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Loss of interneuron LTD and attenuated pyramidal cell LTP in Trpv1 and Trpv3 KO mice

Authors

  • Travis E. Brown,

    1. Department of Molecular Pharmacology, Physiology, and Biotechnology, Brown University, Providence, Rhode Island
    Current affiliation:
    1. School of Pharmacy, University of Wyoming, Laramie, WY 82071
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    • Travis E. Brown and Anda M. Chirila contributed equally to this work.

  • Anda M. Chirila,

    1. Department of Molecular Pharmacology, Physiology, and Biotechnology, Brown University, Providence, Rhode Island
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    • Travis E. Brown and Anda M. Chirila contributed equally to this work.

  • Benjamin R. Schrank,

    1. Department of Molecular Pharmacology, Physiology, and Biotechnology, Brown University, Providence, Rhode Island
    2. Department of Neuroscience, Brown University, Providence, Rhode Island
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  • Julie A. Kauer

    Corresponding author
    1. Department of Neuroscience, Brown University, Providence, Rhode Island
    • Department of Molecular Pharmacology, Physiology, and Biotechnology, Brown University, Providence, Rhode Island
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Correspondence to: Julie A. Kauer, Brown University, 171 Meeting Street BioMed 487, Box GB-4, Providence, RI 02912. E-mail: Julie_Kauer@brown.edu

ABSTRACT

TRPV (transient receptor potential, vanilloid) channels are a family of nonselective cation channels that are activated by a wide variety of chemical and physical stimuli. TRPV1 channels are highly expressed in sensory neurons in the peripheral nervous system. However, a number of studies have also reported TRPV channels in the brain, though their functions are less well understood. In the hippocampus, the TRPV1 channel is a novel mediator of long-term depression (LTD) at excitatory synapses on interneurons. Here we tested the role of other TRPV channels in hippocampal synaptic plasticity, using hippocampal slices from Trpv1, Trpv3 and Trpv4 knockout (KO) mice. LTD at excitatory synapses on s. radiatum hippocampal interneurons was attenuated in slices from Trpv3 KO mice (as well as in Trpv1 KO mice as previously reported), but not in slices from Trpv4 KO mice. A previous study found that in hippocampal area CA1, slices from Trpv1 KO mice have reduced tetanus-induced long-term potentiation (LTP) following high-frequency stimulation; here we confirmed this and found a similar reduction in Trpv3 KO mice. We hypothesized that the loss of LTD at the excitatory synapses on local inhibitory interneurons caused the attenuated LTP in the mutants. Consistent with this idea, blocking GABAergic inhibition rescued LTP in slices from Trpv1 KO and Trpv3 KO mice. Our findings suggest a novel role for TRPV3 channels in synaptic plasticity and provide a possible mechanism by which TRPV1 and TRPV3 channels modulate hippocampal output. © 2013 Wiley Periodicals, Inc.

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