The role of α2-adrenoceptors in the hypothermic effect of clonidine in the rat

Zacny, Elżbieta

doi:10.1111/j.2042-7158.1982.tb04758.x

Cited by 28 publications

(10 citation statements)

References 16 publications

(4 reference statements)

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“…Clonidine, probably due to a reduction in LC activity, leads to a fall in body temperature both in experimental animals [241, 366, 461, 511] and humans [15, 138]. The hypothermic effect of clonidine is antagonised by yohimbine [366, 461] and by high ambient temperature, leading to an increase in body temperature [15].…”

Section: Pharmacological Alterations Of Locus Coeruleus Activitymentioning

confidence: 99%

Functional Neuroanatomy of the Noradrenergic Locus Coeruleus: Its Roles in the Regulation of Arousal and Autonomic Function Part II: Physiological and Pharmacological Manipulations and Pathological Alterations of Locus Coeruleus Activity in Humans

Samuels

Szabadi²

2008

396

365

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The locus coeruleus (LC), the major noradrenergic nucleus of the brain, gives rise to fibres innervating most structures of the neuraxis. Recent advances in neuroscience have helped to unravel the neuronal circuitry controlling a number of physiological functions in which the LC plays a central role. Two such functions are the regulation of arousal and autonomic activity, which are inseparably linked largely via the involvement of the LC. Alterations in LC activity due to physiological or pharmacological manipulations or pathological processes can lead to distinct patterns of change in arousal and autonomic function. Physiological manipulations considered here include the presentation of noxious or anxiety-provoking stimuli and extremes in ambient temperature. The modification of LC-controlled functions by drug administration is discussed in detail, including drugs which directly modify the activity of LC neurones (e.g., via autoreceptors, storage, reuptake) or have an indirect effect through modulating excitatory or inhibitory inputs. The early vulnerability of the LC to the ageing process and to neurodegenerative disease (Parkinson’s and Alzheimer’s diseases) is of considerable clinical significance. In general, physiological manipulations and the administration of stimulant drugs, α2-adrenoceptor antagonists and noradrenaline uptake inhibitors increase LC activity and thus cause heightened arousal and activation of the sympathetic nervous system. In contrast, the administration of sedative drugs, including α2-adrenoceptor agonists, and pathological changes in LC function in neurodegenerative disorders and ageing reduce LC activity and result in sedation and activation of the parasympathetic nervous system.

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Section: Pharmacological Alterations Of Locus Coeruleus Activitymentioning

confidence: 99%

Functional Neuroanatomy of the Noradrenergic Locus Coeruleus: Its Roles in the Regulation of Arousal and Autonomic Function Part II: Physiological and Pharmacological Manipulations and Pathological Alterations of Locus Coeruleus Activity in Humans

Samuels

Szabadi²

2008

396

365

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“…Clonidine-and guanfacine-induced analgesia, hypothermia and hypoactivity served as the index of central a-2 receptor function (Spyraki & Fibiger 1982;Zacny 1982;Kameyama et al 1986).…”

mentioning

confidence: 99%

Adaptive Changes in α‐2 Adrenoceptor Mediated Responses: Analgesia, Hypothermia and Hypoactivity

Minor¹,

Danysz

Jonsson³

et al. 1989

Pharmacology & Toxicology

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The acute effects of the alpha-2 adrenoceptor agonists, clonidine and guanfacine, upon antinociception, hypothermia and motor activity were compared under conditions of receptor antagonism, denervation, and chronic administration of a tricyclic antidepressant compound. The analgesic actions of clonidine and guanfacine were antagonised by idazoxan, an alpha-2 receptor antagonist, but potentiated by pretreatment with the noradrenaline neurotoxin DSP4, and attenuated by chronic treatment with desipramine (DMI). Clonidine- and guanfacine-induced hypothermia was antagonised by idazoxan, potentiated by prior treatment with DSP4 and attenuated by chronic administration with DMI. Both clonidine and guanfacine produced decreases in motor activity that were attenuated by idazoxan but unaffected by prior DSP-4 treatment. Chronic DMI administration also attenuated clonidine-induced hypoactivity but potentiated guanfacine-induced hypoactivity. These diverse results describe both similar and differential adaptive mechanisms modulating the functional effect of alpha-2 receptor systems in the central nervous system.

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“…Earlier studies have shown that the hypothermia caused by low dose clonidine (0.05 mg kg-', i.p.) was antagonized by central or periphal yohimbine (Zacny, 1982). The selective a2-agonists, UK-14,304 and BHT 933, also elicit hypothermia by central actions (Colpaert, 1986;Bill et al, 1989).…”

Section: Discussionmentioning

confidence: 98%

“…McKenzie & Trulson (1978) reported a blunted sensitivity to indirect 5-hydroxytryptamine (5-HT) receptor agonists, while an apparent subsensitivity to central diuretic and natriuretic effects of the a2-adrenoceptor agonist clonidine has also been reported in STZ-treated rats (Zhang & Patel, 1991 of the CNS likely to be directly sensitive to lack of peripheral insulin (Leedom & Meechan, 1989), and the involvement of the hypothalamus in several other functions altered in diabetes, suggests that an effect at an hypothalamic site could underlie the abnormality in temperature regulation. The sensivity of a2-adrenoceptors may be pharmacologically monitored by challenge with acute clonidine, followed by measurement of temperature response (Zacny, 1982;Livingstone et al, 1984;Colpaert, 1986). The present investigation examined the effects of STZ diabetes on the temperature response to clonidine in rats.…”

Section: Introductionmentioning

confidence: 99%

Altered thermoregulatory responses to clonidine in streptozotocin‐diabetic rats

O’Donnell

Bányász

Kovács

1996

British J Pharmacology

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temperature occurred in control rats given clonidine challenge (0.05-2.0 mg kg-', s.c.); this response was inhibited by prior administration of either yohimbine or idazoxan (2 mg kg-1, s.c.) but not by the peripherally-acting a2-adrenoceptor antagonist L-659,066(10 mg kg-', s.c.).3 In rats treated with STZ (65 mg kg-', i.v.) administration of clonidine elicited a dose-independent hyperthermia (circa 1°C.); this effect was unaltered by prior administration of yohimbine or idazoxan. 4 Naloxone (5 mg kg-', s.c.) elicited a small fall in temperature(< 1°C.) in both control and STZtreated rats; naloxone pretreatment did not alter the temperature response to clonidine in either group. 5 Nicotinic acid (10 mg kg-', s.c.) caused a similar small elevation in temperature in both groups. 6 Administration of replacement insulin to STZ-treated rats maintained weight gain and low blood glucose while the thermoregulatory response to clonidine slowly reverted to normal. 7 These results show that altered central temperature control is an element of the generalised abnormality of a2 receptor function induced by STZ.

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The role of α2-adrenoceptors in the hypothermic effect of clonidine in the rat

Cited by 28 publications

References 16 publications

Functional Neuroanatomy of the Noradrenergic Locus Coeruleus: Its Roles in the Regulation of Arousal and Autonomic Function Part II: Physiological and Pharmacological Manipulations and Pathological Alterations of Locus Coeruleus Activity in Humans

Functional Neuroanatomy of the Noradrenergic Locus Coeruleus: Its Roles in the Regulation of Arousal and Autonomic Function Part II: Physiological and Pharmacological Manipulations and Pathological Alterations of Locus Coeruleus Activity in Humans

Adaptive Changes in α‐2 Adrenoceptor Mediated Responses: Analgesia, Hypothermia and Hypoactivity

Altered thermoregulatory responses to clonidine in streptozotocin‐diabetic rats

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