Deficiency in transmitter release triggers homeostatic transcriptional changes that increase presynaptic excitability.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 40729383.
- Also identified by DOI 10.1073/pnas.2322714122 and PMC identifier 12337328.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Weakening of synaptic transmission at the <i>Drosophila</i> larval neuromuscular junction triggers two forms of homeostatic compensation, one that increases the probability of glutamate release per action potential (<i>P<sub>r</sub></i>) 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.
Medical subject headings
- Motor Neurons
- Homeostasis
- Synaptic Transmission
- Neurotransmitter Agents
- Presynaptic Terminals
- Transcription, Genetic