Abstract:
:To evaluate the role in synaptic plasticity of ryanodine receptor type 3 (RyR3), which is normally enriched in hippocampal area CA1, we generated RyR3-deficient mice. Mutant mice exhibited facilitated CA1 long-term potentiation (LTP) induced by short tetanus (100 Hz, 100 ms) stimulation. Unlike LTP in wild-type mice, this LTP was not blocked bythe NMDA receptor antagonist D-AP5 but was partially dependent on L-type voltage-dependent Ca2+ channels (VDCCs) and metabotropic glutamate receptors (mGluRs). Long-term depression (LTD) was not induced in RyR3-deficient mice. RyR3-deficient mice also exhibited improved spatial learning on a Morris water maze task. These results suggest that in wild-type mice, in contrast to the excitatory role of Ca2+ influx, RyR3-mediated intracellular Ca2+ ([Ca2+]i) release from endoplasmic reticulum (ER) may inhibit hippocampal LTP and spatial learning.
journal_name
Neuronjournal_title
Neuronauthors
Futatsugi A,Kato K,Ogura H,Li ST,Nagata E,Kuwajima G,Tanaka K,Itohara S,Mikoshiba Kdoi
10.1016/s0896-6273(00)81123-xsubject
Has Abstractpub_date
1999-11-01 00:00:00pages
701-13issue
3eissn
0896-6273issn
1097-4199pii
S0896-6273(00)81123-Xjournal_volume
24pub_type
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