Impaired long‐term memory and long‐term potentiation in N‐type Ca2+channel‐deficient mice

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Abstract
Voltage‐dependent N‐type Ca2+ channels, along with the P/Q‐type, have a crucial role in controlling the release of neurotransmitters or neuromodulators at presynaptic terminals. However, their role in hippocampus‐dependent learning and memory has never been examined. Here, we investigated hippocampus‐dependent learning and memory and synaptic plasticity at hippocampal CA3–CA1 synapses in mice deficient for the α1B subunit of N‐type Ca2+ channels. The mutant mice exhibited impaired learning and memory in the Morris water maze and the social transmission of food preference tasks. In particular, long‐term memory was impaired in the mutant mice. Interestingly, among activity‐dependent long‐lasting synaptic changes, theta burst‐ or 200‐Hz‐stimulation‐induced long‐term potentiation (LTP) was decreased in the mutant, compared with the wild‐type mice. This type of LTP is known to require brain‐derived neurotrophic factor (BDNF). It was found that both BDNF‐induced potentiation of field excitatory postsynaptic potentials and facilitation of the frequency of miniature excitatory postsynaptic currents (mEPSCs) were reduced in the mutant. Taken together, these results demonstrate that N‐type Ca2+ channels are required for hippocampus‐dependent learning and memory, and certain forms of LTP.