Effect of ?- and ?-adrenergic blocking agents and para-chlorophenylalanine on morphine- and caffeine-stimulated locomotor activity of mice

Estler, C.‐J.

doi:10.1007/bf00429306

Cited by 34 publications

(13 citation statements)

References 23 publications

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“…Supportive evidence for the involvement of catecholamines is the fact that morphine reduces the brain catecholamine content of mice (1,15) and increases the incorporation of 14C-tyrosine into 14C-dopamine and 14C-norepine phrine in the mouse brain (16). The present investigation is consistent with the suggestion that brain catecholamines play a role in the mechanism by which morphine and related narcotic analgesics increase the locomotor activity of mice (1,2,17,18).…”

Section: Resultssupporting

confidence: 89%

Effect of Humoral Modulators on Morphine-induced Increase in Locomotor Activity of Mice

Oka

Hosoya

1976

Japanese Journal of Pharmacology

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Abstract-The effect of humoral modulators on the morphine-induced increase in locomotor activity of mice was studied. The subcutaneous administration of 10 mg/kg of morphine-HC1 produced a marked increase in locomotor activity in mice. The morphine-induced hyperactivity was potentiated by scopolamine and attenuated by physostigmine.In contrast, both methscopolamine and neostigmine, which do not penetrate the blood-brain barrier, had no effect on the hyperactivity produced by morphine.Pretreatment of mice with a-methyltyrosine (20 mg/kg i.p., one hour), an inhibitor of tyrosine hydroxylase, significantly decreased the activity-increasing effects of morphine.On the other hand, pretreatment with p-chlorophenylalamine (3 x 320 mg/kg i.p., 24 hr), a serotonin depletor, caused no significant change in the hyperactivity.The study suggests that the activity-increasing effects of morphine are mediated by the release of catecholamines from adrenergic neurons in the brain. And the results are consistent with the hypothesis that morphine acts by retarding the release of acetylcholine at some central cholinergic synapses. It is also suggested from col lected evidence that the activity-increasing effects of morphine in mice are mediated by mechanisms different from those which mediate the activity-increasing effects of morphine in rats.It is well known that morphine has a different effect on locomotor activity in mice and rats. In mice, an increase in running activity is produced by a wide range of doses of mor phine (1, 2). In contrast, only small amounts of morphine induce an increase in locomotor activity in rats whereas with moderate doses, a dual action on locomotor is observed; initial depression followed by stimulation (3,4,5). With repeated administration of the narcotic, tolerance to an increase in motor activity develops as readily as tolerance to the analgesic effect in mice (1, 6, 7) whereas such does not develop in rats (3,8). On the other hand, tolerance to a decrease in locomotor activity of rats by morphine is easily developed (5, 9). Accordingly, morphine induces a prominent increase in locomotor activity in morphine tolerant rats even with high doses. Thus, morphine seems to produce three quantitatively different stimulant effects on locomotor activity in rodents.A marked increase in locomotor activity in morphine-tolerant rats by morphine was significantly inhibited by cholinergic blocking drugs (8,10). An increase in motor activity in nontolerant rats induced by small amounts of morphine was also suppressed by anti cholinergics or a-MT (4). On the other hand, a prominent increase in locomotor activity * Present address:

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Section: Resultssupporting

confidence: 89%

Effect of Humoral Modulators on Morphine-induced Increase in Locomotor Activity of Mice

Oka

Hosoya

1976

Japanese Journal of Pharmacology

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“…An enhancement was seen with propranolol plus pentobarbital, however. Estler (1973) found that the excitation produced by morphine in mice was not blocked by propranolol but it was blocked by the ereceptor blocking drug, phenoxybenzamine. Evidence that the increase in motor activity seen after ETOH is mediated by catecholamines is furnished by the finding that ~-methyl-p-tyrosine inhibits ETOHinduced stimulation of SLMA (Carlsson et al, 1972).…”

