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

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Abstract
1 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. 2 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). 3 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. 4 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. 5 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. 6 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.