Premium
Doc2α is an activity‐dependent modulator of excitatory synaptic transmission
Author(s) -
Sakaguchi Gaku,
Manabe Toshiya,
Kobayashi Katsunori,
Orita Satoshi,
Sasaki Takuya,
Naito Akira,
Maeda Miki,
Igarashi Hisanaga,
Katsuura Goro,
Nishioka Hideo,
Mizoguchi Akira,
Itohara Shigeyoshi,
Takahashi Tomoyuki,
Takai Yoshimi
Publication year - 1999
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 - 10.1046/j.1460-9568.1999.00855.x
Subject(s) - neural facilitation , neurotransmission , excitatory postsynaptic potential , long term potentiation , neuroscience , synaptic fatigue , synaptic plasticity , facilitation , synaptic augmentation , hippocampal formation , synaptic vesicle , biology , chemistry , inhibitory postsynaptic potential , vesicle , biochemistry , receptor , membrane
Doc2α is a synaptic vesicle‐associated Ca 2 + ‐binding protein. To study the role of Doc2α in synaptic transmission and modulation, we generated homozygous null Doc2α mutant mice. In the CA1 region of hippocampal slices in the mutant mice, excitatory synaptic responses evoked with prolonged 5 Hz stimulation showed a significantly larger frequency facilitation followed by a steeper depression than those in wild‐type mice, whereas there was no difference in synaptic transmission at lower frequencies or in paired‐pulse facilitation. These results suggest that Doc2α regulates synaptic transmission when high Ca 2 + concentrations in the presynaptic terminal are sustained. Furthermore, the mutant mice showed impairment in long‐term potentiation and passive avoidance task. Thus, Doc2α may regulate transmitter release during repetitive synaptic activation, thereby contributing to memory formation.