An Animal Model of Electroconvulsive‐Therapy‐Induced Amnesia

Lerer, Bernard; Stanley, Michael; Altman, Harvey J.; Keegan, Michael

doi:10.1111/j.1749-6632.1986.tb51243.x

Cited by 9 publications

(4 citation statements)

References 9 publications

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“…It has been postulated from rodent studies that cumulative changes in DA, NA and 5HT function within limbic structures underly the therapeutic effect of ECT (Grahame-Smith; Green and Costain, 1978;Green and Nutt, 1987;Orzi et al, 1987) and that alterations in cholinergic function underly ECT-induced amnesia (Lerer et al, 1986). Limbic (particularly hippocampal) dysfunction is thought to underly the ECT-induced (reversible) amnestic syndrome (Squire, 1986), and it is known that these struc-tures are most vulnerable to seizure activity (Inglis 1970;Siesjo, Ingvar and Wieloch, 1986;Evans and Meldrum, 1984).…”

Section: Discussionmentioning

confidence: 99%

“…In addition to the cumulative (but reversible) effect of ECT and chronic ECS on memory, (Squire, 1986;Reichert et al, 1976;Lerer et al, 1986), ECT/ECS is associated with a short-term period of post-ictal confusion (in common with spontaneous seizures, Trimble and Thompson, 1986). We hypothesize that sub-convulsive seizure activity in hippocampal and limbic structures underlies post-ECT/ECS confusion, and that it is the degree of this short-term dysfunction, and cumulative number of such episodes in a given period of time, which determines the degree of amnesia and hippocampal dysfunction induced by multiple electroconvulsions.…”

Section: Discussionmentioning

confidence: 99%

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Local cerebral glucose utilization after chronic electroconvulsive shock: implications for the mode of action of electroconvulsive therapy

Lock

McCulloch

1991

J Psychopharmacol

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The [(14)C]2-deoxyglucose autoradiographic technique measures local rates of glucose utilization simul taneously in all functional and anatomical subunits of the CNS and provides a measure of the functional consequences in the CNS of any manipulation. Glucose utilization was measured in 24 regions of the CNS in conscious rats one day after the end of a 7-day course of electroconvulsive shock (chronic ECS). Chronic ECS had minimal effects on local glucose utilization in most brain areas (including extrapyramidal, cortical, hippocampal and other limbic structures) with only the nucleus accumbens displaying a significant alteration (reduced by 25% from sham-treated animals). These data suggest that functional alterations in the nucleus accumbens may underly a unique therapeutic mechanism of electroconvulsive therapy (ECT), which is known to be effective in a wide variety of psychiatric syndromes characterized by mixed depressive and 'positive' psychotic symptoms. Our findings (supported by preliminary data from a study of sub-convulsive ECS) suggest that the functional sequelae of repeated electroconvulsions in selectively vulnerable limbic and hippocampal structures-more likely to underly ECT's unwanted cognitive side effect than its wanted therapeutic effect-may be attenuated by reducing the power of the stimulus required to induce seizures.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Local cerebral glucose utilization after chronic electroconvulsive shock: implications for the mode of action of electroconvulsive therapy

Lock

McCulloch

1991

J Psychopharmacol

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“…Memory impairment induced by ECS was recently suggested to be related to ECS-induced muscarinic receptor subsensitivity (Lerer et al 1986), but the hypothesis is still premature and further studies are needed to determine whether a correlation exists between the severity of memory impairment and the degree of rnuscarinic receptor down regulation. The central cholinergic systems have been implicated in the mc~dulation of learning and memory (cf.…”

Section: Discussionmentioning

confidence: 99%

Interactions of cholecystokinin, β-endorphin, and their antagonists on passive avoidance behavior in rats

Itoh¹,

Katsuura²,

Takashima³

1987

Can. J. Physiol. Pharmacol.

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The effects of cholecystokinin octapeptide (CCK-8), cholecystokinin tetrapeptide amide (CCK-4), beta-endorphin, proglumide, and naloxone on passive avoidance behavior were studied in rats. Intracerebroventricular (i.c.v.) injection of beta-endorphin (1-10 micrograms) had no significant influence on the latency of the avoidance response in intact rats. Also, beta-endorphin (0.05-5 micrograms, i.c.v.) did not affect the response in rats treated with electroconvulsive shock (ECS). The preventive effect of CCK-8 (0.1-1.0 micrograms, i.c.v.) on ECS-induced amnesia was partly antagonized by beta-endorphin (0.05-10 micrograms, i.c.v.). Intraperitoneal (i.p.) injection of naloxone (1-10 mg/kg) could not prevent ECS-induced amnesia, but continuous subcutaneous infusion of this drug (2 mg/day, 7 days) completely abolished the amnesia. Naloxone (1 and 10 mg/kg, i.p.) also partly antagonized amnesia induced by proglumide (1 and 10 micrograms, i.c.v.) and prevented it when induced by CCK-4 (5 and 10 micrograms, i.c.v.). The results indicate the facilitating action of naloxone and the inhibitory effect of beta-endorphin on memory, suggesting that the endogenous opiate systems are involved in some way in the memory processes.

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“…Exactly how or why ECT is effective in such a wide range of psychiatric disorders remains unclear. Studies on animals using experimental paradigms mimicking a clinical course of treatment provide evidence of neurotransmitter receptor changes (upregulation and down-regulation), which are thought to underlie the therapeutic effects of ECT and cognitive side-effects ( Lever et al, 1986;Green & Nutt, 1987).A similar pattern of receptor alterations is seen with antidepressant drugs, and affects sero tonin and noradrenalin receptors in particular.…”

Section: Mode Of Action Of Ectmentioning

confidence: 99%

Advances in the practice of electroconvulsive therapy

Lock¹

1994

Adv. psychiatr. treat

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The first electroconvulsive treatment was administered by Cerletti and Bini in 1938. The event was essentially an experiment, carried out like a military operation (Endler, 1988). The patient was stimulated three times, each time increasing the intensity of the stimulus before a generalised seizure was induced. He had been suffering from an acute psychosis with a poor prognosis, but responded to a course of 11 treatments and was discharged free of symptoms two months later. The first paper on electroconvulsive therapy (ECT) in English was published in theLancet(Kalinowski) in 1939. At that time, somatic treatment alternatives for the severely ill in large mental institutions included lobotomy and insulin coma therapy. In comparison, unmodified ECT (albeit associated with a significant risk of serious physical morbidity) was predictable, efficient, quick and effective. It is understandable why the treatment became widely and fairly indiscriminately adopted before systematic objective evidence of its efficacy was collected.

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An Animal Model of Electroconvulsive‐Therapy‐Induced Amnesia

Cited by 9 publications

References 9 publications

Local cerebral glucose utilization after chronic electroconvulsive shock: implications for the mode of action of electroconvulsive therapy

Local cerebral glucose utilization after chronic electroconvulsive shock: implications for the mode of action of electroconvulsive therapy

Interactions of cholecystokinin, β-endorphin, and their antagonists on passive avoidance behavior in rats

Advances in the practice of electroconvulsive therapy

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