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W L Veale

Publications and source records attributed to W L Veale.

At least 19 recordsLinked to original sources
PubMed1992

Vasopressin-induced motor effects: localization of a sensitive site in the amygdala.

Arginine vasopressin (AVP) induces motor effects when administered into the cerebral ventricles, the ventral septal area (VSA), or the vestibular cerebellum of the rat brain. Because AVP-like immunoreactivity and AVP-binding sites exist in the central medial amygdala (cmeA), and because the amygdala can be kindled to produce motor effects, we hypothesized that the amygdala might play a role in AVP-induced motor effects. This hypothesis was tested by observing motor behavior in response to injection of AVP into the central medial region of the amygdala. Our results demonstrate that an initial injection of AVP into the cmeA caused minor motor effects, including immobility, prostration and ataxia, whereas a similar injection, given 24 h later, caused severe motor effects including barrel rotations and myoclonic/myotonic-like convulsive behavior. A potential receptor basis for the AVP-induced motor and sensitization effects in the cmeA was investigated using AVP analogues. A V1 antagonist, d(CH2)5Tyr(Me)AVP, blocked both the motor and sensitization effects produced by cmeA AVP injection. A V2 receptor agonist, DDAVP, did not affect motor activity upon cmeA injection, but did, however, sensitize animals to subsequent cmeA AVP injection. These results suggest that the cmeA is a sensitive site for AVP-induced motor effects and that these motor effects are sensitized by prior exposure to AVP. While the motor effects observed after cmeA AVP injection are mediated via AVP receptors that resemble the V1 type, the sensitization effect may be mediated via multiple receptor systems.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1992

Vasopressin perfusion within the medial amygdaloid nucleus attenuates prostaglandin fever in the urethane-anaesthetized rat.

The antipyretic effect of arginine vasopressin (AVP) introduced into the ventral septal area (VSA) by push-pull perfusion was investigated in the urethane-anaesthetized rat. In addition, experiments were carried out to determine whether AVP could suppress fever when similarly perfused within the medial amygdaloid nucleus (meA). During push-pull perfusion of artificial cerebrospinal fluid within the VSA or meA, PGE1 injected intracerebroventricularly evoked fevers with respective magnitudes of 1.3 +/- 0.2 degrees C and 1.4 +/- 0.3 degrees C above baseline. Perfusion of AVP (6.5 micrograms/ml) within the VSA had significantly reduced the magnitude of PGE1 fever to 0.3 +/- 0.3 degrees C above baseline, while having no significant effect on afebrile colonic temperature. Perfusion of AVP (6.5 micrograms/ml) within the meA had significantly attenuated the magnitude of PGE1 fever to 0.7 +/- 0.2 degrees C above baseline, while having no significant effect on afebrile colonic temperature. These results support further the utility of the urethane-anaesthetized rat model for future investigations of the central control of fever and antipyresis. In addition, these data are consistent with the hypothesis that AVP may act within the meA as an endogenous antipyretic.

Alprostadil↗
PubMed1992

Hypothalamic neuropeptide Y inhibits gastric acid output in rat: role of the autonomic nervous system.

Injection of neuropeptide Y (NPY) into the hypothalamic paraventricular nucleus (PVN) inhibits gastric acid secretion in anesthetized rats. The role of the autonomic nervous system in mediation of this response was investigated. Unilateral microinjection of 200 pmol NPY into the PVN of anesthetized rats inhibited spontaneous and pentagastrin-stimulated gastric acid output. Inhibition was abolished by subdiaphragmatic vagotomy, atropine, and bethanechol but was restored by electrical stimulation of the distal cut end of the vagus in cervically vagotomized rats. Although sympathectomy, phenoxybenzamine, and yohimbine abolished the inhibition, it was not affected by prazosin treatment. Gastric blood flow was not altered by injection of NPY. These results suggest that the antisecretory effect of NPY in the PVN was sympathetically mediated via suppression of gastric vagal cholinergic tone through activation of alpha 2-adrenoceptors.

Animals↗
PubMed1992

Vasopressin-induced antipyresis in the medial amygdaloid nucleus of conscious rats.

