التفاصيل البيبلوغرافية
| العنوان: |
Suppression of Presynaptic Glutamate Release by Postsynaptic Metabotropic NMDA Receptor Signalling to Pannexin-1. |
| المؤلفون: |
Bialecki, Jennifer, Werner, Allison, Weilinger, Nicholas L., Tucker, Catharine M., Vecchiarelli, Haley A., Egaña, Jon, Mendizabal-Zubiaga, Juan, Grandes, Pedro, Hill, Matthew N., Thompson, Roger J. |
| المصدر: |
Journal of Neuroscience; 1/22/2020, Vol. 40 Issue 4, p729-742, 14p |
| مصطلحات موضوعية: |
TRPV cation channels, GLUTAMATE receptors, METHYL aspartate receptors, GLUTAMIC acid, IMMUNOELECTRON microscopy, NEURAL transmission |
| مستخلص: |
The impact of pannexin-1 (Panxl) channels on synaptic transmission is poorly understood. Here, we show that selective block of Panxl in single postsynaptic hippocampal CA1 neurons from male rat or mouse brain slices causes intermittent, seconds long increases in the frequency of sEPSC following Schaffer collateral stimulation. The increase in sEPSC frequency occurred without an effect on evoked neurotransmission. Consistent with a presynaptic origin of the augmented glutamate release, the increased sEPSC frequency was prevented by bath-applied EGTA-AM or TTX. Manipulation of a previously described metabotropic NMDAR pathway (i.e., by preventing ligand binding to NMDARs with competitive antagonists or blocking downstream Src kinase) also increased sEPSC frequency similar to that seen when Panxl was blocked. This facilitated glutamate release was absent in transient receptor potential vanilloid 1 (TRPV1) KO mice and prevented by the TRPV1 antagonist, capsazepine, suggesting it required presynaptic TRPV1. We show presynaptic expression of TRPV1 by immunoelectron microscopy and link TRPV1 to Panxl because Panxl block increases tissue levels of the endovanilloid, anandamide. Together, these findings demonstrate an unexpected role for metabotropic NMDARs and postsynaptic Panxl in suppression of facilitated glutamate neurotransmission. [ABSTRACT FROM AUTHOR] |
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