Gjd2b-mediated gap junctions promote glutamatergic synapse formation and dendritic elaboration in Purkinje neurons

eLife

Vatsala Thirumalai¹  Meha Jadhav¹  Shaista Jabeen¹  Sahana Sitaraman¹  Shivangi Verma¹  Vandana Agarwal¹  Gnaneshwar Yadav¹ 

[1] National Centre for Biological Sciences, Tata Institute of Fundamental Research, Bangalore, India;

关键词: Cx35;    Cx36;    electrical synapse;    cerebellum;    zebrafish;    synaptogenesis;    Zebrafish;   

DOI  :  10.7554/eLife.68124

来源: eLife Sciences Publications, Ltd

【 摘 要 】

Gap junctions between neurons serve as electrical synapses, in addition to conducting metabolites and signaling molecules. During development, early-appearing gap junctions are thought to prefigure chemical synapses, which appear much later. We present evidence for this idea at a central, glutamatergic synapse and provide some mechanistic insights. Loss or reduction in the levels of the gap junction protein Gjd2b decreased the frequency of glutamatergic miniature excitatory postsynaptic currents (mEPSCs) in cerebellar Purkinje neurons (PNs) in larval zebrafish. Ultrastructural analysis in the molecular layer showed decreased synapse density. Further, mEPSCs had faster kinetics and larger amplitudes in mutant PNs, consistent with their stunted dendritic arbors. Time-lapse microscopy in wild-type and mutant PNs reveals that Gjd2b puncta promote the elongation of branches and that CaMKII may be a critical mediator of this process. These results demonstrate that Gjd2b-mediated gap junctions regulate glutamatergic synapse formation and dendritic elaboration in PNs.

【 授权许可】

CC BY