Gjd2b-mediated gap junctions promote glutamatergic synapse formation and dendritic elaboration in Purkinje neurons.
Elife
; 102021 08 04.
Article
em En
| MEDLINE
| ID: mdl-34346310
ABSTRACT
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.
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Base de dados:
MEDLINE
Assunto principal:
Células de Purkinje
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Sinapses
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Peixe-Zebra
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Junções Comunicantes
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Conexinas
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Proteínas de Peixe-Zebra
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Proteínas do Olho
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Plasticidade Neuronal
Limite:
Animals
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article