle or morphine sulphate (0.4 mg/kg) were given after 40 min and intracerebroventricular injections of oCRH (0, 5 or 20 micrograms) were administered after 60 min. Sustained, dose-related, increases in cortisol were induced by oCRH and, in agreement with findings in stressed sheep, these responses were reduced by pretreatment with morphine. Prolactin levels appeared to increase after morphine but oCRH, on its own, did not increase prolactin secretion in this study. There was no change in growth hormone concentrations after oCRH whereas morphine transiently stimulated release.

Animals↗
PubMed1992

Prolactin secretion in sheep after dehydration followed by restraint or administration of ovine corticotrophin-releasing factor.

Plasma concentrations of prolactin were measured in male sheep (wethers, n = 8) during 120 min exposure to mild physical stress (restraint), and also following I.V. injection of 30 micrograms ovine corticotrophin-releasing factor (CRF), when the animals were water replete and when they had been deprived of water for 48 h. Restraint stress produced a small increase in prolactin secretion (n.s.) when the animals were euhydrated and a large increase (P less than 0.001) when they were dehydrated. Administration of CRF had no effect on prolactin concentrations in either experimental condition. In a further study in which euhydrated animals (n = 6) were subjected to restraint while receiving infusions of vasopressin (1 microgram/h), there was no enhancement of basal or stress-induced prolactin secretion. Thus, dehydration enhances stress-induced prolactin release in sheep through a process that does not involve a pituitary action of CRF or circulating vasopressin.

Animals↗
PubMed1992

CCK-A receptors mediate the effect of cholecystokinin on vasopressin but not on cortisol in pigs.

Bolus intravenous injections of cholecystokinin (CCK) octapeptide induce a rapid rise in plasma vasopressin and a later increase in cortisol in the prepubertal pig. To determine whether these endocrine responses involve CCK-A or CCK-B receptors, this experiment investigated the effect of CCK (1 microgram/kg) in pigs (n = 7) pretreated with the CCK-A antagonist L 364718 (70 microgram/kg) or the CCK-B antagonist L 365260 (10 ng/kg and 10 micrograms/kg). The animals were prepared with jugular vein catheters and given the antagonist vehicle, L 364718, or L 365260 10 min before administration of CCK or saline. Analysis of hormone concentrations in blood samples taken 2, 5, 10, and 20 min after the second injection indicated that an abrupt rise in vasopressin, detectable within 2 min of CCK administration, occurred after vehicle or L 365260 pretreatment but not when CCK was preceded by L 364718. In contrast, the rise in plasma cortisol that was observed approximately 15 min after CCK injection was not prevented by either antagonist. Thus peripherally administered CCK induces vasopressin release by CCK-A receptor activation, in agreement with its inhibitory effect on food intake in this species. However, the effect of CCK on cortisol secretion does not appear to involve either CCK-A or CCK-B receptors.

Animals↗
PubMed1991

Operant food intake in pigs following intracerebroventricular (i.c.v.) administration of prolactin.

1. It has previously been shown that systemic administration of prolactin stimulates food intake in a number of animal species. 2. In the present study we investigated whether central administration of prolactin would increase food intake in satiated pigs trained to make operant responses for food and water. 3. Prolactin (25-100 U) administered by intracerebroventricular (i.c.v.) injection produced no significant effects on food intake during the 60 min measurement period after injection. 4. Furthermore, none of these doses of prolactin had any effect on the daily (24 hr) consumption of food in these animals. 5. Similarly prolactin (25-100 U) i.c.v. had no significant short or long-term effects on water intake. 6. These results indicate that prolactin does not stimulate food intake in pigs by a central mode of action.

Animals↗
PubMed1991

Central and peripheral doses of cholecystokinin that inhibit feeding in pigs also stimulate vasopressin and cortisol release.

The effects on vasopressin and cortisol secretion of centrally and peripherally administered cholecystokinin octapeptide (CCK) were investigated in conscious prepubertal pigs. Injection of 1.3 micrograms CCK into the lateral cerebral ventricle resulted in a sustained increase in plasma vasopressin after a latency of 5 min but no change in cortisol concentrations. Intravenous injection of 0.7 and 1.3 micrograms/kg CCK initiated a rapid surge (within 2 min) in plasma vasopressin and a later increase in cortisol secretion. The time course of the vasopressin response to the central injection of CCK was found to be similar to the period of behavioural inhibition induced when an equivalent dose of the peptide was given by the same route in an earlier feeding experiment. An analogous situation was also observed when CCK was given peripherally and, in this case, the threshold dose at which the behavioural and endocrine responses were induced was found to be the same.

