Fever produced by prostaglandin E<sub>1</sub>

Feldberg, W.; Saxena, Parul

doi:10.1113/jphysiol.1971.sp009585

Cited by 167 publications

(47 citation statements)

References 18 publications

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“…For implantation of the cannula into the lateral ventricle, the method described by Feldberg & Shaligram (1972) and for implantation into the posterior hypothalamus, that described by Feldberg & Saxena (1971), was used.…”

Section: Methodsmentioning

confidence: 99%

Morphine hyperglycaemia

Feldberg¹,

Gupta²

1974

The Journal of Physiology

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2. Microinfusions of morphine into the posterior hypothalamus did not produce hyperglycaemia.3. Infusion of morphine into the liquor space at the entrance of the aqueduct or of the fourth ventricle produced hyperglycaemia. Any structures in the walls of the third ventricle as well as the peri-aqueductal grey are thus excluded as the site of action.4. Infusion of morphine into the subarachnoid space just above the corpora quadrigemina or below the ventral surface of the brain stem produced hyperglycaemia. With these routes the morphine does not enter any part of the ventricular cavities and the action would appear to be on structures at the ventral surface of the brain stem.5. Injection of morphine into the cisterna magna produces hyperglycaemia when the doses are larger than those already effective on injection into the cerebral ventricles. This also suggests an action on structures at the ventral surface of the brain stem, as this surface is reached more readily from the ventricles than from the cisterna.6. It is concluded that on injection into the cerebral ventricles, the morphine has to pass into the subarachnoid space, through the foramina of Luschka, in order to produce hyperglycaemia. It then reaches the ventral surface of the brain stem and probably acts there on structures in the upper part of the medulla oblongata.

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Section: Methodsmentioning

confidence: 99%

Morphine hyperglycaemia

Feldberg¹,

Gupta²

1974

The Journal of Physiology

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“…Nanogram quantities of PGE1 administered into the lateral ventricles of unanaesthetized cats with permanently implanted cannulae are hyperthermic (Feldberg & Saxena, 1971a). In our experiments with anaesthetized dogs much higher doses were needed.…”

Section: Drugsmentioning

confidence: 98%

“…The effects on body temperature of intraventricularly or intrahypothalamically injected noradrenaline and adrenaline, 5-hydroxytryptamine, acetylcholine and PGE1 have been extensively investigated in several species of animals (Feldberg & Myers, 1963, 1964a, 1964b, 1965Feldberg, Hellon & Lotti, 1967;Myers, 1967;Cooper, Granston & Honour, 1965;Bligh, 1966;Findlay & Robertshaw, 1967;Anderson, Jobin & Olsson, 1966;Brittain & Handley, 1967;Myers & Yaksh, 1969;Feldberg & Saxena, 1971a, 1971bMilton & Wendlandt, 1971).…”

Section: Introductionmentioning

confidence: 99%

Analysis of the Effects on Body Temperature of Intracerebroventricular Injection in Anaesthetized Dogs of Gamma‐aminobutyric Acid

Dhumal

Gulati

Raghunath

et al. 1974

British J Pharmacology

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1 The cerebral ventricles of dogs under intravenous pentobarbitone sodium anaesthesia, were perfused with artificial cerebro-spinal fluid (CSF) at a rate of 0.4-0.5 ml/min from the ventricular to the aqueductal cannulae. The effluent was collected from the aqueductal cannula in 20 min samples. The animals' temperatures were recorded from the rectum.2 y-Aminobutyric acid (GABA) 0.1-5 mg when injected into the ventricles produced variable temperature effects. Doses of 0.1 and 0.5 mg always produced hyperthermia and 1 and 5 mg doses sometimes produced hyperthermia and sometimes hypothermia. 3 Intraventricular perfusion with 2-bromolysergic acid diethylamide (BOL) and hyoscine did not block hyperthermia. Tests on the rat isolated stomach strip or the guinea-pig isolated superfused ileum for the possible release, respectively, of 5-hydroxytryptamine or acetylcholine by GABA were negative. 4 When tested for the presence of prostaglandin E(PGE)-like substances on the isolated rat stomach strip, both the control effluent and the GABA effluent showed activity, the latter being much more potent. There was a temporal correlation between this effect and hyperthermia. Intraventricularly administered sodium salicylate converted the GABA-induced hyperthermia to hypothermia and blocked the release of PGE-like substances. 5Hypothermia induced by GABA alone or in the presence of sodium salicylate was associated with the release of noradrenaline into the effluent. 6 Intraventricular administration of GABA in reserpinized dogs produced hyperthermia and not hypothermia. Similar results were obtained with phentolamine perfusion in normal dogs. 7 Perfusion with calcium-free solution blocked both the noradrenaline-releasing and hypothermic actions of GABA. 8 It is concluded that hyperthermia associated with intraventricular injections of GABA is due to the release of PGE-like substance and hypothermia is due to the release of noradrenaline.

