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Inhibition by anandamide of gap junctions and intercellular calcium signalling in striatal astrocytes

  • Author(s): Venance, L
  • Piomelli, D
  • Glowinski, J
  • Glaume, C
  • et al.

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https://doi.org/10.1038/376590a0Creative Commons Attribution 4.0 International Public License
Abstract

Anandamide, an endogenous arachidonic acid derivative that is released from neurons and activates cannabinoid receptors1, may act as a transcellular cannabimimetic messenger in the central nervous system2-4. The biological actions of anandamide and the identity of its target cells are, however, still poorly documented5. Here we show that anandamide is a potent inhibitor of gap-junction conductance and dye permeability in striatal astrocytes. This inhibitory effect is specific for anandamide as compared to co-released congeners4or structural analogues, is sensitive to pertussis toxin and to protein-alkylating agents, and is neither mimicked by cannabinoid-receptor agonists nor prevented by a cannabinoid-receptor antagonist. Glutamate released from neurons evokes calcium waves in astrocytes6that propagate via gap junctions7-9, and may, in turn, activate neurons distant from their initiation sites in astrocytes10-12. We find that anandamide blocks the propagation of astrocyte calcium waves generated by either mechanical stimulation or local glutamate application. Thus, by regulating gap-junction permeability, anandamide may control intercellular communication in astrocytes and therefore neuron-glial interactions. © 1995, Nature Publishing Group. All Rights Reserved.

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