PUBLICATION

Glycinergic transmission and postsynaptic activation of CaMKII are required for glycine receptor clustering in vivo

Authors
Yamanaka, I., Miki, M., Asakawa, K., Kawakami, K., Oda, Y., and Hirata, H.
ID
ZDB-PUB-130201-11
Date
2013
Source
Genes to cells : devoted to molecular & cellular mechanisms   18(3): 211-224 (Journal)
Registered Authors
Hirata, Hiromi, Kawakami, Koichi, Oda, Yoichi
Keywords
none
MeSH Terms
  • Animals
  • Calcium Channel Blockers/pharmacology
  • Calcium Channels, L-Type/drug effects
  • Calcium Channels, L-Type/metabolism
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2/antagonists & inhibitors
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism*
  • Glycine/metabolism*
  • Neurons/metabolism
  • Receptors, Glycine/antagonists & inhibitors
  • Receptors, Glycine/metabolism*
  • Rhombencephalon/cytology
  • Rhombencephalon/growth & development
  • Strychnine/pharmacology
  • Synapses/drug effects
  • Synapses/metabolism
  • Synapses/ultrastructure
  • Synaptic Transmission*/drug effects
  • Zebrafish/metabolism
PubMed
23347046 Full text @ Genes Cells
Abstract

Synaptic transmission-dependent regulation of neurotransmitter receptor accumulation at postsynaptic sites underlies the formation, maintenance and maturation of synaptic function. Previous in vitro studies showed that glycine receptor (GlyR) clustering requires synaptic inputs. However, in vivo GlyR regulation by synaptic transmission is not fully understood. Here, we established a model system using developing zebrafish, in which GlyRs are expressed in Mauthner cells (M-cells), a pair of giant, reticulospinal, hindbrain neurons, thereby enabling analysis of GlyR clusters over time in identifiable cells. Bath application of a glycinergic blocker, strychnine, to developing zebrafish prevented postsynaptic GlyR cluster formation in the M-cells. After strychnine removal, the GlyR clusters appeared in the M-cells. At a later stage, glycinergic transmission blockade impaired maintenance of GlyR clusters. We also found that pharmacological blockade of either L-type Ca2+ channels or calcium-/calmodulin-dependent protein kinase II (CaMKII) disturbed GlyR clustering. In addition, the M-cell-specific CaMKII inactivation using the Gal4-UAS system significantly impaired GlyR clustering in the M-cells. Thus, the formation and maintenance of GlyR clusters in the M-cells in the developing animals are regulated in a synaptic transmission-dependent manner, and CaMKII activation at the postsynapse is essential for GlyR clustering. This is the first demonstration of synaptic transmission-dependent modulation of synaptic GlyRs in vivo.

Genes / Markers
Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes