Journal
CELLS
Volume 8, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/cells8060586
Keywords
astrocytes; opioids; synaptic transmission
Categories
Funding
- NIH-National Institute on Drug Abuse (NIDA) [1F30DA042510-01]
- NIH-National Institute of Neurological Disorders and Stroke (NINDS) [R01NS097312-01]
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Major hallmarks of astrocyte physiology are the elevation of intracellular calcium in response to neurotransmitters and the release of neuroactive substances (gliotransmitters) that modulate neuronal activity. While mu -opioid receptor expression has been identified in astrocytes of the nucleus accumbens, the functional consequences on astrocyte-neuron communication remains largely unknown. The present study has investigated the astrocyte responsiveness to mu -opioid signaling and the regulation of gliotransmission in the nucleus accumbens. Through the combination of calcium imaging and whole-cell patch clamp electrophysiology in brain slices, we have found that mu -opioid receptor activation in astrocytes elevates astrocyte cytoplasmic calcium and stimulates the release of the gliotransmitter glutamate, which evokes slow inward currents through the activation of neuronal N-methyl-D-aspartate (NMDA) receptors. These results indicate the existence of molecular mechanisms underlying opioid-mediated astrocyte-neuron signaling in the nucleus accumbens.
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