Experiments were undertaken to characterize a possible receptor mediating antipyretic action of arginine vasopressin (AVP) within the medial amygdaloid nucleus (meA) in the conscious rat. Additional experiments were directed at determining whether the action of endogenously released AVP can be revealed in the meA during fever in the conscious rat. These objectives were achieved using vasopressin analogues directed against vasopressor (V1a) and antidiuretic (V2) receptors. Bilateral injection of AVP (40 pmol) into the meA of conscious rats suppressed fever evoked by intracerebroventricular (icv) administration of prostaglandin E1 (PGE1, 50 ng). The V2 receptor agonist 1-desamino-8-D-AVP (40 pmol) injected into the meA evoked only moderate antipyresis compared with AVP, possibly because of interaction of this agonist with V1a receptors. The antipyretic effect of AVP was blocked when injection of the peptide was preceded by a bilateral injection of the V1a antagonist 1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)-2-(O-methyl)tyrosine AVP [d(CH2)5Tyr(Me)AVP, 400 pmol] into the meA. Injection of d(CH2)5Tyr(Me)AVP alone into the meA was without significant effect on afebrile core temperature. Injection of d(CH2)5Tyr(Me)AVP or 1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)-2-D-valine,4-valine AVP (a V2 antagonist) alone into the meA before icv PGE1 resulted in fevers that were not significantly different from artificial cerebrospinal fluid controls. These data are consistent with the possibility that AVP might act within the meA to evoke antipyresis via receptors that resemble V1a (vasopressor) receptors. However, the action of AVP endogenously released into the meA does not appear to be an absolute requisite in the normal modulation of PGE1 fever.

Alprostadil↗
PubMed1991

Modulation of brown adipose tissue-mediated thermogenesis by lesions to the nucleus tractus solitarius in the rat.

Given that relatively little is known regarding the central control of brown adipose tissue (BAT)-mediated thermogenesis the present study assessed whether the direct pharmacological stimulation of beta- or alpha-adrenergic receptors located on the brown adipocytes would result in a typical thermogenic response following electrolytic lesions to the nucleus tractus solitarius (NTS). Bilateral electrolytic lesions to the NTS in the rat effectively disrupted the baroreceptor reflex arc. It was observed that the metabolic and temperature responses to either norepinephrine (1, 5, or 25 micrograms/kg/min) or to the beta-agonist isoproterenol (0.5 micrograms/kg/min) were significantly attenuated in the NTS-lesioned rats relative to the control animals with an intact baroreflex. Conversely, the cardiovascular effects of norepinephrine or of the alpha-agonist phenylephrine (10 micrograms/kg/min) were enhanced in the NTS-lesioned animals. The results suggest that the functional capacity of the brown adipocytes was reduced following NTS lesions and points to an alteration in the ability of beta-receptors to respond to pharmacological stimulation with a typical thermogenic response.

Adipose Tissue, Brown↗
PubMed1991

Nucleus tractus solitarii lesions alter the metabolic and hyperthermic response to central prostaglandin E1 in the rat.

1. Given that the nucleus tractus solitarii (NTS) may regulate the ability of brown adipose tissue to evoke non-shivering thermogenesis and that brown fat may mediate the rise in whole-body metabolism observed following central pyrogen administration, we assessed whether interruption of baroreceptor afferents coursing though the NTS would interfere with the ability of prostaglandin E1 to evoke a normal fever response profile. 2. Infusion of 150-600 ng of prostaglandin E1 (PGE1) into a lateral cerebral ventricle of the conscious rat resulted in a rise in core temperature, and also an increase in whole-body metabolic rate, brown adipose tissue temperature, arterial blood pressure and heart rate. 3. Following bilateral electrolytic lesions to the NTS, resting core and brown fat temperatures, metabolic rates, blood pressures and heart rates in the NTS-lesioned animals were comparable to control rats. However, the PGE1-evoked increase in metabolic rate, along with the rise in core and brown adipose tissue temperatures and heart rate were attenuated. The pressor response was, however, enhanced, possibly due to the demonstrated interference by the lesions with normal baroreflex control. 4. The findings suggest that the nucleus tractus solitarii region of the rats' brain may be important in mediating the thermogenesis evoked by central PGE1.

