Synapsin I regulates glutamate release from rat brain synaptosomes.
Introduction of the dephosphorylated from of synapsin I into rat brain synaptosomes using freeze-thaw (transient) permeabilization significantly decreased the K(+)-induced release of glutamate. In contrast, introduction of synapsin I that had been phosphorylated by Ca2+/calmodulin-dependent protein kinase II was without effect on glutamate release. Addition of dephosphosynapsin I after freeze-thaw treatment also had no effect. Thus, the action of synapsin I was dependent on the phosphorylation state of synapsin I and on its entry into the synaptosomes. Our results implicate synapsin I as an important component in the regulation of neurotransmitter release in the mammalian nervous system.
Nichols
R A
RA
Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, New York 10021.
Chilcote
T J
TJ
Czernik
A J
AJ
Greengard
P
P
D000818:Animals; D001921:Brain / Q000378:metabolism*; D005470:Fluorometry / Q000379:methods; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D015759:Ionomycin / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D016704:Synapsins / Q000494:pharmacology*; D013574:Synaptosomes / Q000378:metabolism*
D005971:Glutamates; D016704:Synapsins; D018698:Glutamic Acid; D015759:Ionomycin; D011188:Potassium