A sustained effect of electroconvulsive shock on the turnover of norepinephrine in the central nervous system of the rat.

Kety, Seymour S.; Javoy, F.; Thierry, Anne‐Marie; Julou, L; Głowiński, J.

doi:10.1073/pnas.58.3.1249

Cited by 137 publications

(19 citation statements)

References 15 publications

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“…Repetitive ECS treatment is known to produce a variety of delayed and persistent perturbations in central neurotransmitter systems, including increased norepinephrine content and turnover (27), decreased postsynaptic p-adrenergic receptor density (28), increased tyrosine hydroxylase protein and activity (29,30), increased serotonin content (27), and increased content of dynorphin [1][2][3][4][5][6][7][8] immunoreactivityt in specific brain regions. We expect that the elevated hypothalamic preproenkephalin mRNA abundance described here is only one of several ECS-produced alterations in specific mRNA levels.…”

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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“…43 for review). While ECS may increase (44) or decrease (12) LC activity, perhaps depending on stimulus intensity and the associated stress of the procedure, repeated ECS, like TCAs, consistently decreased NT-3 in the LC. Whether the decrease in NT-3 caused by TCAs and ECS is a consequence of a sustained decrease in LC firing rate, or some other factor remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

Stress and antidepressants differentially regulate neurotrophin 3 mRNA expression in the locus coeruleus.

Smith

Makino

Altemus

et al. 1995

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

101

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The mechanisms by which stress and antidepressants exert opposite effects on the course of clinical depression are not known. However, potential candidates might include neurotrophic factors that regulate the development, plasticity, and survival of neurons. To explore this hypothesis, we examined the effects of stress and antidepressants on neurotrophin expression in the locus coeruleus (LC), which modulates many of the behavioral and physiological responses to stress and has been implicated in mood disorders. Using in situ hybridization, we demonstrate that neurotrophin 3 (NT-3) is expressed in noradrenergic neurons of the LC. Recurrent, but not acute, immobilization stress increased NT-3 mRNA levels in the LC. In contrast, chronic treatment with antidepressants decreased NT-3 mRNA levels. The effect occurred in response to antidepressants that blocked norepinephrine uptake, whereas serotonin-specific reuptake inhibitors did not alter NT-3 levels. Electroconvulsive seizures also decreased NT-3 expression in the LC as well as the hippocampus. Ntrk3 (neurotrophic tyrosine kinase receptor type 3; formerly TrkC), the receptor for NT-3, is expressed in the LC, but its mRNA levels did not change with stress or antidepressant treatments. Because NT-3 is known to be trophic for LC neurons, our results raise the possibility that some of the effects of stress and antidepressants on LC function and plasticity could be mediated through NT-3. Moreover, the coexpression of NT-3 and its receptor in the LC suggests the potential for autocrine mechanisms of action.The behavioral and physiological responses to stress closely resemble the symptoms of clinical depression (1). Stress can precipitate episodes of depression (2), and chronic, uncontrollable stress has been proposed as a model of depression (3). How stress might exacerbate depression in vulnerable patients is not known. However, the locus coeruleus (LC), which plays a major role in behavioral arousal in response to novel or stressful stimuli (4), has long been a focus of investigation. Stress increases the firing rate of LC noradrenergic neurons as well as levels of norepinephrine (NE) and tyrosine hydroxylase (TH), the rate-limiting enzyme in the synthesis of catecholamines (5-9). As a consequence, chronic stress increases the magnitude of NE release in response to a novel stressor (10). In contrast, tricyclic antidepressants (TCAs) decrease LC firing (11) and TH mRNA and protein in the LC (12, 13). Pretreatment with imipramine for 18 days, but not 1 or 7 days, prevents the induction of TH in the LC by cold stress (14). Generally, both the therapeutic and neurochemical effects of antidepressants require several weeks to develop.The mechanisms underlying LC adaptation in response to stress and antidepressants are not presently known. However, a possible candidate for the regulation of LC plasticity might be a neurotrophic factor such as neurotrophin 3 (NT-3). This hypothesis is supported by a recent study demonstrating that enhances the survival of adult LC n...

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“…One explanation for the increase in NA after chronic ECS comes from studies in brain slices in which the synthesis and utilisation of NA has been shown to be increased (Kety, 1967;Modigh et al, 1976). This effect also lasted 24 h beyond the last treatment.…”

Section: Discussionmentioning

confidence: 99%

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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A sustained effect of electroconvulsive shock on the turnover of norepinephrine in the central nervous system of the rat.

Cited by 137 publications

References 15 publications

Electroconvulsive shock increases preproenkephalin messenger RNA abundance in rat hypothalamus.

Electroconvulsive shock increases preproenkephalin messenger RNA abundance in rat hypothalamus.

Stress and antidepressants differentially regulate neurotrophin 3 mRNA expression in the locus coeruleus.

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

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