Adipose Tissue, Brown↗
PubMed1991

Contribution of brown adipose tissue to central PGE1-evoked hyperthermia in rats.

The relative contribution of several effector systems to a prostaglandin E1-(PGE1) evoked hyperthermia was examined. Infusion of 150 ng of PGE1 into a lateral cerebral ventricle increased core temperature and whole body metabolic rate, brown adipose tissue temperature, systolic blood pressure, and heart rate. Pretreating the animals with a nonselective beta-antagonist propranolol (1 mg/kg iv in 0.3 ml followed by 3 mg.kg-1.h-1 in 0.3 ml/h) not only attenuated the rise in metabolism observed after the central administration of 150 ng PGE1 but also diminished the elevation in both core and brown fat tissue temperatures as well as the increase in heart rate. Pretreating the animals with the alpha-antagonist prazosin (2 mg/kg im followed by 50 micrograms.kg-1.h-1 iv in 0.3 ml/h) somewhat reduced the rise in whole body metabolism, suppressed the elevation in core temperature, but failed to alter the rise in brown adipose tissue temperature normally seen after the central administration of PGE1. Moreover, both the rise in systolic blood pressure and heart rate were attenuated when the PGE1 administration was preceded by prazosin. These results suggest that brown adipose tissue is an important effector organ responsible for mediating the hyperthermic response observed after the intracerebral injection of PGE1. In addition, the results indicate that alterations in vasomotor tone may also be important in producing or sustaining the elevated core temperature found after a pyrogen administration.

Adipose Tissue↗
PubMed1990

Depletion of brain alpha-MSH alters prostaglandin and interleukin fever in rats.

Alpha-melanocyte stimulating hormone (alpha-MSH), a putative endogenous antipyretic agent, is synthesized largely within neurons in the arcuate nucleus. To test the hypothesis that destruction of this area would increase the febrile response, male Wistar rats, treated as neonates with intraperitoneal injections of monosodium glutamate (MSG) or saline, were given intracerebroventricular (i.c.v.) injections of prostaglandin E1 (20 ng; 200 ng) or purified interleukin-1 (20 U) and body temperature was monitored. The fevers displayed by the MSG-treated animals were significantly greater (P less than 0.05) than those of the controls for the lower dose of PGE1 at 10-30 min and for IL-1 at 3-6 h after the injections. MSG-treated rats showed significant reduction (P less than 0.01) in alpha-MSH content of the medial basal hypothalamus and lateral septum when compared to saline controls. Body temperature response of non-febrile animals to high ambient temperature was not affected by the MSG treatment. These data support the hypothesis that alpha-MSH is an endogenous antipyretic in the rat.

Alprostadil↗
PubMed1990

The effectiveness of arginine vasopressin and sodium salicylate as antipyretics in the Brattleboro rat.

The infusion of either 30 micrograms/microliters (approx. 100 micrograms/kg/h) of sodium salicylate or 10 ng/microliters (10(-5) M) arginine vasopressin within the ventral septal area of the Brattleboro rat brain reduced a centrally induced prostaglandin E1 (PGE1) hyperthermia when compared with infusions of artificial cerebrospinal fluid. Conversely, the infusion of a related peptide, oxytocin (10 ng/microliters (10(-5) M), or 33 ng/kg/h) failed to alter the rise in core temperature following the PGE1 injection. These results suggest that the vasopressin receptors reported to be present in the Brattleboro rat may respond normally to exogenously administered vasopressin, thus allowing for the antipyretic action. Moreover, the antipyretic effects of sodium salicylate suggest that aspirin-like drugs may induce the release of alpha-melanocyte-stimulating hormone which, in turn, attenuates the PGE1-evoked fever. Given recent evidence, however, which suggests that the Brattleboro rat may contain vasopressin both peripherally and within the brain, the antipyretic action of sodium salicylate may be alternatively explained through the endogenous release of vasopressin.

Alprostadil↗
PubMed1990

Release of vasopressin and oxytocin by paraventricular stimulation in rats.

