Repeated electroconvulsive shock attenuates clonidine-induced hypoactivity in rodents

Heal, David J.; Akagi, Hiroko; Bowdler, Julie M.; Green, A.Richard

doi:10.1016/0014-2999(81)90549-5

Cited by 106 publications

(40 citation statements)

References 14 publications

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“…The present findings are in general agreement with previous results, in so far as repeated administration of DMI or ECS has been shown to decrease presynaptic X2-adrenoceptor function (Tang et al, 1979;McMillen et al, 1980;Heal et al, 1981;1987a;Sugrue, 1983) and cortical f-adrenoceptor number (Bergstrom & Kellar, 1979a, b;Sellinger-Barnette et al, 1980;Asakura et al, 1982;Sugrue, 1982;1983;Stanford & Nutt, 1982;Stanford et al, 1983). Moreover, chronic ECS has previously been demonstrated to reduce cortical a2-adrenoceptors (Pilc & Vetulani, 1982;Stanford & Nutt, 1982;Heal et al, 1987a).…”

Section: Discussionsupporting

confidence: 93%

“…Since the behavioural parameters assessed by the method of Drew et al (1979) are specifically CX2-adrenoceptor-mediated (Drew et al, 1979;Heal et al, 1981) and are not induced by other sedative agents, such as pentobarbitone or diazepam (Heal et al, 1981), this strongly suggests a difference in central aC2-adrenoceptor function between male and female rats. This is unlikely to result from a generalised increase in activity in females because Heal et al (1987b) have shown that the parameters scored by the method of Drew et al (1979) were not influenced by increased locomotor activity after apomorphine injection (Heal et al, 1987b).…”

Section: Discussionmentioning

confidence: 99%

“…This behaviour was rated 0-3 on 4 separate parameters (passivity, tactile responsiveness, posture and gait) by an observer who was unaware of the treatment received by the animals. This protocol is based on the method described by Drew et al (1979) and is fully described by Heal et al (1981).…”

Section: Methods Animalsmentioning

confidence: 99%

“…However, presynaptic x2-adrenoceptor func-1 Author for correspondence. tion is also decreased by repeated administration of desipramine (DMI;Tang et al, 1979;McMillen et al, 1980;Sugrue, 1983;Heal et al, 1983;1987a) and ECS (Heal et al, 1981;1987a;Sugrue, 1983). Several groups have also shown that postsynaptic a2-adrenoceptors are decreased by repeated ECS (Stanford & Nutt, 1982;Pilc & Vetulani, 1982;Heal et al, 1987a), but the effect of chronic DMI treatment is much more controversial (Johnson et al,function which are produced by DMI and ECS treatment are markedly influenced by the circulating levels of oestradiol (Bristow et al, 1986;Heal et al, 1988) and the thyroid hormone, triiodothyronine (T3; Heal et al, 1987a).…”

Section: Introductionmentioning

confidence: 99%

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Sex‐related differences in central adrenergic function and responsiveness to repeated administration of desipramine or electroconvulsive shock

Heal

Bristow

Hurst

et al. 1989

British J Pharmacology

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1 Clonidine induces hypoactivity in rodents. Male rats were found to be markedly more susceptible to the sedative effects of this a2-adrenoceptor agonist than females. Thus to obtain identical hypoactivity responses for subsequent experiments, clonidine was administered to male and female rats at doses of 0.2 and 0.5 mg kg-1, respectively. 2 The clonidine-induced hypoactivity response of female rats was not affected by the oestrous cycle. 3 Repeated injection of desipramine (DMI; 5mg kg-1 b.d.) for up to 14 days progressively attenuated clonidine-induced hypoactivity in both male and female rats. However, in males the attenuation was more rapid in onset and a greater overall reduction was obtained. This a2-adrenoceptor-mediated response was also progressively reversed by repeated daily administration of an electroconvulsive shock (ECS; 110 V, 1 s). In this case, although the maximum decrease was greater in males, the time of onset was identical in both sexes.4 There were no sex-related differences in either the number or affinity of a2-and ,B-adrenoceptors in rat cortex. Cortical a2-adrenoceptors were decreased by 14 days of DMI injection or 10 days of ECS treatment (ECS x 10) and these effects were identical in both sexes. These receptors were not altered by 2 days administration of DMI or ECS. Cortical fi-adrenoceptors were reduced in male and female rats by 2 and 14 days of DMI injection and by ECS x 10, but not ECS x 2. 5 Viewed overall, the data show differences in a2-adrenoceptor function between the sexes, as determined by clonidine-induced hypoactivity and the responsiveness of this paradigm to repeated administration of DMI and ECS. In contrast, no differences were observed in complementary a2-and /-adrenoceptor binding experiments using rat cortical tissue.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Methods Animalsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Sex‐related differences in central adrenergic function and responsiveness to repeated administration of desipramine or electroconvulsive shock

