Prefrontal cortical distribution of muscarinic M2 and cannabinoid-1 (CB1) receptors in adult male mice with or without chronic adolescent exposure to Δ9-tetrahydrocannabinol.

Autor:	Garzón M; Departamento de Anatomía, Histología y Neurociencia, Facultad de Medicina UAM, 28029 Madrid, Spain.; Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, 407 East 61st Street, New York, NY 10065, USA., Chan J; Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, 407 East 61st Street, New York, NY 10065, USA., Mackie K; Linda and Jack Gill Center for Biomolecular Science, Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN 47405, USA., Pickel VM; Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, 407 East 61st Street, New York, NY 10065, USA.
Jazyk:	angličtina
Zdroj:	Cerebral cortex (New York, N.Y. : 1991) [Cereb Cortex] 2022 Nov 21; Vol. 32 (23), pp. 5420-5437.
DOI:	10.1093/cercor/bhac024
Abstrakt:	Chronic adolescent administration of marijuana's major psychoactive compound, ∆9-tetrahydrocannabinol (Δ9-THC), produces adaptive changes in adult social and cognitive functions sustained by prelimbic prefrontal cortex (PL-PFC). Memory and learning processes in PL-PFC neurons can be regulated through cholinergic muscarinic-2 receptors (M2R) and modulated by activation of cannabinoid-1 receptors (CB1Rs) targeted by Δ9-THC. Thus, chronic exposure to Δ9-THC during adolescence may alter the expression and/or distribution of M2Rs in PL-PFC neurons receiving CB1R terminals. We tested this hypothesis by using electron microscopic dual CB1R and M2R immunolabeling in adult C57BL/6 J male mice that had received vehicle or escalating dose of Δ9-THC through adolescence. In vehicle controls, CB1R immunolabeling was mainly localized to axonal profiles virtually devoid of M2R but often apposing M2R-immunoreactive dendrites and dendritic spines. The dendrites received inputs from CB1R-labeled or unlabeled terminals, whereas spines received asymmetric synapses exclusively from axon terminals lacking CB1Rs. Adolescent Δ9-THC significantly increased plasmalemmal M2R-immunogold density exclusively in large dendrites receiving input from CB1R-labeled terminals. In contrast, cytoplasmic M2R-immunogold density decreased in small spines of the Δ9-THC-treated adult mice. We conclude that Δ9-THC engagement of CB1Rs during adolescence increases M2R plasmalemmal accumulation in large proximal dendrites and decreases M2R cytoplasmic expression in small spines of PL-PFC. (© The Author(s) 2022. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
Databáze:	MEDLINE
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