期刊
MOLECULAR AND CELLULAR NEUROSCIENCE
卷 31, 期 3, 页码 481-492出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2005.11.002
关键词
inhibitory; homeostatic plasticity; mIPSC; TrkB; NMDA receptor; AMPA receptor
资金
- NINDS NIH HHS [R01 NS040337-06, R01 NS044370, R01 NS040337, F31 NS 43831, R01 NS 44370, R01 NS044370-03, F31 NS043831-01, F31 NS043831, R01 NS 040337] Funding Source: Medline
The homeostatic plasticity hypothesis suggests that neuronal activity scales synaptic strength. This study analyzed effects of activity deprivation on GABAergic synapses in cultured hippocampal neurons using patch clamp electrophysiology to record mIPSCs and immunocytochemistry to visualize presynaptic GAD-65 and the gamma 2 subunit of the GABA(A) receptor. When neural activity was blocked for 48 h with tetrodotoxin (TTX, 1 mu M), the amplitude of mIPSCs was reduced, corresponding with diminished sizes of GAD-65 puncta and gamma 2 clusters. Treatment with the NMDA receptor antagonist APV (50 mu M) or the AMPA receptor antagonist DNQX (20 mu M) mimicked these effects, and co-application of brain-derived neurotrophic factor (BDNF, 100 ng/mL) overcame them. Moreover, when neurons were treated with BDNF alone for 48 h, these effects were reversed via the TrkB receptor. Overall, these results suggest that activity-dependent scaling of inhibitory synaptic strength can be modulated by BDNF/TrkB-mediated signaling. (c) 2005 Elsevier Inc. All rights reserved.
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