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Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy.

Neurobiology of disease | Oct 16, 2008

Many animal models of temporal lobe epilepsy (TLE) begin with status epilepticus (SE) followed by a latency period. Increased hippocampal pyramidal neuron excitability may contribute to seizures in TLE. I(h), mediated by h channels, regulates intrinsic membrane excitability by modulating synaptic integration and dampening dendritic calcium signaling. In a rat model of TLE, we found bidirectional changes in h channel function in CA1 pyramidal neurons. 1-2 d after SE, before onset of spontaneous seizures, physiological parameters dependent upon h channels were augmented and h channel subunit surface expression was increased. 28-30 d following SE, after onset of spontaneous seizures, h channel function in dendrites was reduced, coupled with diminished h channel subunit surface expression and relocalization of subunits from distal dendrites to soma. These results implicate h channel localization as a molecular mechanism influencing CA1 excitability in TLE.

Pubmed ID: 18657617 RIS Download

Mesh terms: Animals | Channelopathies | Cyclic Nucleotide-Gated Cation Channels | Epilepsy, Temporal Lobe | Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels | Male | Membrane Proteins | Mice | Nerve Tissue Proteins | Potassium Channels | Protein Subunits | Protein Transport | Rats | Rats, Sprague-Dawley

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Associated grants

  • Agency: NINDS NIH HHS, Id: NS37444
  • Agency: NIMH NIH HHS, Id: MH48432
  • Agency: NINDS NIH HHS, Id: P01 NS037444
  • Agency: NINDS NIH HHS, Id: K02 NS055995
  • Agency: NINDS NIH HHS, Id: R21 NS052595-01A1
  • Agency: NINDS NIH HHS, Id: R21 NS052595
  • Agency: NIMH NIH HHS, Id: R37 MH044754
  • Agency: NIMH NIH HHS, Id: R01 MH048432
  • Agency: NIMH NIH HHS, Id: MH44754
  • Agency: NINDS NIH HHS, Id: K02 NS055995-01
  • Agency: NINDS NIH HHS, Id: R21 NS052595-02
  • Agency: NINDS NIH HHS, Id: K02 NS055995-02

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NeuroMab

A national mouse monoclonal antibody generating resource for biochemical and immunohistochemical applications in mammalian brain. NeuroMabs are generated from mice immunized with synthetic and recombinant immunogens corresponding to components of the neuronal proteome as predicted from genomic and other large-scale cloning efforts. Comprehensive biochemical and immunohistochemical analyses of human, primate and non-primate mammalian brain are incorporated into the initial NeuroMab screening procedure. This yields a subset of mouse mAbs that are optimized for use in brain (i.e. NeuroMabs): for immunocytochemical-based imaging studies of protein localization in adult, developing and pathological brain samples, for biochemical analyses of subunit composition and post-translational modifications of native brain proteins, and for proteomic analyses of native brain protein networks. The NeuroMab facility was initially funded with a five-year U24 cooperative grant from NINDS and NIMH. The initial goal of the facility for this funding period is to generate a library of novel NeuroMabs against neuronal proteins, initially focusing on membrane proteins (receptors/channels/transporters), synaptic proteins, other neuronal signaling molecules, and proteins with established links to disease states. The scope of the facility was expanded with supplements from the NIH Blueprint for Neuroscience Research to include neurodevelopmental targets, the NIH Roadmap for Medical Research to include epigenetics targets, and NIH Office of Rare Diseases Research to include rare disease targets. These NeuroMabs will then be produced on a large scale and made available to the neuroscience research community on an inexpensive basis as tissue culture supernatants or purified immunoglobulin by Antibodies Inc. The UC Davis/NIH NeuroMab Facility makes NeuroMabs available directly to end users and is unable to accommodate sales to distributors for third party distribution. Note, NeuroMab antibodies are now offered through antibodiesinc.

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