التفاصيل البيبلوغرافية
| العنوان: |
Suppression of AMPA Receptor Exocytosis Contributes to Hippocampal LTD. |
| المؤلفون: |
Shumpei Fujii, Hiromitsu Tanaka, Tomoo Hirano |
| المصدر: |
Journal of Neuroscience; 6/13/2018, Vol. 38 Issue 24, p5523-5537, 15p |
| مصطلحات موضوعية: |
ENDOCYTOSIS, EXOCYTOSIS, HIPPOCAMPUS (Brain), IMAGING systems, NEUROPLASTICITY |
| مستخلص: |
The decrease in number of AMPA-type glutamate receptor (AMPAR) at excitatory synapses causes LTD, a cellular basis of learning and memory. The number of postsynaptic AMPARs is regulated by the balance of exocytosis and endocytosis, and enhanced endocytosis of AMPAR has been suggested to underlie the LTD expression. However, it remains unclear how endocytosis and exocytosis of AMPAR change during LTD. In this study, we addressed this question by analyzing exocytosis and endocytosis of AMPAR by imaging superecliptic pHlorin (SEP)-tagged AMPAR around postsynaptic structure formed directly on the glass surface in the hippocampal culture prepared from rat embryos of both sexes. Contrary to a prevailing view on the LTD expression by endocytosis enhancement, the LTD induction by NMDA application only transiently enhanced endocytosis of SEP-tagged GluAl subunits of AMPAR, which was counteracted by sim ultaneous augmentation of exocytosis. As a result, soon after the start of the LTD induction (~ 1 min), the surface AMPAR did not markedly decrease. Thereafter, the surface GluAl-SEP gradually decreased (2-5 min) and kept at a low level until the end of observation (>30 min). Surprisingly, this gradual and sustained decrease of surface AMPAR was accompanied not by the enhanced endocytic events of GluAl, but by the suppression of exocytosis. Together, our data highlight an unprecedented mechanism for the LTD expression by attenuation of exocytosis of AMPAR, but not by enhanced endocytosis, together with a reduction of postsynaptic AMPAR scaffolding protein PSD95. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
