Modification of Brain Acetylcholine Release by Morphine and Its Antagonists in Normal and Morphine‐dependent Rats

Jhamandas, Khem; Sutak, Maaja

doi:10.1111/j.1476-5381.1974.tb09592.x

Cited by 56 publications

(23 citation statements)

References 19 publications

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“…The release of cortical ACh was investigated in the presence of neostigmine (50 j±g/ml) and atropine (0.5 gig/ml) using the cup technique of MacIntosh & Oborin (1953). Experimental details of the procedure, as employed in the rat, have been described fully in a previous paper (Jhamandas & Sutak, 1974 …”

Section: Methodsmentioning

confidence: 99%

“…Studies reported from this and other laboratories show that the opiate antagonist naloxone, when administered to chronically morphine-treated animals, enhances the output of ACh in the cerebral cortex (Jhamandas & Sutak, 1974;Labrecque & Domino, 1974;Mullins & Phillis, 1974). Morphine itself can inhibit the release of ACh in the CNS and this effect can be antagonized by naloxone administered before or after morphine treatment (Jhamandas, Phillis & Pinsky, 1971; Matthews, Labrecque & Domino, 1973;Yaksh & Yamamura, 1975).…”

Section: Introductionmentioning

confidence: 99%

“…Weights of drugs refer to the salts. Chronic morphine injections were administered to rats as described in a previous paper (Jhamandas & Sutak, 1974).…”

Section: Drugs and Treatmentmentioning

confidence: 99%

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Morphine–naloxone Interaction in the Central Cholinergic System: The Influence of Subcortical Lesioning and Electrical Stimulation

Jhamandas

Sutak

1976

British J Pharmacology

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I The opiate antagonist naloxone, injected or topically applied to the cerebral cortex, had no significant effect on the spontaneous output of cortical acetylcholine (ACh) in rats. 2 Morphine (2.5 mg/kg) administered intravenously inhibited the release of cortical ACh. A subsequent injection of naloxone rapidly reversed morphine-induced inhibition, and produced a sustained increase in the release of ACh. Topical application of naloxone solutions, after morphine, produced a slow and weak reversal of its inhibitory action. 3 Destruction of the medial thalamus abolished both the inhibitory effects of morphine on the cortical ACh release, and its antagonism by naloxone administered after the agonist. 4 Injection of naloxone in a low dose (0.1 mg/kg) increased the release of cortical ACh provoked by electrical stimulation of either the medial thalamus or the reticular formation in normal rats. In the morphine-dependent rat, naloxone also facilitated the evoked release and its action was greater than in control animals. The facilitatory effect of naloxone on the cortical release evoked by stimulation of the medial thalamus was greater than its effect on the release evoked by stimulation of the reticular formation in both normal and morphine-dependent rats. Naltrexone, a narcotic antagonist, also facilitated the electrically stimulated release of cortical ACh. 6 It is suggested that (a) morphine and naloxone act at a subcortical site, probably the medial thalamus, to modify the cortical ACh release and that (b) naloxone may facilitate the electricallyinduced release of ACh in the CNS by antagonizing the effect of the endogenous morphine-like factor, enkephalin.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Morphine–naloxone Interaction in the Central Cholinergic System: The Influence of Subcortical Lesioning and Electrical Stimulation

Jhamandas

Sutak

1976

British J Pharmacology

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“…However, some reports argue against this view. First, cortical ACh release has repeatedly been found to increase, rather than decrease, during naloxone-precipitated morphine abstinence in the rat (Jhamandas & Sutak, 1974; 'Correspondence. Casamenti et al, 1980;Crossland & Ahmed, 1984).…”

Section: Introductionmentioning

confidence: 99%

Cortical acetylcholine release is increased and γ‐aminobutyric acid outflow is reduced during morphine withdrawal

Antonelli

Beani

Bianchi

et al. 1986

British J Pharmacology

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The effects of naloxone on acetylcholine (ACh) and γ‐aminobutyric acid (GABA) outflow from the cerebral cortex of freely moving, morphine‐dependent guinea‐pigs was studied. The cortical efflux of ACh in chronically‐treated guinea‐pigs was about half of that of normal animals. GABA efflux was unaffected. During opioid withdrawal precipitated by naloxone (0.1–10 mg kg−1, i.p.) the guinea‐pigs showed jumping, hyperactivity and wet dog shakes, the intensity of which was directly related to the dose of naloxone. The withdrawal syndrome was accompanied by a dose‐dependent increase in ACh release and reduction in GABA outflow; ACh release was increased by naloxone at doses lower (0.1–3 mg kg−1) than those acting on GABA efflux (1–10 mg kg−1). Atropine (10 mg kg−1) and diazepam (5 mg kg−1) did not prevent GABA and ACh changes.

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“…Morphine-related opiates and enkephalins act on specific opiate receptors to depress the peripheral and central release of acetylcholine (ACh) (Jhamandas & Sutak, 1974;Jhamandas, Hron & Sutak, 1975). The inhibitory actions of morphine on the release of ACh from the guinea-pig ileum or the rat cerebral cortex can be selectively antagonized by the methylxanthines, theophylline (Theo) and caffeine .…”

Section: Introductionmentioning

confidence: 99%

Antagonism of enkephalin action on acetylcholine release by methylxanthines: lack of a purine link

Elliott

Jhamandas

Notman

et al. 1983

British J Pharmacology

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Modification of Brain Acetylcholine Release by Morphine and Its Antagonists in Normal and Morphine‐dependent Rats

Cited by 56 publications

References 19 publications

Morphine–naloxone Interaction in the Central Cholinergic System: The Influence of Subcortical Lesioning and Electrical Stimulation

Morphine–naloxone Interaction in the Central Cholinergic System: The Influence of Subcortical Lesioning and Electrical Stimulation

Cortical acetylcholine release is increased and γ‐aminobutyric acid outflow is reduced during morphine withdrawal

Antagonism of enkephalin action on acetylcholine release by methylxanthines: lack of a purine link

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