The nucleus tractus solitarius/dorsal motor nucleus of the vagus nerve (NTS/DMV) area was perfused by the push-pull perfusion technique in anesthetized rats, and perfusates were assayed for arginine vasopressin (AVP) and oxytocin (OXT) immunoreactivity. As compared with controls, electrical stimulation of the ipsilateral paraventricular nucleus (PVN) resulted in increased amounts of both AVP (approximately 5-fold) and OXT (approximately 10-fold, P less than 0.05 each) in the perfusates. During the poststimulation perfusion period, peptide concentrations were found to return to control levels. Elevation of circulating AVP and OXT by an osmotic stimulus did not result in increases of AVP and OXT in NTS/DMV perfusates. These data suggest that AVP and OXT are released from NTS/DMV area fiber terminals during electrical stimulation of descending PVN neurons. Furthermore, they are consistent with the view that both peptides are involved as neurotransmitters in autonomic regulation.

Animals↗
PubMed1990

Cerebrospinal fluid pressure in conscious rats during prostaglandin E1 fever.

Intraperitoneal body temperature was monitored from groups of 10 conscious adult male Wistar rats. The daily body temperature rhythm was determined, and an intraperitoneal body temperature dose response relationship was established for prostaglandin E1 (PGE1) delivered into a lateral cerebral ventricle (LCV). Cerebrospinal fluid pressure was measured by direct cannulation of a LCV. Heart rate, arterial and central venous blood pressure, and blood gases were also measured in groups of 10 animals. It was found that there was a daily rhythm in intraperitoneal body temperature that was higher at night than during the day but stable between 0800 and 1600 h. A significant temperature dose (20-2,000 ng)-response relationship was established for administration of PGE1 into the LCV. Cerebrospinal fluid pressure when measured from the LCV increased significantly during the "chill" phase of the PGE1-induced fever. Carotid arterial blood pressure also significantly increased at this time as did central venous pressure, particularly so with vigorous shivering. There was a significant fall in arterial CO2 partial pressure, a slight rise in pH, and no change in arterial O2 partial pressure. These data support the hypothesis that a significant increase in cerebrospinal fluid pressure occurs during the chill phase of a PGE1-induced fever in the conscious rat.

Alprostadil↗
PubMed1990

Vasopressin and oxytocin in rat brain in response to prostaglandin fever.

Urethan-anesthetized rats were used to identify effective stimuli for the release of the peptides arginine vasopressin (AVP) and oxytocin into the ventral septal area (VSA) of the brain. Febrile responses to intracerebroventricular injection of prostaglandin E1 (PGE1) were observed in rats whose body temperatures were maintained at 35, 37, or 39 degrees C. Microinjection of the AVP antagonist d(CH2)5Tyr(Me)AVP into the VSA enhanced fever only when PGE1 administration was associated with a significant rise in body temperature. Passive elevation ("artificial fever") or reduction of body temperature in the absence of a PGE1 stimulus was not affected by the antagonist. Push-pull perfusion of the VSA and the dorsal hippocampus, followed by radioimmunoassay of perfusates for AVP and oxytocin, revealed enhanced release into the VSA of AVP only when PGE1 administration was followed by a rise in body temperature. Oxytocin was released whenever body temperature was raised. Peptide concentrations in simultaneous perfusates of dorsal hippocampus did not change in response to PGE1 administration or to passive elevation of body temperature. We conclude that AVP is released into the VSA, but not the dorsal hippocampus, of the rat during a fever induced by PGE1. Oxytocin is released into the VSA, but not the hippocampus, when temperature is elevated.

Alprostadil↗
PubMed1989

Indomethacin-induced antipyresis in the rat: role of vasopressin receptors.

Infusion of 15 micrograms/microliters (approximately 120 micrograms/kg/h) of indomethacin within the ventral septal area of the rat brain significantly reduced a centrally induced prostaglandin E1 (PGE1) hyperthermia when compared with infusions of artificial cerebrospinal fluid. A bolus injection of a V1 receptor antagonist, d(CH2)5Try(Me)AVP, (200, 2000, or 20,000 pmol) within the ventral septal area had no effect of body temperature alone but did suppress the PGE1-induced fever. Similar bolus injections of the V1 receptor antagonist within the ventral septal area failed to alter the antipyretic action of indomethacin on the hyperthermia resulting from centrally administered PGE1. Central injections of a V2 receptor antagonist failed to alter either the PGE1-induced fever or the indomethacin-evoked antipyresis. The results suggest that the V1 receptor antagonist may exert non-specific neurodepressant effects which may interfere with the expression or production of PGE1 hyperthermia and may further mask any contribution of arginine vasopressin to the antipyretic effects of indomethacin.