Section: Discussionmentioning

confidence: 97%

Alteration of ethanol-induced changes in locomotor activity by adrenergic blockers in mice

Matchett

Erickson

1977

Psychopharmacology

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The effects of various doses of ethanol (ETOH) on spontaneous locomotor activity (SLMA) in mice were measured using photocell activity chambers. Of the 4 i.p. doses injected, the 2 lowest doses (0.5 and 1.0 g/kg) stimulated SLMA, the next higher dose (2.0 g/kg) produced a biphasic effect of depression followed by stimulation, and the highest dose (4.0 g/kg) depressed SLMA. The mechanism of the biphasic effect of the 2.0 g/kg dose was studied in tests with central catecholamine antagonists at various doses 30 min before ETOH. Doses of 5, 10, and 20 mg/kg of propranolol, a beta-receptor blocker, significantly antagonized the depressant effect of ETOH but had no influence on the stimulant effect. High doses (10 and 20 mg/kg) of phentolamine, an alpha-receptor blocker, significantly antagonized the stimulant phase of ETOH action but had no significant effect on the depressant phase. All doses (0.062-0.250 mg/kg) of spiroperidol, a dopaminergic blocking drug, significantly enhanced the SLMA depression produced by ETOH. These results indicate that the SLMA-depressant effect of ETOH may be mediated by central "beta-type" receptors, that the SLMA-stimulant effect of ETOH may be mediated by central "alpha-type" receptors, and that at least part of ETOH's action may be due to dopaminergic mechanisms.

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“…Moreover, pretreatment with FLA-63, a DBH inhibitor, reduces morphine-induced locomotion in rats (Ayhan and Randrup, 1973). In addition, the a-adrenergic antagonist, phenoxybenzamine, decreases the locomotion induced by morphine in mice (Estler, 1973) and rats (Ayhan and Randrup, 1973). Recent research has identified noradrenergic receptors within the PFC as being particularly important in subserving the locomotor effects of morphine.…”

Section: Ne and Opiate-induced Locomotion/sensitizationmentioning

confidence: 99%

There and Back Again: A Tale of Norepinephrine and Drug Addiction

Weinshenker

Schroeder

2006

Neuropsychopharmacol

323

277

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Fueled by anatomical, electrophysiological, and pharmacological analyses of endogenous brain reward systems, norepinephrine (NE) was identified as a key mediator of both natural and drug-induced reward in the late 1960s and early 1970s. However, reward experiments from the mid-1970s that could distinguish between the noradrenergic and dopaminergic systems resulted in the prevailing view that dopamine (DA) was the primary 'reward transmitter' (a belief holding some sway still today), thereby pushing NE into the background. Most damaging to the NE hypothesis of reward were studies demonstrating that NE receptor antagonists and NE reuptake inhibitors failed to impact drug self-administration. In recent years new tools, such as genetically engineered mice, and new experimental paradigms, such as reinstatement of drug seeking following withdrawal, have propelled NE back into the awareness of addiction researchers. Of particular interest is disulfiram, an inhibitor of the NE biosynthetic enzyme dopamine b-hydroxylase, which has demonstrated promising efficacy in the treatment of cocaine dependence in preliminary clinical trials. The purpose of this review is to synthesize the new data linking NE to critical aspects of DA signaling and drug addiction, with a focus on psychostimulants (eg, cocaine), opiates (eg, morphine), and alcohol.

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Effect of ?- and ?-adrenergic blocking agents and para-chlorophenylalanine on morphine- and caffeine-stimulated locomotor activity of mice

Cited by 34 publications

References 23 publications

Effect of Humoral Modulators on Morphine-induced Increase in Locomotor Activity of Mice

Effect of Humoral Modulators on Morphine-induced Increase in Locomotor Activity of Mice

Alteration of ethanol-induced changes in locomotor activity by adrenergic blockers in mice

There and Back Again: A Tale of Norepinephrine and Drug Addiction

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