scholarly journals Opioid-Mediated Astrocyte–Neuron Signaling in the Nucleus Accumbens

Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 586 ◽  
Author(s):  
Michelle Corkrum ◽  
Patrick E. Rothwell ◽  
Mark J. Thomas ◽  
Paulo Kofuji ◽  
Alfonso Araque

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 μ-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 μ-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 μ-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.

2012 ◽  
Vol 235 (2) ◽  
pp. 189-194 ◽  
Author(s):  
M. Morales-Mulia ◽  
E. Estrada-Camarena ◽  
M.I. Amaya ◽  
S. Mejía-Mauríes ◽  
I. Sollozo-Dupont ◽  
...  

2000 ◽  
Vol 20 (24) ◽  
pp. 9333-9340 ◽  
Author(s):  
Alexis C. Thompson ◽  
Agustin Zapata ◽  
Joseph B. Justice ◽  
Roxanne A. Vaughan ◽  
Lawrence G. Sharpe ◽  
...  

Epigenomics ◽  
2016 ◽  
Vol 8 (12) ◽  
pp. 1583-1599 ◽  
Author(s):  
Claudia Knothe ◽  
Bruno G Oertel ◽  
Alfred Ultsch ◽  
Mattias Kettner ◽  
Peter Harald Schmidt ◽  
...  

1994 ◽  
Vol 24 (1-4) ◽  
pp. 347-352 ◽  
Author(s):  
Takeshi Houtani ◽  
Teizo Ueyama ◽  
Hiroshi Takeshima ◽  
Shigehisa Kato ◽  
Kazuhiko Fukuda ◽  
...  

Nature ◽  
2020 ◽  
Vol 584 (7820) ◽  
pp. E16-E16
Author(s):  
Weijiao Huang ◽  
Aashish Manglik ◽  
A. J. Venkatakrishnan ◽  
Toon Laeremans ◽  
Evan N. Feinberg ◽  
...  

2002 ◽  
Vol 88 (3) ◽  
pp. 1407-1419 ◽  
Author(s):  
L. Barakat ◽  
A. Bordey

Although glial GABA uptake and release have been studied in vitro, GABA transporters (GATs) have not been characterized in glia in slices. Whole cell patch-clamp recordings were obtained from Bergmann glia in rat cerebellar slices to characterize carrier-mediated GABA influx and efflux. GABA induced inward currents at −70 mV that could be pharmacologically separated into GABAA receptor and GAT currents. In the presence of GABAA/B/C receptor blockers, mean GABA-induced currents measured −48 pA at −70 mV, were inwardly rectifying between −70 and +50 mV, were inhibited by external Na+ removal, and were diminished by reduction of external Cl−. Nontransportable blockers of GAT-1 (SKF89976-A and NNC-711) and a transportable blocker of all the GAT subtypes (nipecotic acid) reversibly reduced GABA-induced transport currents by 68 and 100%, respectively. A blocker of BGT-1 (betaine) had no effect. SKF89976-A and NNC-711 also suppressed baseline inward currents that likely result from tonic GAT activation by background GABA. The substrate agonists, nipecotic acid and β-alanine but not betaine, induced voltage- and Na+-dependent currents. With Na+ and GABA inside the patch pipette or intracellular GABA perfusion during the recording, SKF89976-A blocked baseline outward currents that activated at −60 mV and increased with more depolarized potentials. This carrier-mediated GABA efflux induced a local accumulation of extracellular GABA detected by GABAA receptor activation on the recorded cell. Overall, these results indicate that Bergmann glia express GAT-1 that are activated by ambient GABA. In addition, GAT-1 in glia can work in reverse and release sufficient GABA to activate nearby GABA receptors.


Neuroscience ◽  
2019 ◽  
Vol 408 ◽  
pp. 400-417 ◽  
Author(s):  
Allison M. Cleymaet ◽  
Shannon K. Gallagher ◽  
Ryan E. Tooker ◽  
Mikhail Y. Lipin ◽  
Jordan M. Renna ◽  
...  

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