Heal

Bristow

Hurst

et al. 1989

British J Pharmacology

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“…The effects of chronic ECS on a-adrenoceptors are less clearly defined, but point to a downregulation of a2-receptors (Bergstrom et al, 1979;Stanford et al, 1982). Behavioural data are also consistent with downregulation (Heal et al, 1981;Pilc et al, 1984). The fact that ECS decreases both P-and a2-adrenoceptor number and function suggests the possibility that brain NA processes are a common site of antidepressant action.…”

Section: Introductionmentioning

confidence: 96%

Effects of acute and chronic electroconvulsive shock on noradrenaline release in the rat hippocampus and frontal cortex

Thomas

Nutt

Holman

1992

British J Pharmacology

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Changes in the extracellular content of endogenous noradrenaline (NA) in frontal cortex and hippocampus were determined by in vivo microdialysis following acute and chronic electroconvulsive shock (ECS) in rats anaesthetized with chloral hydrate. Basal release of NA in the frontal cortex (4.9 ± 0.3 pg/sample) did not differ significantly from that in the hippocampus (4.6 ± 0.2 pg/sample). A single ECS resulted in an increase of NA release in the hippocampus (21.1 ± 1.3 pg/sample) and in the frontal cortex (11.6 ± 1.2 pg/sample). In both brain regions extracellular NA had returned to basal values within 30 min. Animals were treated chronically with ECS (once per day for seven days). Twenty‐four h later (day 8), basal release of NA into dialysis samples from the frontal cortex was significantly increased (50%) as compared to chronic sham controls. Basal release in the hippocampus was not significantly different from the sham controls. In the chronic ECS animals the increase in NA released in both brain areas following an ECS on day 8 did not differ from either the chronic sham controls or from animals given acute ECS. Animals were challenged 24 h after eight ECS or sham control treatments (once per day) with the α2‐adrenoceptor antagonist, idazoxan (10 mg kg−1, s.c). Idazoxan increased NA release in the hippocampus in both groups. There was no difference in the magnitude of the response in ECS‐ and in sham‐treated rats. In the frontal cortex, idazoxan increased the extracellular NA content in the chronic sham controls, but the response to idazoxan was significantly attenuated in the chronic ECS animals. Chronic but not acute ECS was found to elicit a sustained (> 24 h) increase in the release of NA in the frontal cortex, but not in the hippocampus. The idazoxan data suggest that the increase may be due to a downregulation of presynaptic α2‐adrenoceptors in the frontal cortex. The difference in response of these two brain regions to chronic ECS is discussed in terms of differences in the regulation of extracellular NA content by uptake and autoreceptor activation.

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Clinical and Biochemical Effects of Catecholamine Depletion on Antidepressant-Induced Remission of Depression

Miller

Delgado²,

Salomon³

et al. 1996

Arch Gen Psychiatry

170

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The therapeutic effects of norepinephrine reuptake inhibitors, but not serotonin reuptake inhibitors, are reversed by catecholamine depletion. Considered with previous reports that serotonin depletion produces depressive relapses in patients in remission maintained with serotonin reuptake inhibitors, but not norepinephrine reuptake inhibitors, these findings suggest that antidepressants may not work via a single monoamine-related mechanism.

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Repeated electroconvulsive shock attenuates clonidine-induced hypoactivity in rodents

Cited by 106 publications

References 14 publications

Sex‐related differences in central adrenergic function and responsiveness to repeated administration of desipramine or electroconvulsive shock

Sex‐related differences in central adrenergic function and responsiveness to repeated administration of desipramine or electroconvulsive shock

Effects of acute and chronic electroconvulsive shock on noradrenaline release in the rat hippocampus and frontal cortex

Clinical and Biochemical Effects of Catecholamine Depletion on Antidepressant-Induced Remission of Depression

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