Angiotensin Receptor Antagonists↗
PubMed1989

Single-unit activity in the bed nucleus of the stria terminalis during fever.

Arginine vasopressin, released from nerve terminals in the septal region, probably exerts endogenous antipyretic activity. A major source of vasopressin to this area is the bed nucleus of the stria terminalis (BST). In order to characterize electrophysiologically the BST-septal pathway and its potential role in the control of fever, single-unit, extracellular recordings were made from neurons in the BST of anesthetized rats. Afferent and efferent connections were identified by electrical stimulation of the medial amygdaloid nucleus and the ventral septal area (VSA). BST neurons received both inhibitory and excitatory synaptic input from the amygdala and VSA. Efferents to the VSA were identified by stimulus-evoked antidromic spike invasion. Some BST neurons were responsive to peripheral skin temperature (thermoresponsive). The activity of putative vasopressin neurons was studied during prostaglandin E1-induced fever. Although a majority of BST units was unaffected by fever, a proportion of the cells examined increased their firing rates in accordance with reported release of vasopressin in the VSA during fever.

Action Potentials↗
PubMed1989

Sodium salicylate: alternate mechanism of central antipyretic action in the rat.

Infusion of sodium salicylate (50.0 or 100.0 micrograms/microliters) into the ventral septal area (VSA) of the rat brain suppressed Prostaglandin-E1-induced hyperthermia. Infusion of artificial cerebrospinal fluid (aCSF) or 10.0 micrograms doses of salicylate did not. The suppression of intracerebroventricularly-induced (icv) Prostaglandin E1 (PGE1) hyperthermia was not due to a hypothermic action of salicylate since salicylate infusions given during cold exposure (10.0 degrees C) did not lower core body temperatures. A possible interaction between salicylate and endogenous arginine vasopressin (AVP) was investigated. Infusion of both salicylate (50.0 micrograms/microliters) and either AVP antiserum or AVP antagonist into the VSA resulted in PGE hyperthermias occurring at levels which were not different from control levels as opposed to enhanced hyperthermia (antiserum or antagonist alone) or suppressed hyperthermia (salicylate alone). These results are consistent with the notion that sodium salicylate infusions within the VSA enhance AVP action and thus bring about the attenuation of PGE-induced hyperthermia.

Alprostadil↗
PubMed1988

Plasma catecholamines in conscious rabbits after central administration of vasopressin.

Arterial levels of epinephrine (E) were significantly raised for all times sampled, after intracerebroventricular (i.c.v.) injection of arginine vasopressin (AVP) (1 nmol) into conscious rabbits. Venous levels of norepinephrine (NE) were significantly raised within the first 4 min after a similar i.c.v. injection of AVP. The significant increases in arterial E and venous NE correspond in time and therefore could account for changes in heart rate and blood pressure elicited by centrally injected AVP. Therefore, AVP could influence cardiovascular function by increasing the activity of the sympatho-adrenomedullary system.

Animals↗
PubMed1988

Injection of neuropeptide Y into the paraventricular nucleus of the hypothalamus inhibits gastric acid secretion in the rat.

Neuropeptide Y (NPY) was injected into the paraventricular nucleus (PVN) of the hypothalamus of anesthetized rats in order to assess its effect on gastric acid secretion. NPY evoked a dose-dependent decrease of interdigestive gastric acid output when injected directly into the PVN or immediately ventral to it. Intracerebroventricular NPY and saline injections did not alter acid output. Injection of NPY into adjacent non-PVN hypothalamic areas resulted in either an elevated acid output or had no effect depending on the site of injection. Mean arterial blood pressure and heart rate were not consistently affected by NPY. These results show that injection of NPY into the PVN of anesthetized rats inhibits interdigestive gastric acid output in a dose-dependent manner.

Animals↗