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Biomedical subjects

E L Way

Publications and source records attributed to E L Way.

At least 109 records · Page 6Linked to original sources
PubMed1977

Behavioral interactions between naloxone and dopamine agonists.

A fixed-interval schedule of food presentation was used to study the effects of apomorphine, ET-495 and clonidine and interactions between these drugs and naloxone in the rat. The rate of responding under this schedule was decreased by low doses of apomorphine (0.03--0.3 mg/kg), ET-495 (0.3-1.0 mg/kg) and clonidine (0.03--0.3 mg/kg). Naloxone, at a dose (3 mg/kg) which did not itself alter responding, potentiated the rate decreasing effects of apomorphine and ET-495 but did not alter the effects of clonidine. It is suggested that the rate decreasing effects of low doses of apomorphine and ET-495 may be related to presynaptic inhibition of dopamine neurons and that under certain circumstances naloxone may also inhibit dopaminergic activity.

Animals↗
PubMed1977

Comparison of the effects of morphine on locomotor activity, analgesia and primary and protracted physical dependence in six mouse strains.

Mice of the DBA/2J, A/J, C3H, C57BL/L, ICR and Swiss strains were studied with respect to acute and chronic morphine administration. The acute administration of morphine resulted in a dose-dependent running response in C57BL/6, C3H, ICR and Swiss strains, but no running response in DBA/2J and A/J strains. Strain differences in sensitivity to morphine-induced running activity did not parallel differences in sensitivity to morphine-induced running activity did not parallel differences in sensitivity to antinociception in the abdominal constriction test (r = 0.404), but significantly correlated with differences in the expression of physical dependence as measured by either precipitated (r = 0.957) or abrupt (r = 0.927) withdrawal jumping behavior in mice made dependent by morphine pellent implantation. Mortality for 3 days of pellet implantation ranged from 5% in ICR mice to 84% in A/J mice. Strain differences in degree of initial physical dependence. These results suggest the possibility that the running response and withdrawal jumping may involve at least part of the same neuronal pathway. This pathway may include dopamine-containing neurons which terminate in the neostriatum.

Analgesia↗
PubMed1976

Circling behavior in rats with 6-hydroxydopamine or electrolytic nigral lesions,.

Unilateral destruction of dopaminergic cell bodies in the substantia nigra zona compacta (SNC) was performed in rats using either electrocoagulation or chemical lesioning (6-hydroxydopamine, 6-OHDA). Neostriatal dopamine concentration ipsilateral to an electrolytic lesion was 34% of the contralateral side 2-3 weeks after operation; serotonin and noradrenaline brain levels were not altered. In contrast, dopamine and noradrenaline forebrain concentrations ipsilateral to a 6-OHDA lesion were 20 and 31%, respectively, of the contralateral side. After 6-OHDA, dopamine concentrations in the ipsilateral neostriatum were reduced to levels below the sensitivity of the fluorometric assay; cortical, brainstem and neostriatal serotonin levels, on the other hand, were not altered after 6-OHDA. Ipsilateral circling behavior was elicited by d-amphetamine after electrolytic and chemical lesioning. In contrast, the direction of circling produced after apomorphine differed between the two lesion models: contralateral circling behavior was exhibited by 6-OHDA-lesioned rats, whereas ipsilateral circling was produced in animals with electrolytic lesions. Contralateral circling was induced in both lesion-type models by haloperidol or pimozide. S.c. atropine administration induced ipsilateral circling in rats with 6-OHDA lesions, whereas contralateral circling was observed after arecoline. Animals with electrolytic SNC lesions turn ipsilaterally after s.c. administrations of either arecoline or atropine. The data indicate that the electrolytic and 6-OHDA circling behavior models represent two different neuropharmacological states and it is, therefore, suggested that comparisons of data obtained from models using different methods of lesioning be made with caution.

Animals↗
PubMed1976

Alterations in the efficacy of naloxone induced by stress, cyclic adenosine monophosphate, and morphine tolerance.

Pretreatment of mice with a single injection of morphine or by chronic implantation of morphine pellets increased the ability of naloxone to antagonize the analgetic effects of morphine. However, this increased effectiveness of naloxone was also produced by pretreatment with diethylether, ACTH, corticosterone or dexamethasone. Thus, the increased potency of naloxone observed after pretreatment with narcotics may be due, at least in part, to those pretreatments on the pituitary--adrenal axis. In addition, in animals made highly tolerant and dependent by cAMP administration during morphine pellet implantation, the narcotic antagonist potency of naloxone was similar to that of untreated animals.

Adrenocorticotropic Hormone↗
PubMed1976

Dopaminergic-cholinergic interactions in naloxone-induced circling in morphine-dependent rats with nigral lesions.

3-4 weeks after placement of a unilateral, electrolytic lesion of the substantia nigra zona compacta, rats were highly dependent on morphine by the s.c. morphine pellet implantation technique. Following challenge with a supramaximal naloxone dose of 20 mg/kg i.p., both continuous contralateral circling behavior and severe withdrawal signs in morphine-dependent, lesioned rats were elicited. After various drug pretreatments, the contralaeral circling behavior precipitated by naloxone was: (a) reversed to ipsilateral circling by i.p. apomorphine or d-amphetamine, (b) unaltered by i.p. haloperidol or intraneostriatal arecoline administered into the intact neostriatum, and (c) reversed to ipsilateral circling by the administration of atropine into the intact neostriatum. Atropine, apomorphine and amphetamine all interfered with the manifestation of naloxone-precipitated abstinence. These data suggest that a diminution of dopaminergic or an enhancement of cholinergic activities, or both, occur at the level of the neostriatum during naloxone-precipitated withdrawal in morphine-dependent rats.

Animals↗
PubMed1976

Morphine tolerance and physical dependence: influence of cholinergic agonists and antagonists.

The effects of centrally acting agents which alter cholinergic activity were assessed in mice rendered tolerant to and dependent on morphine (M mice) and in naive mice (N mice). In both N and M mice, physostigmine potentiated morphine analgesia slightly, and this action was blocked by atropine and scopolamine. When administered 10 min before naloxone in dependent mice atropine enhanced precipitated withdrawal jumping; when given 30 min before naloxone, atropine produced an inhibition of the response. Physostigmine abd oxotremorine greatly inhibited the jumping response, while echothiophate had no effect. The inhibitory effect of physostigmine on naloxone precipitated withdrawal jumpimg was reversed by atropine and scopolamine but atropine did not alter morphine tolerance and dependence development. Brain acetylcholine (ACh) levels in both N and M mice were increased by physostigmine, the increase being greater in M mice. This increase was blocked by prior administration of atropine or scopolamine. When atropine was administered to M mice 10 min before sacrifice, brain AC-h levels decreased. However, when brain ACh levels were determined 30 min after atropine, no change was found. It was concluded that ACh does not play a major direct role in the development of tolerance and dependence, but that ACh is involved in the manifestations of acute morphine effects and in some of the withdrawal signs in the dependent state.

Acetylcholine↗