Electroconvulsive shock differentially increases binding to alpha-1 adrenergic receptor subtypes in discrete regions of rat brain

Julie A. Blendy, Linda J. Grimm, David C. Perry, Lisa West-Johnsrud, Kenneth J. Kellar*

*Corresponding author for this work

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Quantitative in vitro autoradiographic methods were used to examine for the effect of repeated administration of electroconvulsive shock (ECS) on binding to subtypes of the α-1 receptor in rat brain. Rats were treated once daily for 10 d with ECS or sham ECS, then killed, and brains were removed and sectioned for autoradiographic analysis. Total α-1 binding (including both α-1a and α-1b subtypes) was assessed with [3H]prazosin; α-1b binding was assessed with [3H]prazosin in the presence of 10 nM WB4101 to mask α-1a binding; and α-1a binding was assessed with [3H]WB4101. ECS caused a significant increase in [3H]prazosin binding in most cortical regions; this increase was confined to a band corresponding to cortical laminae I-III. Subtype analysis indicated that the increase in cortical binding was due to an increase in binding to the α-1b subtype. Dense α-1 binding was detected in most thalamic nuclei; however, only 1 small area, the parafascicular nucleus, showed a significant increase in α-1 binding following repeated ECS. The only other region where ECS was shown to significantly affect α-1 binding was the amygdala. Binding to all regions of the amygdala except the central nuclei was increased by ECS; in the lateral amygdala, this was due primarily to an increase in α-1b binding, while in the remaining regions the increase was primarily an α-1a phenomenon. Thus the effect of repeated ECS on α-1 binding in rat brain was found to be confined to several specific regions of the cortex, thalamus, and amygdala. Furthermore, in each of these regions, the ECS effect was limited to 1 or the other of the 2 subtypes of the α-1 receptor.

Original languageEnglish
Pages (from-to)2580-2586
Number of pages7
JournalJournal of Neuroscience
Volume10
Issue number8
DOIs
Publication statusPublished - 1 Aug 1990
Externally publishedYes

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