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

• Published in: The Journal of neuroscience Vol. 10; no. 8; pp. 2580 - 2586
• Main Authors: Blendy, JA, Grimm, LJ, Perry, DC, West-Johnsrud, L, Kellar, KJ
• Format: Journal Article
• Language: English
• Published: Washington, DC Soc Neuroscience 01-08-1990; Society for Neuroscience
• Subjects: Adrenergic alpha-Antagonists; Animals; Autoradiography; Biological and medical sciences; Brain - metabolism; Central nervous system; Central neurotransmission. Neuromudulation. Pathways and receptors; Dioxanes - metabolism; Dioxanes - pharmacology; Electroshock; Fundamental and applied biological sciences. Psychology; Male; Osmolar Concentration; Prazosin - antagonists & inhibitors; Prazosin - metabolism; Rats; Rats, Inbred Strains; Receptors, Adrenergic, alpha - metabolism; Reference Values; Tissue Distribution; Vertebrates: nervous system and sense organs; Cartography; Brain; Molecular form; Rat; Electrical stimulus; Rodentia; Central nervous system; Binding site; Autoradiography; Vertebrata; Mammalia; Convulsion; α1-»Adrenergic receptor; α-Adrenergic receptor
• ISSN: 0270-6474; 1529-2401
• DOI: 10.1523/jneurosci.10-08-02580.1990

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 alpha-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 alpha-1 binding (including both alpha-1a and alpha-1b subtypes) was assessed with [3H]prazosin; alpha-1b binding was assessed with [3H]prazosin in the presence of 10 nM WB4 101 to mask alpha-1a binding; and alpha-1a binding was assessed with [3H]WB4 101. 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 alpha-1b subtype. Dense alpha-1 binding was detected in most thalamic nuclei: however, only 1 small area, the parafascicular nucleus, showed a significant increase in alpha-1 binding following repeated ECS. The only other region where ECS was shown to significantly affect alpha-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 alpha-1b binding, while in the remaining regions the increase was primarily an alpha-1a phenomenon. Thus the effect of repeated ECS on alpha-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 alpha-1 receptor.