Acetylcholinesterase activity in the pons and medulla oblongata of rats after chronic electroconvulsive shock

Abstract

An imbalance between cholinergic and noradrenergic neurotransmission has been proposed for the etiology of affective disorders. According to this hypothesis, depression would be the result of enhanced cholinergic and reduced noradrenergic neurotransmission. Repeated electroconvulsive shock (ECS) is an effective treatment for depression; moreover, in laboratory animals it induces changes in brain noradrenergic neurotransmission similar to those obtained by chronic treatment with antidepressant drugs (down-regulation of beta-adrenergic receptors). The aim of the present study was to determine whether repeated ECS in rats changes acetylcholinesterase (Achase) activity. Achase controls the level of acetylcholine (Ach) in the synaptic cleft and its levels seem to be regulated by the interaction between Ach and its receptor. Thus, a decrease in Achase activity would suggest decreased cholinergic activity. Adult male Wistar rats received one ECS (80 mA, 0.2 s, 60 Hz) daily for 7 days. Control rats were handled in the same way without receiving the shock. Rats were sacrificed 24 h after the last ECS and membrane-bound and soluble Achase activity was assayed in homogenates obtained from the pons and medulla oblongata. A statistically significant decrease in membrane-bound Achase activity (nmol thiocholine formed min -1 mg protein -1 ) (control 182.6 ± 14.8, ECS 162.2 ± 14.2, P<0.05) and an increase in soluble Achase activity in the medulla oblongata (control 133.6 ± 4.2, ECS 145.8 ± 12.3, P<0.05) were observed. No statistical differences were observed in Achase activity in the pons. Although repeated ECS induced a decrease in membrane-bound Achase activity, the lack of changes in the pons (control Achase activity: total 231.0 ± 34.5, membrane-bound 298.9 ± 18.5, soluble 203.9 ± 30.9), the region where the locus coeruleus, the main noradrenergic nucleus, is located, does not seem to favor the existence of an interaction between cholinergic and noradrenergic neurotransmission after ECS treatment. Key wordsElectroconvulsive shock (ECS) is a classical antidepressive treatment (1) and its therapeutical effect is observed after repeated sessions. The time span between the onset of treatment and the improvement in mood seems to be related to adaptive biochemical changes that occur in the brain. In laboratory animals, repeated ECS treatment induces changes in noradrenergic neurotransmission which are similar to those produced by chronic antidepressant drugs, including down-regulation of beta-adrenergic receptors and reduced synthesis of cyclic adenosine monophosphate (cAMP) induced by

Acetylcholinesterase inhibitors for electroconvulsive therapy‐induced cognitive side effects: a systematic review

“…With regard to the cholinergic system, previous studies examined postictal brains in rats and revealed a decrease in the number of muscarinic binding sites without compensatory increase in the affinity of the ligand for this receptor. Also, significant reductions in acetylcholine levels and an increased activity of the enzyme choline acetyltransferase directly after ECT were seen (Longoni et al ., ; Camarini and Benedito, ). These pathophysiological findings support the hypothesis that acetylcholine is involved in cognitive side effects induced by ECT.…”