Synaptotagmin and synaptic transmission alterations in apolipoprotein E-deficient mice

Prog Neuropsychopharmacol Biol Psychiatry. 1999 Apr;23(3):519-31. doi: 10.1016/s0278-5846(99)00013-5.


1. Aged apoE-deficient mice and age-matched controls were tested for cognitive alterations in the Morris water maze. 2. Water maze results were correlated with in vivo electrophysiology and expression of the synaptic protein synaptotagmin (p65). 3. Compared to age-matched controls, apolipoprotein E-deficient mice displayed significant performance impairment accompanied by in vivo electrophysiological alterations in the dentate gyrus. 4. Apolipoprotein E-deficient mice also showed a significant increase in the synaptic protein, synaptotagmin, a synaptic calcium sensor involved in neurotransmitter release. 5. Cognitive impairments in these animals may be associated with decreased synaptic excitability in hippocampal neurons and the regulatory role of apolipoprotein E in synaptic function might be mediated by modulation of the expression of calcium sensor proteins.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aging / physiology*
  • Alzheimer Disease / physiopathology
  • Animals
  • Apolipoproteins E / deficiency*
  • Calcium-Binding Proteins*
  • Cognition Disorders / physiopathology*
  • Dentate Gyrus / physiopathology
  • Female
  • Male
  • Maze Learning
  • Membrane Glycoproteins / pharmacology*
  • Mice
  • Nerve Tissue Proteins / pharmacology*
  • Synaptic Transmission / physiology*
  • Synaptotagmin I
  • Synaptotagmins


  • Apolipoproteins E
  • Calcium-Binding Proteins
  • Membrane Glycoproteins
  • Nerve Tissue Proteins
  • Synaptotagmin I
  • Synaptotagmins