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“…In addition, PGE2 injected into the cerebral ventricles (icv) was pyrogenic at low doses (Feldberg and Gupta, 1973;Feldberg and Saxena, 1971a;Feldberg and Saxena, 1971b;Milton and Wendlandt, 1971;Philipp-Dormston and Siegert, 1974). And additionally, if injected intradermally or intravascularly, PGE2 decreased the pain threshold to induce hyperalgesia (Ferreira, 1972;Ferreira et al, 1973).…”

Section: Immune-to-brain Signalingmentioning

confidence: 99%

Talking to the Brain at the Blood-Brain Barrier through Inflammation-Induced Prostaglandin E2

Vasilache¹

2015

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The immune-to-brain signaling is a critical survival factor when the body is confronted by pathogens, and in particular by microorganisms. During infections, the ability of the immune system to engage the central nervous system (CNS) in the management of the inflammatory response is just as important as its ability to mount a specific immune response against the pathogen, since the CNS can provide a systemic negative feed-back to the immune activation by release of stress hormones and also can prioritize the usage of the energy resources by the vital organs. Prostaglandin E2 (PGE2) and pro-inflammatory cytokines were among the first mediators to be identified to participate in the immune-to-brain signaling, a process that is clinically recognized by the development of manifestations of common illness such as fever, anorexia, decreased social interactions, lethargy, sleepiness, and hyperalgesia.In this thesis the contribution of PGE2 to the immune-to-brain signaling was further characterized at the blood-brain-barrier (BBB) and in the anterior preoptic area (POA) of the hypothalamus (i.e. the thermoregulatory region or, in sickness, the fever generating region).BBB is the major interface region between peripheral circulating cytokines and the neuronal parenchyma and a critical source of PGE2. Using chimeric mice lacking the inducible enzyme for PGE2 synthesis, microsomal PGE synthase-1 (mPGES-1), in either hematopoietic or nonhematopoietic cells, we demonstrate in paper I that brain endothelial cells are the critical source of PGE2 in BBB during peripheral inflammation. For the demonstration of the mPGES-1 expression in the BBB cells we developed in paper I a method for enzymatic dissociation of these cells, followed by fluorescence activated cell sorting (FACS). Using the same method, we show in paper II that the BBB response to immune stimuli is towards an increased production of PGE2 in endothelial cells and an increased sensitivity of these cells for proinflammatory cytokines. These changes are supported by decreased PGE2 degradation and decreased synthesis of other prostanoids in perivascular macrophages, which hence respond in concordance with the endothelial cells in enhancing PGE2 signaling.Once released in the neuronal tissue, PGE2 has been shown to be critical for the fever response by acting on the type 3 PGE2 receptors (EP3) within POA. By laser capture microdissection (LCM) we extracted the EP3 receptor expressing region in POA, defined by in situ hybridization histochemistry, from mouse brain sections. We demonstrate in paper III that the predominant subtypes of the EP3 receptor in POA are EP3α and EP3γ. In paper IV we further analyze the effect of PGE2 on the LCM dissected EP-rich POA using gene expression microarrays. We demonstrate that PGE2 has a limited effect on the gene expression changes within POA, suggesting that the neuronal activity is modulated by PGE2 in a transcriptionindependent manner and that the profound gene expression changes that are seen in the CNS during inflammation ...

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Fever produced by prostaglandin E₁

Abstract: SUMMARYProstaglandin E1 (PGE1) produces a rise in rectal temperature when injected into the cerebral ventricles of unanaesthetized cats, rabbits and rats. An effect is obtained with as little as 20, and sometimes even with 10 ng.

Cited by 167 publications

References 18 publications

Morphine hyperglycaemia

Morphine hyperglycaemia

Analysis of the Effects on Body Temperature of Intracerebroventricular Injection in Anaesthetized Dogs of Gamma‐aminobutyric Acid

Talking to the Brain at the Blood-Brain Barrier through Inflammation-Induced Prostaglandin E2

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Fever produced by prostaglandin E1

Abstract: SUMMARYProstaglandin E1 (PGE1) produces a rise in rectal temperature when injected into the cerebral ventricles of unanaesthetized cats, rabbits and rats. An effect is obtained with as little as 20, and sometimes even with 10 ng.

Cited by 167 publications

References 18 publications

Morphine hyperglycaemia

Morphine hyperglycaemia

Analysis of the Effects on Body Temperature of Intracerebroventricular Injection in Anaesthetized Dogs of Gamma‐aminobutyric Acid

Talking to the Brain at the Blood-Brain Barrier through Inflammation-Induced Prostaglandin E2

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Product

Resources

About

Fever produced by prostaglandin E₁