Effect of single and repeated convulsions on glutamate decarboxylase (GAD) activity and [3H]muscimol binding in the rat brain

Atterwill, C.K.; Batts, C C; Bloomfield, M

doi:10.1111/j.2042-7158.1981.tb13793.x

Cited by 21 publications

(2 citation statements)

References 15 publications

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“…An investigation has therefore been made of the effect of repeated seizures on GABA release in regions ofrat brain and on the rate ofGABA synthesis in various brain regions, the latter study being designed to try to confirm and extend an earlier investigation (Green et al, 1978) by use of a different methodology. In addition a study has been made of the activity of glutamic acid decarboxylate activity in rat brain both in the absence and presence of added cofactor (pyridoxal 5-phosphate), following repeated ECS since there is one report that activity is increased following repeated seizures (Atterwill et al, 1981). Such a change although reportedly small (Atterwill et al, 1981) is difficult to reconcile with a decreased rate of GABA synthesis.…”

Section: Introductionmentioning

confidence: 99%

“…In addition a study has been made of the activity of glutamic acid decarboxylate activity in rat brain both in the absence and presence of added cofactor (pyridoxal 5-phosphate), following repeated ECS since there is one report that activity is increased following repeated seizures (Atterwill et al, 1981). Such a change although reportedly small (Atterwill et al, 1981) is difficult to reconcile with a decreased rate of GABA synthesis.…”

Section: Introductionmentioning

confidence: 99%

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The effect of repeated electroconvulsive shock on GABA synthesis and release in regions of rat brain

Green

Vincent

1987

British J Pharmacology

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1 The release of endogenous y-aminobutyric acid (GABA) from slices of rat cortex, hippocampus and striatum prepared both 30 min and 24 h after the last of a series of electroconvulsive shocks (5 seizures given spread out over 10 days) has been investigated. 2 No change in spontaneous (basal) release was observed. However, 30 min after the last convulsion, K+-evoked GABA release above basal release was inhibited in both hippocampus (20%) and striatum (33%) but not in the cortex. Release was still inhibited in striatum (22%) 24 h after the last seizure. 3 In confirmation of an earlier report, chronic electroconvulsive shock was found to increase basal GABA content in striatum and inhibit synthesis by 34%. The synthesis rate was also inhibited in the hippocampus (44%) but not in the cortex. 4 Glutamic acid decarboxylase activity was unchanged in all regions after repeated electroconvulsive shock treatment. 5 It is proposed that repeated electroconvulsive shocks lead to a substantial inhibition of release in the striatum and hippocampus and a long-term inhibition of GABA synthesis in these regions. Such changes may be associated with the altered monoamine biochemistry and function observed after repeated electroconvulsive shock and with the mechanism of the antidepressant action of electroconvulsive therapy.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The effect of repeated electroconvulsive shock on GABA synthesis and release in regions of rat brain

Green

Vincent

1987

British J Pharmacology

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Psychopharmacology of Repeated Seizures: Possible Relevance to the Mechanism of Action of Electroconvulsive Therapy

Green¹,

Nutt

1987

Handbook of Psychopharmacology

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Long lasting effect of a single audiogenic seizure on GABA turnover rates and steady-state levels

Clement¹,

Ciesielski²,

Simler

et al. 1989

Neurochem Res

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GABA turnover rates (TOR) and steady-state levels (SSL) were determined, 16-18 h after a single acoustic stimulation, in 15 brain areas of 3 mouse sublines. Each subline differs in its response to an acoustic stimulation (Rb1 mice are clonic-tonic seizure-prone, Rb2: clonic seizure-prone, Rb3: seizure-resistant). TOR and SSL were compared to those of unstimulated control mice and to those of repeatedly stimulated mice of the same subline. Following a single acoustic stimulation long-lasting alterations of GABA metabolism, mainly large alterations of GABA TOR, are observed. Most of the effects elicited after repeated stimulations, either on SSL or TOR, are not those of the last stimulation and repeated seizures (and/or stimulations) strengthen the effect of a single one. It appears that, for each of the Rb sublines, a specific and quite simple profile of the alterations of GABA metabolism in response to a single or repeated audiogenic seizures (and/or stimulations) can be given. The global analysis through the correlation of GABA TOR and SSL gives an indication that the alterations of the parameters of the correlation observed are to be allocated to the audiogenic seizures. Furthermore the tonic and clonic components of the audiogenic seizures can be distinguished.

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Effect of single and repeated convulsions on glutamate decarboxylase (GAD) activity and [3H]muscimol binding in the rat brain

Cited by 21 publications

References 15 publications

The effect of repeated electroconvulsive shock on GABA synthesis and release in regions of rat brain

The effect of repeated electroconvulsive shock on GABA synthesis and release in regions of rat brain

Psychopharmacology of Repeated Seizures: Possible Relevance to the Mechanism of Action of Electroconvulsive Therapy

Long lasting effect of a single audiogenic seizure on GABA turnover rates and steady-state levels

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