Animals↗
PubMed1991

Hormonal effects of apomorphine and cholecystokinin in pigs: modification of the response to cholecystokinin by a dopamine antagonist (metoclopramide) and a kappa opioid agonist (PD117302).

Three experiments were carried out to investigate some of the mechanisms involved in the endocrine responses of pigs to the emetic agents apomorphine and cholecystokinin. In Experiment 1, plasma levels of vasopressin and cortisol were measured in prepubertal pigs (N = 5) treated with i.v. apomorphine (25 micrograms/kg) or saline vehicle. In Experiment 2, concentrations of vasopressin and cortisol were determined in pigs given iv sulphated cholecystokinin octapeptide (1.3 micrograms/kg), metoclopramide (300 micrograms/kg), metoclopramide + cholecystokinin, and an oral dose of the kappa opioid agonist PD 117302 (20 micrograms) alone, or followed by i.v. cholecystokinin. In Experiment 3, operant feeding behaviour was quantified in pigs (N = 4) given cholecystokinin (1 microgram/kg) or cholecystokinin preceded by oral PD 117302. Following apomorphine injection in Experiment 1, there was a rapid, transient, rise in plasma vasopressin. Cholecystokinin had a similar effect on vasopressin secretion in Experiment 2 and also induced a later rise in plasma cortisol. Pre-treatment with metoclopramide appeared to reduce both of these effects of cholecystokinin, but only the decrease in cortisol was statistically significant. However, oral administration of PD 117302 abolished the effect of cholecystokinin on vasopressin release and reduced the subsequent rise in cortisol. The inhibitory effect of cholecystokinin on feeding was unaltered by PD 117302 treatment in Experiment 3. The results obtained with apomorphine and metoclopramide, together, suggest that the neuroendocrine effects of cholecystokinin in the pig may involve an action on central dopamine receptors while the effects of PD 117302 indicate that kappa opioids may modify the hormonal responses to cholecystokinin by a peripheral action.

Animals↗
PubMed1991

Dehydration, but not vasopressin infusion, enhances the adrenocortical responses of sheep to corticotropin-releasing hormone or restraint.

Two experiments were carried out using adult castrated sheep prepared with jugular vein catheters. In Experiment 1, sheep (N = 8) were injected iv with saline vehicle, vehicle + 15 or 30 micrograms oCRH, or subjected to 120 min mild physical stress (restraint), following a 48 h period during which water was freely available or withheld. Blood samples were taken for 30 min before and 120 min after oCRH injection, and before and during restraint, and the plasma analysed for AVP and cortisol content. Levels of AVP increased by over 500% after dehydration, but were unaffected by oCRH or restraint. In contrast, plasma cortisol was unchanged after dehydration, but increased after oCRH and restraint. Moreover, these cortisol responses were significantly greater when the sheep were dehydrated. In Experiment 2, euhydrated sheep (N = 6) were infused iv with saline vehicle or vehicle + AVP for a 5-h pretreatment period, followed by a 2-h experimental period in which the animals were injected with 15 micrograms oCRH or subjected to 120 min restraint, as in Experiment 1. Blood samples were taken throughout the experiment from a contralateral catheter and the plasma analysed for AVP and cortisol content. The AVP infusion produced plasma levels of the hormone approximately twice those seen after 48 h dehydration in Experiment 1, but did not affect cortisol secretion. Furthermore, the cortisol response to oCRH, or restraint, was not enhanced by the AVP infusion. These results suggest that pituitary responsiveness to exogenous or endogenous CRH (restraint stress) may be enhanced in sheep by dehydration through a mechanism that does not involve an adrenal or pituitary action of circulating AVP.

Adrenal Cortex↗
PubMed1990

Central administration of corticotropin releasing factor in the pig: effects on operant feeding, drinking and plasma cortisol.

