Deficiency in transmitter release triggers homeostatic transcriptional changes that increase presynaptic excitability
成果类型：
Article
署名作者：
Cypranowska, Caroline A.; Feldthouse, Maya; Choi, Yoon Gi; Bakshinska, Dariya; Li, Rachel; Newman, Zachary L.; Isacoff, Ehud Y.
署名单位：
University of California System; University of California Berkeley; University of California System; University of California Berkeley; University of California System; University of California Berkeley; University of California System; University of California Berkeley; University of California System; University of California Berkeley; United States Department of Energy (DOE); Lawrence Berkeley National Laboratory; Francis Crick Institute; University of California System; University of California San Diego; University of Minnesota System; University of Minnesota Twin Cities
刊物名称：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
ISSN/ISSBN：
0027-14748
DOI：
10.1073/pnas.2322714122
发表日期：
2025-08-05
关键词：
hyperkinetic beta-subunit
neurotransmitter release
drosophila-melanogaster
synaptic-transmission
binding-protein
gene-expression
active zone
slowpoke channel
central neurons
inactivation
摘要：
Weakening of synaptic transmission at the Drosophila larval neuromuscular junction triggers two forms of homeostatic compensation, one that increases the probability of glutamate release per action potential (Pr) and another that increases motoneuron (MN) activity. We investigated the molecular changes in MNs that underlie the increase in MN activity. RNA sequencing (RNA-seq) analysis on MNs whose glutamate release is weakened by knockdown of components of the MN transmitter release machinery reveals a reduction in expression of a group of genes that encode potassium channels and their positive modulators. These results identify a mechanism of compensation for weakened synaptic transmission by MNs, which engages a transcriptional program in those cells to increase firing and, thereby, ensure sufficient locomotory drive.