Interactions of Opiates and Endorphins With Cerebral Catecholamines

Bläsig, J; Herz, A.

doi:10.1007/978-3-642-67505-8_11

Cited by 8 publications

(1 citation statement)

References 175 publications

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“…Drugs that manipulate noradrenergic activity markedly influence opioid-induced antinociception (Blasig & Herz, 1980). The LC is a main source of the ascending and descending noradrenergic systems in the CNS (Moore & Card, 1984).…”

Section: Discussionmentioning

confidence: 99%

Effects of the central analgesic tramadol and its main metabolite, O‐desmethyltramadol, on rat locus coeruleus neurones

Ševčı́k

Nieber

Driessen

et al. 1993

British J Pharmacology

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1 Tramadol is a centrally acting analgesic with low opioid receptor affinity and, therefore, presumably additional mechanisms of analgesic action. Tramadol and its main metabolite 0-desmethyltramadol were tested on rat central noradrenergic neurones of the nucleus locus coeruleus (LC), which are involved in the modulation of nociceptive afferent stimuli. 6 The hyperpolarizing effect of noradrenaline (30 JM) was potentiated in the presence of (-)-tramadol (100 JM), but not in the presence of (+ )-O-desmethyltramadol (10 JAM). There was no potentiation of the noradrenaline (30 iAM) effect, when the cells were hyperpolarized by current injection to an extent similar to that produced by (-)-tramadol (100 JM). 7 Both noradrenaline (100 JM) and (-)-tramadol (1I00 jaM) decreased the input resistance.8 The results confirm that the analgesic action of tramadol involves both opioid and non-opioid components. It appears that (-)-tramadol inhibits the uptake of noradrenaline and via a subsequent increase in the concentration of endogenous noradrenaline indirectly stimulates a2-adrenoceptors. (+ )-0-desmethyltramadol seems to stimulate directly opioid "-receptors. The effects of (+)-tramadol and (-)-O-desmethyltramadol consist of combined J-opioid and a2-adrenergic components.

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Section: Discussionmentioning

confidence: 99%

Effects of the central analgesic tramadol and its main metabolite, O‐desmethyltramadol, on rat locus coeruleus neurones

Ševčı́k

Nieber

Driessen

et al. 1993

British J Pharmacology

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Opioid Receptor Types at Noradrenergic Neurons and their Roles in Blood Pressure Regulation

Illéš

Bucher

1988

Opioid Peptides and Blood Pressure Control

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Acceleration of cerebral noradrenaline turnover after morphine withdrawal and its retardation by acute morphine administration in rats

Attila

Ahtee

1984

Naunyn-Schmiedeberg's Arch. Pharmacol.

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To clarify the effects of withdrawal from chronic morphine treatment on cerebral noradrenaline (NA) turnover, we have measured the alpha-methyl-p-tyrosine (alpha MT)-induced depletion of NA in five brain areas of male Wistar rats given morphine twice daily for 40 or 60 days. After the last morphine dose (50 or 70 mg/kg) the rats were withdrawn for 1, 2 or 4 days. In order to study the development of tolerance a challenge dose of 10 mg/kg of morphine was given to some of the rats. Withdrawal of morphine accelerated the alpha MT-induced NA depletion clearly in the hemispheres and the lower brain stem and slightly in the diencephalon. The acceleration was more pronounced in the brains of rats treated for 60 days than of those treated for 40 days. In the hemispheres the acceleration of NA depletion occurred at 1 and 2 days, in the diencephalon at 2 days, and in the lower brain stem at 2 and 4 days after morphine withdrawal. The most pronounced acceleration of NA depletion coincided with the maximum withdrawal-induced weight loss. The challenge dose of morphine clearly retarded the alpha MT-induced NA depletion in the hemispheres of control rats treated chronically with saline. This retardation was even more pronounced in rats withdrawn from chronic morphine treatment for 1 or 2 days. The challenge dose slightly accelerated the alpha MT-induced NA depletion in the lower brain stem of control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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Interactions of Opiates and Endorphins With Cerebral Catecholamines

Cited by 8 publications

References 175 publications

Effects of the central analgesic tramadol and its main metabolite, O‐desmethyltramadol, on rat locus coeruleus neurones

Effects of the central analgesic tramadol and its main metabolite, O‐desmethyltramadol, on rat locus coeruleus neurones

Opioid Receptor Types at Noradrenergic Neurons and their Roles in Blood Pressure Regulation

Acceleration of cerebral noradrenaline turnover after morphine withdrawal and its retardation by acute morphine administration in rats

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