Enkephalins interfere with acquisition of an active avoidance response

Rigter, Henk; Hanna, Tracy J.; Messing, Rita B.; Martinez, Joe L.; Vasquez, Beatriz J.; Jensen, Robert A.; Veliquette, John; McGaugh, James L.

doi:10.1016/0024-3205(80)90149-6

Cited by 83 publications

(21 citation statements)

References 13 publications

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“…Studies by Izquierdo et al (1980) and Rigter et al (1980) have provided evidence suggesting that endorphins and enkephalins can cause impairment of memory storage, and the opiate-mediated inhibition of hippocampal acetylcholine might play a role in this phenomenon considering the known importance of cholinergic influences on cognitive function (Bartus et al, 1982). Our results indicated that dynorphin A (1-13) acts at K-receptors in the rat hippocampus and/or frontal cortex modulating acetylcholine release when cholinergic neurotransmission is depressed.…”

Section: Resultsmentioning

confidence: 56%

Improvement by dynorphin A (1–13) of galanin‐induced impairment of memory accompanied by blockade of reductions in acetylcholine release in rats

Hiramatsu

Mori

Murasawa

et al. 1996

British J Pharmacology

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1 Human galanin (0.32 nmol per rat, i.c.v.), an endogenous neuropeptide, administered 30 min before acquisition or retention trials, significantly impaired the acquisition of learning and recall of memory in a step-through type passive avoidance performance. 2 The role of dynorphin A (1 -13) in learning and memory is controversial. Dynorphin A (1-13) (0.5 nmol per rat, i.c.v.) administered 5 min before galanin injection, completely antagonized these impairments. 3 Galanin significantly decreased acetylcholine release in the hippocampus 40 to 120 min after injection as determined by in vivo brain microdialysis. This peptide also decreased acetylcholine release, albeit to a lesser extent, from the frontal cortex. 4 Dynorphin A (1-13) (0.5 nmol per rat, i.c.v.) 5 min before galanin injection, completely blocked the decrease in extracellular acetylcholine concentration induced by galanin. 5 These antagonistic effects of dynorphin A (1-13) were abolished by treatment with norbinaltorphimine (5.44 nmol per rat, i.c.v.), a selective K-opioid receptor antagonist, 5 min before dynorphin A (1-13). 6 Dynorphin A (1-13) (0.5 nmol) itself had no effect on learning and memory and on the acetylcholine concentration in the hippocampus or the frontal cortex in normal rats. 7 These results suggest that the neuropeptide dynorphin A (1-13) ameliorates the galanin-induced impairment of learning and memory accompanied by abolition of reductions in acetylcholine release via K-opioid receptors.

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Section: Resultsmentioning

confidence: 56%

Improvement by dynorphin A (1–13) of galanin‐induced impairment of memory accompanied by blockade of reductions in acetylcholine release in rats

Hiramatsu

Mori

Murasawa

et al. 1996

British J Pharmacology

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“…Such findings have led to the speculation that opiate-sensitive mechanisms within the amygdala may provide a common substrate for the effects of opiates on memory processes and regulation of emotional states including fear (6). On the other hand, peripherally administered opioid peptides have been reported to affect both acquisition and consolidation of avoidance responses (7)(8)(9). Such effects are time dependent, suggesting that these peptides acted to alter some aspect of learning and memory processes.…”

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confidence: 99%

Opiates and classical conditioning: selective abolition of conditioned responses by activation of opiate receptors within the central nervous system.

