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Protein kinase Cγ is a signaling molecule required for the developmental speeding of α‐amino‐3‐hydroxyl‐5‐methyl‐4‐isoxazole‐propionate receptor kinetics
Author(s) -
Patten Shunmoogum A.,
Roy Birbickram,
Cunningham Marcus E.,
Stafford James L.,
Ali Declan W.
Publication year - 2010
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2010.07216.x
Subject(s) - ampa receptor , microbiology and biotechnology , biology , chemistry , receptor , glutamate receptor , biochemistry
A key step in the maturation of glutamate synapses is the developmental speeding of α‐amino‐3‐hydroxyl‐5‐methyl‐4‐isoxazole‐propionate receptor (AMPA‐R) kinetics, which occurs via a switch in receptor subtypes. However, the molecular components required for the switch in receptors are unknown. Here, we used the zebrafish preparation to show that activation of protein kinase C (PKC)γ is necessary for the developmental speeding of AMPA‐R kinetics. Targeted knockdown of PKCγ with an antisense morpholino oligonucleotide [PKCγ‐morpholino (PKCγ‐MO)], prevents the normal speeding up of AMPA‐R kinetics in Mauthner cells. PKCγ‐MO‐injected embryos are incapable of trafficking AMPA‐Rs following application of phorbol 12‐myristate 13‐acetate or PKCγ. PKCγ‐MO‐injected embryos do not hatch or exhibit the C‐start escape response. Increasing synaptic activity (33 h post‐fertilization embryos) by application of an elevated K + medium or by application of N ‐methyl‐ d ‐aspartate induces rapid PKCγ‐dependent trafficking of fast AMPA‐Rs to synapses. Our findings reveal that PKCγ is a molecular link underlying the developmental speeding of AMPA‐Rs in zebrafish Mauthner cells.