Adolescent ethanol intake alters cannabinoid type‐1 receptor localization in astrocytes of the adult mouse hippocampus

Cannabinoid type‐1 (CB1) receptors are widely distributed in the brain and play important roles in astrocyte function and the modulation of neuronal synaptic transmission and plasticity. However, it is currently unknown how CB1 receptor expression in astrocytes is affected by long‐term exposure to s...

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Published in:Addiction biology Vol. 24; no. 2; pp. 182 - 192
Main Authors: Bonilla‐Del Rίo, Itziar, Puente, Nagore, Peñasco, Sara, Rico, Irantzu, Gutiérrez‐Rodrίguez, Ana, Elezgarai, Izaskun, Ramos, Almudena, Reguero, Leire, Gerrikagoitia, Inmaculada, Christie, Brian R., Nahirney, Patrick, Grandes, Pedro
Format: Journal Article
Language:English
Published: United States John Wiley & Sons, Inc 01-03-2019
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Summary:Cannabinoid type‐1 (CB1) receptors are widely distributed in the brain and play important roles in astrocyte function and the modulation of neuronal synaptic transmission and plasticity. However, it is currently unknown how CB1 receptor expression in astrocytes is affected by long‐term exposure to stressors. Here we examined CB1 receptors in astrocytes of ethanol (EtOH)‐exposed adolescent mice to determine its effect on CB1 receptor localization and density in adult brain. 4–8‐week‐old male mice were exposed to 20 percent EtOH over a period of 4 weeks, and receptor localization was examined after 4 weeks in the hippocampal CA1 stratum radiatum by pre‐embedding immunoelectron microscopy. Our results revealed a significant reduction in CB1 receptor immunoparticles in astrocytic processes of EtOH‐exposed mice when compared with controls (positive astrocyte elements: 21.50 ± 2.80 percent versus 37.22 ± 3.12 percent, respectively), as well as a reduction in particle density (0.24 ± 0.02 versus 0.35 ± 0.02 particles/μm). The majority of CB1 receptor metal particles were in the range of 400–1200 nm from synaptic terminals in both control and EtOH. Altogether, the decrease in the CB1 receptor expression in hippocampal astrocytes of adult mice exposed to EtOH during adolescence reveals a long lasting effect of EtOH on astrocytic CB1 receptors. This deficiency may also have negative consequences for synaptic function. CB1 receptors on GFAP‐immunoreactive astrocytes in the CA1 stratum radiatum of adult mice were significantly reduced following EtOH exposure during adolescence. However, the CB1 receptor expression on inhibitory synaptic terminals remained unchanged. The low concentration of CB1 receptor immunogold particles on excitatory synaptic terminals in the adult CA1 stratum radiatum also decreased after adolescent EtOH exposure.
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ISSN:1355-6215
1369-1600
DOI:10.1111/adb.12585