Mauk¹,

Madden²,

Barchas³

et al. 1982

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

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It has previously been shown that opiates produce selective abolition of aversively motivated classically conditioned responses in the rabbit. The experiments reported here show that these effects are mediated by specific activation of opiate receptors within the central nervous system in that this central activation is both necessary and sufficient to produce opiate-induced abolition of conditioned responding. Further characterization suggests that selective activation through opiate-si-receptor interactions within the periaqueductal gray/periventricular region of the fourth ventricle may be critical in mediating this abolition.In recent literature, it is suggested that opiate-sensitive processes are involved in the modulation of various aspects of learning and memory formation (1-3). Among these reports are findings that microadministration of opiate agonists into the amygdala complex can alter the retention of passive-avoidance conditioning and the acquisition of fear-motivated conditioned heart-rate responses (4, 5). Such findings have led to the speculation that opiate-sensitive mechanisms within the amygdala may provide a common substrate for the effects of opiates on memory processes and regulation of emotional states including fear (6). On the other hand, peripherally administered opioid peptides have been reported to affect both acquisition and consolidation of avoidance responses (7-9). Such effects are time dependent, suggesting that these peptides acted to alter some aspect of learning and memory processes. Moreover, these effects occur at doses that indicate that the primary site of action may be in the peripheral rather than the central nervous system.We have recently reported that intravenous (i.v.) administration ofmorphine produces complete and naloxone-reversible abolition of a simple aversively motivated learned responsethe classically conditioned eyelid/nictitating membrane (NM) response in the rabbit (10). Morphine has no effect on performance of the unconditioned reflex response nor on tone-conditioned stimulus-evoked neuronal activity in the primary auditory pathway. Further, the conditioned response (CR) is selectively abolished on the trial immediately following morphine injection, before the animal has experienced the next aversive unconditioned stimulus (US). It would appear that morphine is acting selectively and possibly directly on the associative process-that is, some as yet to be localized portion of the neural circuitry that is essential for the expression of the learned response.As a first step in the localization and characterization of the opiate-sensitive process in question, we felt that it is necessary to determine the relative contributions ofperipheral and central opiate-sensitive sites in the mediation of the opiate-induced abolition of aversively motivated conditioned responding. To this end, we report a series of experiments in which we determined the relative effects of both systemic and central administration ofseveral opiate agonists and antagonists on the ...

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“…For example, the endogenous opioid peptide LE, when administered to a variety of species in a multitude of tasks, most frequently impairs learning (Rigter et al 1980a(Rigter et al , 1980b 0893-133X/94/$7.00 al. 1980; Izquierdo and Dias 1981;Martinez et al 1981Martinez et al , 1984Martinez et al , 1985aMartinez et al , 1985bMartinez et al , 1988Martinez et al , 1990Martinez and Rigter 1982;Introini et al 1985;Dana and Martinez 1986;Lin den and Martinez 1986;Schulteis et al 1988Pat terson et al 1989;Janak and Martinez 1990;Sandi et al 1990;Schulteis and Martinez 1992b).…”

mentioning

confidence: 99%

“…[Leu]enkepha lin impairs active avoidance acquisition in mice (Marti nez et al 1985b;Dana and Martinez 1986;Janak and Martinez 1990) and in rats (Rigter et al 1980a(Rigter et al , 1980bMartinez and Rigter 1982;Mar tinez et al 1985a). …”

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confidence: 99%

“…For example, al though ME is reported to impair acquisition (Rigter et al 1980a) and retention (Introini et al 1985;Izquierdo and Dias 1981) of avoidance conditioning in rats and mice, other reports indicate that ME enhances acquisi tion of Y-maze (Martinez et al 1984) and complex maze (Kastin et al 1976) learning and delays extinction of a pole-jump response (de Wied et al 1978) in rats.…”

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confidence: 99%

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[Leu]Enkephalin Enhances Active Avoidance Conditioning in Rats and Mice

Janak

Manly

Martinez

1994

Neuropsychopharmacol

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The effects of intraperitoneal (IP) administration of the endogenous opioid peptide, [Leu1enkephalin (LE), on avoidance conditioning in rodents were investigated. At a dose of 30 /lglkg (IP), LE enhanced acquisition of a one-way step-through active avoidance response when administered 2 minutes before training to Swiss Webster mice. [Leu1enkephalin produced aU-shaped dose-response function because both lower and higher doses of LE did not affect avoidance responding. fLeu1enkephalin-induced enhancement of avoidance ac quisition was also observed in Sprague-Dawley rats; the intraperitoneal injection of 10 /lglkg LE, administered 5 minutes before training, enhanced acquisition of a tinez et al. 1991a;Koob 1987;Gold 1989;McGaugh 1989). Two of these defming characteristics are that 1) the dose-response functions produced by modulatory substances are V-shaped, rather than hyperbolic, and 2) each modulatory substance has the ability to either

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Enkephalins interfere with acquisition of an active avoidance response

Cited by 83 publications

References 13 publications

Improvement by dynorphin A (1–13) of galanin‐induced impairment of memory accompanied by blockade of reductions in acetylcholine release in rats

Improvement by dynorphin A (1–13) of galanin‐induced impairment of memory accompanied by blockade of reductions in acetylcholine release in rats

Opiates and classical conditioning: selective abolition of conditioned responses by activation of opiate receptors within the central nervous system.

[Leu]Enkephalin Enhances Active Avoidance Conditioning in Rats and Mice

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