Electroconvulsive shock treatment decreases β-adrenergic receptor sensitivity in rat brain

Pandey, Ghanshyam N.; Heinze, W; Brown, Barbara D.; Davis, John M.

doi:10.1038/280234a0

Cited by 171 publications

(32 citation statements)

References 12 publications

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“…In particular it has been shown that many different antidepressant treatments, including repeated electroconvulsive shock (ECS), reduce P-adrenoceptor binding in certain regions of rat brain (Bergstrom & Kellar, 1979;Pandey, Heinze, Brown & Davis, 1979;Sellinger-Barnette, Mendels & Frazer, 1980). The reduction in 1-adrenoceptor ligand binding is often, but not invariably (Mishra, Janowsky & Sulser, 1980), associated with a reduction in the responsiveness of noradrenaline-sensitive adenylate cyclase (Vetulani & Sulser, 1975;Wolfe, Harden, Sporn & Molinoff, 1978).…”

Section: Introductionmentioning

confidence: 99%

The effect of chronic antidepressant administration on β‐adrenoceptor function of the rat pineal

Cowen¹,

Fraser²,

Grahame‐Smith³

et al. 1983

British J Pharmacology

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1 The 1-adrenoceptor agonist, isoprenaline (1.5-3.0 mg kg-intravenously), produced a doserelated increase in rat pineal melatonin content. This increase was prevented by pretreatment with the selective PI-adrenoceptor antagonist, atenolol (2mgkg 1), but not by the P2-adrenoceptor antagonist, butoxamine (2 mg kg-1). The P2-adrenoceptor agonist, terbutaline (5.0mg kg-1), produced a moderate increase in pineal melatonin content. 2 Repeated daily administration of desmethylimipramine (10mg kg-for 10 days) and maprotiline (10mg kg-for 10 days), antidepressants predominantly inhibiting noradrenaline (NA) uptake, reduced the isoprenaline-induced increase in pineal melatonin content. Amitriptyline (20 mg kg-I for 14 days), a drug which inhibits both NA and 5-hydroxytryptamine (5-HT) uptake, had a similar effect. The P-adrenoceptor agonist, clenbuterol (5 mg kg-for 14 days), also attenuated the increase in pineal melatonin produced by isoprenaline. 3 In contrast, chronic administration of the selective 5-HT uptake inhibitor, fluoxetine (10mg kg-for 10 days), or the antidepressants, iprindole and mianserin (both 20mg kg1 for 14 days), which do not inhibit monoamine uptake, failed to reduce the increase in pineal melatonin following isoprenaline. Repeated electroconvulsive shock was similarly without effect. 4 Ten hours after the final dose of desmethylimipramine (10mg kg-1) once daily for 10 days there was no change in the usual dark phase increase in pineal melatonin. 5 The data suggest that repeated administration of certain antidepressant drugs results in reduced pineal P-adrenoceptor sensitivity. However the lack of change in the dark phase increase in pineal melatonin following repeated desmethylimipramine, implies that the reduced B-adrenoceptor sensitivity may be part of an adaptive process which maintains normal pineal function. Therefore the decrease in 1-adrenoceptor number in the brain reported after chronic antidepressant administration may not be associated with a change in overall synaptic function.

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Section: Introductionmentioning

confidence: 99%

The effect of chronic antidepressant administration on β‐adrenoceptor function of the rat pineal

Cowen¹,

Fraser²,

Grahame‐Smith³

et al. 1983

British J Pharmacology

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“…Accordingly, recent animal studies have assessed the effect on brain NA function of repeated daily administration of TCAs. Particular attention has been directed to changes in post-synaptic I-adrenoceptors since repeated administration of nearly all antidepressant treatments, including TCAs (Banerjee et al, 1977;Sellinger-Barnett et al, 1980), electroconvulsive shock (Pandey et al, 1979a) and monoamine oxidase inhibitors (Sellinger- Barnett et al, 1980), reduces the density of specific ,-adrenoceptor binding and/or the responsiveness of the associated NA-sensitive adenylate cyclase (Vetulani & Sulser, 1975;Sulser, 1979) in various brain regions. The consistency of these changes has led to the proposal that decreased 0-adrenoceptor synaptic function is responsible for the therapeutic effect of antidepressant treatment (Sulser, 1979).…”

Section: Introductionmentioning

confidence: 99%

Plasma melatonin during desmethylimipramine treatment: evidence for changes in noradrenergic transmission.

