IP3 is an important second messenger to release Ca2+ from internal store. IP3 receptor (IP3R) works as an IP3-induced Ca2+ release channel. We studied the role of type 1 IP3R (IP3R1) in neural plasticity. We found that IP3R1 is necessary for the induction of long-term depression (LTD) by using cerebellar slices of IP3R1-deficient mice. We also studied the neural plasticity of the hippocampus. While no differences were seen between mutant and wild-type mice in terms of the mean magnitude of the long-term potentiation (LTP) or LTD induced by a standard tetanus or low-frequency afferent stimulation (LFS), a short tetanus protocol evoked much greater LTP amplitude in the IP3R1-deficient mice than the control. In addition, DP or LTP suppression was attenuated in the mutant mice, the mean magnitude of the responses after delivery of LFS or tetanus being significantly greater than in wild-type mice. These results suggested that IP3R1 is involved in LTP, DP and LTP suppression, but is not essential for LTD. In addition, IP3R1 was involved in the determination of polarity and input specificity of activity-induced synaptic modification in hippocampal CA1 pyramidal cells. We studied the electrophysiological activity and learning behavior of ryanodine receptor (type 3; RyR3) deficient mice. When LTP was evoked using high-frequency stimulation in the CA1 hippocampal neuron, the increase in the initial slope of field excitatory postsynaptic potentials (EPSPs) was not significantly different between homozygous and wild mice, although the increase in the homozygous mice tended to be greater than in the wild mice. With near-threshold stimulation, however, LTP was not induced in wild-type mice but was induced in homozygous mice. In the probe trial test, in which the platform was removed after the training schedule, ryanodine receptor type 3-deficient mice spent significantly more time than the wild-type mice in the quadrant where the platform had been.
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