Different opioid systems may participate in post-electro-convulsive shock (ECS) analgesia and catalepsy

Urca, Gideon; Yitzhaky, Jacob; Frenk, Hanan

doi:10.1016/0006-8993(81)90301-2

Cited by 58 publications

(25 citation statements)

References 27 publications

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“…Whether ECS affects enkephalin release or turnover has not been determined. However, there is indirect evidence for the release of opioid peptides from central neurons after a single ECS treatment; for example, naloxone, an opiate-receptor antagonist, partially blocks several ECSelicited actions, including post-ictal analgesia (23,24), retrograde amnesia (25), and electroencephalographic changes (26). In a possibly related paradigm studied by us and others, treatment of rats with haloperidol, a dopamine-receptor antagonist that increases striatal [Met]enkephalin content, release, and turnover, was shown to increase the striatal preproenkephalin mRNA abundance (7,8).…”

Section: Resultsmentioning

confidence: 99%

Electroconvulsive shock increases preproenkephalin messenger RNA abundance in rat hypothalamus.

Yoshikawa¹,

Hong²,

Sabol³

1985

Proc. Natl. Acad. Sci. U.S.A.

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Daily administration of electroconvulsive shock (ECS) to rats for 10 days increased the content of [Mete]enkephalin in the hypothalamus and the striatum by 64% and 45%, respectively. The effect of ECS on the relative abundance of mRNA coding for the enkephalin precursor preproenkephalin was investigated. Analysis by cell-free translation of polyadenylylated RNA and immunoprecipitation of preproenkephalin revealed ECS-elicited increases of 79% and 14% in preproenkephalin mRNA activity in the hypothalamus and striatum, respectively. ECS treatment did not affect the general translational activity of total polyadenylylated RNA from these brain regions. A 2P-labeled probe prepared from a rat preproenkephalin cDNA clone hybridized with an apparently single species of polyadenylylated RNA of -'1450 nucleotides from both hypothalamus and striatum. Dot-blot hybridization of polyadenylylated RNA with the rat probe indicated that ECS elicits a 76% increase in the preproenkephalin mRNA abundance in the hypothalamus and no significant change in the striatum. These results suggest that ECS treatment leads to enhanced biosynthesis of the enkephalin precursor in hypothalamic neurons.Opioid peptides of the proenkephalin system are widely distributed throughout the nervous system and are believed to play important roles in modulating a variety of neuronal functions. These peptides, which include [Met5]enkephalin (Tyr-Gly-Gly-Phe-Met), [Leu5]enkephalin (Tyr-Gly-GlyPhe-Leu), [Met]enkephalin-Arg6-Phe7, [Met]enkephalinArg6-Gly7-Leu8, and [Met]enkephalin-Arg6-Arg7-Val'-NH2, are generated by processing the primary gene product preproenkephalin (preproenkephalin A) (1-4). Little is known about the factors that regulate enkephalin biosynthesis in enkephalinergic neurons.Hong et al. (5) reported that daily treatment of rats with electroconvulsive shock (ECS) for 6-10 days elicits a delayed and sustained increase in the levels of [Met]enkephalin in specific brain regions, most markedly in the hypothalamus (100% increase), with smaller increases (40-60%) in the striatum, nucleus accumbens, septum, and amygdala. In contrast, ECS does not affect the hypothalamic content of ,-endorphin, an opioid peptide derived from the precursor procorticotropin-,B-endorphin. The temporal characteristics of the [Met]enkephalin increase resembled those of the antidepressive action of electroconvulsive therapy in man. It has not been determined whether the increased enkephalin content is due to an enhancement of proenkephalin biosynthesis or to an inhibition of enkephalin secretion, transport, or degradation.A change in the cellular concentration of preproenkephalin mRNA may indicate a corresponding change in the rate of biosynthesis of proenkephalin and derived peptides. Detection of preproenkephalin mRNA is now possible either by cell-free translation of poly(A)+ RNA followed by immunoprecipitation of synthesized preproenkephalin (6, 7) or by blot hybridization of poly(A)+ RNA with a preproenkephalin cDNA probe (8). In the present study, we have empl...

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Section: Resultsmentioning

confidence: 99%

Electroconvulsive shock increases preproenkephalin messenger RNA abundance in rat hypothalamus.

Yoshikawa¹,

Hong²,

Sabol³

1985

Proc. Natl. Acad. Sci. U.S.A.

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“…Focal penicillin seizures, on the other hand, were similarly inhibited by morphine and naloxone (Spillantini and Masotti, 1986). Naloxone did not influence the threshold of seizures (Corcoran and Wada, 1979), but reversed the postictal inhibition (Kelsey and Belluzzi, 1982) during kindling experiments, pointing to the possible role of opiate receptors in postictal phenomena (Urca et al, 1981).…”

Section: Introductionmentioning

confidence: 82%

Naltrexone potentiates 4-aminopyridine seizures in the rat

Mihály

Bencsik

Solymosi

1990

J. Neural Transmission

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The effects of a pharmacological blockade of the mu opiate receptors on the manifestation of tonic-clonic seizures were investigated in freely moving animals. 4-aminopyridine, a specific blocker of the neuronal K+ channels was used to produce generalized convulsions. After pretreatment of adult rats with 1 mg/kg naltrexone HCl, 3, 5, 7, 9, 14 mg/kg 4-aminopyridine was injected intraperitoneally, and the latencies of the symptoms generated by 4-aminopyridine were measured. Naltrexone HCl decreased these latencies and enhanced the seizures significantly. The experiments provided further evidence for the existence of a tonic anticonvulsant opioid system in the brain.

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“…A more prolonged ECS treatment (e.g. lasting for 2 s) produces catalepsy accompanied by a loss in the righting reflex (for about 5 min) as first reported by Holaday and Belenky (1980) and since confirmed by a number of other workers (Urca et al, 1981;Frenk and Stein, 1984;Furui et al, 1986;Lason et al, 1987). Similar cataleptic effects are produced by high doses of morphine and by central administration of &endorphin and dynorphin (Fog, 1970;Bloom et al, 1976; al., 1977; Herman et a/., 1980).…”

Section: Behavioural Evidencementioning

confidence: 67%

“…Moreover, Urca et a/. have themselves reported strain differences between the antinociceptive effects of ECS in rats (Urca et al, 1981(Urca et al, , 1983. This is an important consideration which should be taken into account in future studies.…”

Section: Behavioural Evidencementioning

confidence: 95%

Does electroconvulsive shock therapy work through opioid mechanisms?

Jackson¹,

Nutt²

1990

Human Psychopharmacology

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It is now well-established that electroconvulsive shock (ECS) is the most effective treatment for severe depression. Over the past two decades a great deal of new information has been obtained regarding its neuropharmacological basis. The present review examines evidence that the behavioural and mood-elevating actions of ECS are mediated through changes in the function of opioid receptors or their endogenous transmitters. The recent discovery of stable, non-peptide ligands for the K-and &receptor subtypes are detailed, and the prospects for a new phase of research in this area are expounded.

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Different opioid systems may participate in post-electro-convulsive shock (ECS) analgesia and catalepsy

Cited by 58 publications

References 27 publications

Electroconvulsive shock increases preproenkephalin messenger RNA abundance in rat hypothalamus.

Electroconvulsive shock increases preproenkephalin messenger RNA abundance in rat hypothalamus.

Naltrexone potentiates 4-aminopyridine seizures in the rat

Does electroconvulsive shock therapy work through opioid mechanisms?

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