Cowen¹,

Green²,

Grahame‐Smith³

et al. 1985

Brit J Clinical Pharma

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Plasma melatonin was used to determine overall beta‐adrenergic transmission through pineal neuro‐effector junctions during desmethylimipramine (DMI) treatment in 10 normal subjects. Changes in plasma melatonin indicated that an initial increase in noradrenaline (NA) transmission produced by DMI was counteracted by adaptive changes which restored transmission to normal by the third week of treatment. A 'rebound' increase in NA transmission was seen on DMI withdrawal. The results suggest that the adaptive changes which occur in NA synapses during DMI treatment do not, as has been proposed, decrease NA transmission below normal levels, but instead restore homeostasis in the presence of the drug.

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“…However, ECS also increases dopamine-mediated behaviour (Modigh, 1975;Evans et al, 1976;Green et al, 1983b) and decreases P-adrenoceptor number (Pandey et al, 1979;Bergstrom & Kellar, 1979).…”

Section: Implicationsfor the Action Ofantidepressant Treatmentsmentioning

confidence: 99%

Some anticonvulsant drugs alter monoamine‐mediated behaviour in mice in ways similar to electroconvulsive shock; implications for antidepressant therapy

Green¹,

Johnson²,

Mountford³

et al. 1985

British J Pharmacology

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1 The effects in mice of administration of the anticonvulsants, progabide, sodium valproate, diazepam, carbamazepine and phenytoin on 5-hydroxytryptophan (5-HTP)-induced head-twitch, apomorphine-induced locomotion, clonidine-induced sedation, and P-adrenoceptor and 5-HT2 receptor number have been examined. 2 Repeated progabide administration (400 mg kg-', i.p. twice daily for 14 days) enhanced the headtwitch response the effect lasting for over 8 days after the last dose, and also increased 5-HT2 receptor number in frontal cortex. 3 Progabide (400 mg kg-', i.p.) enhanced the head-twitch response when given once daily for 10 days and when given intermittently (5 times over 10 days) but not after 1 day of administration. 4 Repeated Na valproate (400mg kg-',i.p.) also increased the 5-HTP-induced head-twitch response and 5-HT2 receptor number in the frontal cortex when given twice daily for 14 days, but no behavioural enhancement was seen after 10 days' treatment. 5 Diazepam (1.25 mg kg-', i.p.) twice daily for 14 days increased the head-twitch response and 5-HT2 receptor number. 6 Repeated progabide and valproate (but not diazepam) administration attenuated the sedation response to the a2-adrenoceptor agonist, clonidine (0.15mg kg-') but neither drug altered 1-adrenoceptor number in the cerebral cortex. 7 No changes in apomorphine-induced locomotor behaviour were seen after progabide, valproate or diazepam.8 Repeated carbamazepine (20 mg kg-') or phenytoin (40 mg kg-1) administration failed to alter any of the biochemical or behavioural parameters listed above. 9 Like repeated electroconvulsive shock (ECS), progabide altered the head-twitch response, clonidine-induced sedation response and 5-HT2 receptor number. Unlike repeated ECS, it did not alter P-adrenoceptor number or the apormorphine-induced locomotor response. These data suggest that ECS may produce some changes in monoamine function by altering GABA metabolism as has previously been postulated.

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Electroconvulsive shock treatment decreases β-adrenergic receptor sensitivity in rat brain

Cited by 171 publications

References 12 publications

The effect of chronic antidepressant administration on β‐adrenoceptor function of the rat pineal

The effect of chronic antidepressant administration on β‐adrenoceptor function of the rat pineal

Plasma melatonin during desmethylimipramine treatment: evidence for changes in noradrenergic transmission.

Some anticonvulsant drugs alter monoamine‐mediated behaviour in mice in ways similar to electroconvulsive shock; implications for antidepressant therapy

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