Four experiments were carried out to investigate the effects of corticotropin releasing factor (CRF) on ingestive behaviour and cortisol secretion in the prepubertal pig. In Experiment 1, 19-hr food-deprived animals were given intracerebroventricular (ICV) injections of 2.5, 10 or 20 micrograms CRF, or saline vehicle, 5 min after the start of a 30-min operant-feeding session. The total number of food reinforcements obtained in the posttreatment period did not change after 2.5 or 10 micrograms CRF, although the latter dose reduced intake in the final 5 min of the test; overall food consumption, however, was reduced after 20 micrograms CRF. In Experiment 2, pigs were treated intravenously with 20 micrograms CRF, or saline, using the same test situation as in Experiment 1; neither treatment significantly affected operant feeding. In Experiment 3, 19-hr water-deprived pigs were given ICV injections of 20 micrograms CRF, or saline, 15 min before the start of a 30-min operant-drinking session. Water intake was increased in the 5-min period directly after CRF injection, but there was no overall reduction in drinking. In Experiment 4, blood samples were taken at 15-min intervals for 30 min before and 90 min after ICV injection of 20 micrograms CRF, or saline, in food and water replete animals. Both treatments appeared to increase plasma cortisol levels, as determined by radioimmunoassay, but the effect was more pronounced after CRF.

Animals↗
PubMed1990

Cortisol release in pigs following peripheral and central administration of ovine and human corticotropin-releasing hormone.

Prepubertal pigs (N = 6) were surgically implanted with iv and intracerebroventricular catheters. The animals were given oCRH or hCRH peripherally (0, 20 or 50 micrograms) or centrally (0, 10 or 20 micrograms) and the effect on plasma cortisol measured. Peak cortisol concentrations were observed 20 min after iv, and 40 min after intracerebroventricular, administration. A larger cortisol response was observed when 20 micrograms oCRH was given by the central, compared to the peripheral, route and intracerebroventricular administration of both 10 and 20 micrograms oCRH caused excitation and vocalisation. By contrast, the effect of hCRH on cortisol secretion was small, regardless of the route of administration, and only one animal displayed a behavioural response when the highest dose was given centrally.

Animals↗
PubMed1989

Opioid influences on pituitary function in sheep under basal conditions and during psychological stress.

The effects of intravenous injections of naloxone (2 mg/kg), morphine (0.3 mg/kg) and saline vehicle on plasma concentrations of cortisol, prolactin, vasopressin and oxytocin were assessed in sheep (N = 10) when in their social groups (basal conditions) and during a period of isolation (psychological stress). Blood samples were collected by jugular venipuncture before and during the 60-min period following drug administration. Plasma hormone concentrations were determined by radioimmunoassay. Under basal conditions, cortisol levels were increased after naloxone (36-48%), but not after morphine or saline, and concentrations of prolactin, vasopressin and oxytocin did not change. Under stress conditions, (1) cortisol concentrations were elevated throughout the 60-min sampling period after naloxone or saline but for only 20 min after morphine; maximum increases observed were 161% (naloxone), 150% (saline) and 112% (morphine); (2) prolactin levels were raised after saline (85-129%) and morphine (55-61%) but were unchanged after naloxone; (3) vasopressin concentrations decreased transiently (43%) after saline but not following naloxone or morphine; and (4) oxytocin levels did not change after any treatment. These results indicate that endogenous and exogenous opioids modulate cortisol release in nonstressed sheep, and cortisol and prolactin secretion in sheep subjected to psychological stress. The nature of the anterior pituitary responses induced, together with the absence of a discernible effect on posterior pituitary function, suggest that the central opioid systems involved are similar in sheep and primates but different from those in the rat.

Animals↗
PubMed1989

Anterior and posterior pituitary hormone release induced in sheep by cholecystokinin.

The effect of an intravenous bolus injection of cholecystokinin octapeptide (CCK-8; 0.85 micrograms/kg) on the release of cortisol, prolactin, vasopressin, and oxytocin was studied in sheep (n = 10). Concentrations of these hormones were measured in blood samples taken before (-10, 0 min) and after (5, 10, 20 min) administration of a saline vehicle or vehicle + CCK. Following CCK treatment, levels of cortisol were raised after 10 and 20 min, prolactin and vasopressin concentrations were increased after 5 min, and oxytocin secretion was unaffected.

Animals↗