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Effect of CRMP3 expression on dystrophic dendrites of hippocampal neurons

Molecular Psychiatry volume 16, pages 689–691 (2011)Cite this article

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We have previously shown that deleting CRMP3 gene altered prepulse inhibition of the acoustic startle response,1 impaired long-term potentiation and induced dendritic dystrophy in hippocampus.2 In cultured hippocampal neurons, CRMP3 expression resulted in numerous long-branched dendrites, which were inhibited by its dominant-negative isoform.3 Because the levels of CRMP3 expression in hippocampal neurons correlated with dendrite morphogenesis, it is conceivable that CRMP3 may be a potential therapeutic target in neuronal dystrophy affecting hippocampal dendrites. In this study, we report that CRMP3 overexpression prevents dystrophy of dendrites occurring in a neurotoxic context.

How does CRMP3 preserve individual dendritic structure? Calcium signals triggered by various effectors control the growth and branching of dendrites, and release of calcium from intracellular stores maintains dendritic branch stability.9 In contrast, after prolonged exposure, PrP106–126 and scrapie homogenate induced neurite alterations and contortions via a reduction in Ca2+ entry and dysfunction of voltage-gated calcium channels, including CaV2.2.10, 11 Relevant to these findings, using whole-cell voltage clamp electrophysiology, we found for the first time that transfection of CRMP3-EGFP enhanced Ca2+ current density via neuronal N- (CaV2.2) and P/Q-type (CaV2.1) voltage-gated calcium channels in hippocampal neurons (Figure 1c). On average, the peak current density increased by ∼2.8-fold, from 10.4±2.2 (n=9) in control neurons to 29.2±2.8 (n=10) pA/pF in CRMP3-expressing neurons (holding potential of 5 mV, P<0.05, ANOVA). Collectively, these observations suggest that CRMP3 activity on calcium flux may mediate its effects on dendrite formation. They provide a new foundation for further studies on the role of CRMP3 in Ca2+ trafficking and signaling, and to determine whether its effect on Ca2+ channel function is associated with its activity on the induction/maintenance of dendritic architecture in the hippocampus.

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Authors and Affiliations

  1. INSERM U842, Université Lyon-1, Lyon, France

    T T Quach, N Chounlamountri, N Auvergnon & J Honnorat

  2. Department of Pharmacology and Toxicology, Paul and Carole Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA

    Y Wang & R Khanna

  3. Hospices Civils de Lyon, Hôpital Neurologique, Neurologie B, Bron, France

    J Honnorat

  4. Université de Lyon1, UMR-S842, Lyon, France

    J Honnorat

  5. Department of Psychiatry, Ohio State University College of Medicine, Columbus, OH, USA

    A-M Duchemin

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  1. T T Quach
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  2. Y Wang
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Correspondence to A-M Duchemin.

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Quach, T., Wang, Y., Khanna, R. et al. Effect of CRMP3 expression on dystrophic dendrites of hippocampal neurons. Mol Psychiatry 16, 689–691 (2011). https://doi.org/10.1038/mp.2011.6

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