THERMOREGULATORY EFFECTS OF N<sup>6</sup>‐2′‐<i>O</i>‐DIBUTYRYL ADENOSINE 3′,5′‐MONOPHOSPHATE IN THE RESTRAINED MOUSE

Dascombe, Michael J.; Milton, A. S.; Nyemitei-Addo, I.; Pertwee, Roger Guy

doi:10.1111/j.1476-5381.1980.tb08723.x

Cited by 7 publications

(2 citation statements)

References 14 publications

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“…The initial fall in body temperature is followed by a later hyperthermia which can be attributed to tissue damage at the injection site. Similar responses to db cyclic AMP have been reported for the cat (Dascombe & Milton, 1975) and the rat (Dascombe & Parkes, 1981). The fall in temperature produced by db cyclic AMP was not mimicked by two activators of adenylate cyclase, cholera toxin and guanyl imidodiphosphate, indicating the hypothermia is of pharmacological rather than pathophysiological interest.…”

Section: Discussionsupporting

confidence: 74%

“…This observation gives substantial support to the proposal by Rosendorff (1976) that endogenous cyclic AMP is involved in the neurochemical events mediating fever. However, this theory cannot be applied to other species used in the study of pyretics and antipyretics, namely the cat and the rat, which develop hypothermia in response to db cyclic AMP in the PO/AH (Dascombe & Milton, 1975;Dascombe & Parkes, 1981).…”

Section: Introductionmentioning

confidence: 99%

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Evidence that cyclic nucleotides are not mediators of fever in rabbits

Dascombe

1984

British J Pharmacology

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1 The N6-2'-O-dibutyryl derivative of adenosine 3',5'-monophosphate (db cyclic AMP) and related compounds have been micro-injected into the preoptic/anterior hypothalamic nuclei (PO/AH) of the unanaesthetized, restrained rabbit and the effects on deep body temperature observed.2 Db cyclic AMP (100-400 jig) produced hypothermia of rapid onset in rabbits at an ambient temperature of 20-23°C. Hypothermia was also produced by N2-2'-O-dibutyryl guanosine 3',5'-monophosphate (db cyclic GMP), but not by saline, sodium n-butyrate, adenosine 3',5'-monophosphate (cyclic AMP), guanosine 3',5'-monophosphate, adenosine 5'-mono-, di-or triphosphate. 3 The initial hypothermic response to db cyclic AMP and db cyclic GMP was followed by a sustained rise in temperature. However, all compounds injected into the PO/AH produced a similar hyperthermia which was attenuated by paracetamol. Development of this tissue-damage fever abolished the hypothermic response to db cyclic AMP in some rabbits. 4 The effects of db cyclic AMP on body temperature and behaviour were not reproduced by the adenylate cyclase activators, cholera toxin (0.125-5 tLg) and guanyl imidodiphosphate (5-400 jig).5 It is concluded that hypothermia is the principal effect of db cyclic AMP on body temperature when injected into the PO/AH in rabbits. These data do not support the proposal that endogenous cyclic AMP in the rabbit brain mediates pyrexia.

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Section: Discussionsupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Evidence that cyclic nucleotides are not mediators of fever in rabbits

Dascombe

1984

British J Pharmacology

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Prostaglandins in Fever and the Mode of Action of Antipyretic Drugs

Milton¹

1982

Pyretics and Antipyretics

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Species differences in behavioural effects of rolipram and other adenosine cyclic 3h, 5h-monophosphate phosphodiesterase inhibitors

Wachtel¹

1983

J. Neural Transmission

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The effect of the phosphodiesterase (PDE) inhibitors rolipram, Ro 20-1724 and isobutylmethylxanthine (IBMX) on motor behaviour and rectal temperature was studied in mice, rats and guinea pigs following intraperitoneal administration (0.39 to 25 mg/kg). The selective adenosine cyclic 3',5'-monophosphate (cAMP) PDE inhibitors rolipram and Ro 20-1724 in each species caused a dissimilar pattern of neurotropic effects: Hypothermia and hypokinesia in mice, hypothermia, hypokinesia and head twitches in rats, hypothermia, hyperkinesia and head twitches in guinea pigs. The head twitches were associated with forepaw shaking and increased grooming. Rolipram was the most potent compound in the three species. In guinea pigs it was less active than in rats or mice. Ro 20-1724 was approx. 15 to 30 times less potent in inducing the characteristic alterations in the various species. The alkylxanthine PDE inhibitor IBMX, 0.39 to 6.25 mg/kg, slightly stimulated the locomotor activity of mice and rats, most probably due to antagonism of central adenosine actions. IBMX, 6.25 to 25 mg/kg, caused a pattern of neurotropic effects identical to that produced by the selective cAMP PDE inhibitors, indicating the prevalence of the cAMP PDE inhibitory action over the adenosine antagonistic action at higher dosages. IBMX was approx. as potent as Ro 20-1724 in this respect. The species differences in the neurotropic responses to cAMP PDE inhibition in vivo presumably reflect similar differences in the extent of cAMP accumulation in brain tissue of the three species in vitro. Enhanced availability of brain cAMP in vivo in the various rodent species seems to be correlated with diverse patterns of more or less complex motor behavioural symptoms.

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THERMOREGULATORY EFFECTS OF N⁶‐2′‐O‐DIBUTYRYL ADENOSINE 3′,5′‐MONOPHOSPHATE IN THE RESTRAINED MOUSE

Cited by 7 publications

References 14 publications

Evidence that cyclic nucleotides are not mediators of fever in rabbits

Evidence that cyclic nucleotides are not mediators of fever in rabbits

Prostaglandins in Fever and the Mode of Action of Antipyretic Drugs

Species differences in behavioural effects of rolipram and other adenosine cyclic 3h, 5h-monophosphate phosphodiesterase inhibitors

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THERMOREGULATORY EFFECTS OF N6‐2′‐O‐DIBUTYRYL ADENOSINE 3′,5′‐MONOPHOSPHATE IN THE RESTRAINED MOUSE

Cited by 7 publications

References 14 publications

Evidence that cyclic nucleotides are not mediators of fever in rabbits

Evidence that cyclic nucleotides are not mediators of fever in rabbits

Prostaglandins in Fever and the Mode of Action of Antipyretic Drugs

Species differences in behavioural effects of rolipram and other adenosine cyclic 3h, 5h-monophosphate phosphodiesterase inhibitors

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Product

Resources

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THERMOREGULATORY EFFECTS OF N⁶‐2′‐O‐DIBUTYRYL ADENOSINE 3′,5′‐MONOPHOSPHATE IN THE RESTRAINED MOUSE