Conditional forebrain deletion of the L-type calcium channel CaV1.2 disrupts remote spatial memories in mice

  1. Jessica A. White1,
  2. Brandon C. McKinney2,3,
  3. Manorama C. John4,
  4. Patricia A. Powers4,
  5. Timothy J. Kamp4,5, and
  6. Geoffrey G. Murphy1,3,6,7
  1. 1 Molecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan 48109-0069, USA;
  2. 2 Medical Scientist Training Program, University of Michigan, Ann Arbor, Michigan 48109-0069, USA;
  3. 3 Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48109-0069, USA;
  4. 4 Department of Physiology, University of Wisconsin, Madison, Wisconsin 53706, USA;
  5. 5 Department of Medicine, University of Wisconsin, Madison, Wisconsin 53706, USA;
  6. 6 Department of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, Michigan 48109-0069, USA

Abstract

To determine whether L-type voltage-gated calcium channels (L-VGCCs) are required for remote memory consolidation, we generated conditional knockout mice in which the L-VGCC isoform CaV1.2 was postnatally deleted in the hippocampus and cortex. In the Morris water maze, both CaV1.2 conditional knockout mice (CaV1.2cKO) and control littermates displayed a marked decrease in escape latencies and performed equally well on probe trials administered during training. In distinct contrast to their performance during training, CaV1.2cKO mice exhibited significant impairments in spatial memory when examined 30 d after training, suggesting that CaV1.2 plays a critical role in consolidation of remote spatial memories.

Footnotes

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