Dopamine D1-deficient mutant mice do not express the late phase of hippocampal long-term potentiation

Neuroreport. 1997 Nov 10;8(16):3533-5. doi: 10.1097/00001756-199711100-00023.


The possible involvement of the dopamine D1 receptor subtype in mechanisms of long-term potentiation (LTP) of the Schaffer collateral-commissural input of CA1 neurones was investigated using D1-deficient mutant mice. In transversal hippocampus slices from mice lacking the D1 receptor a normal post-tetanic and short-term potentiation could be induced after applying a triple 100 Hz tetanization. However, the potentiated fEPSP in the mutant mice declined to control value about 140 min following tetanization, whereas in the wild type mice a normal, non-decremental LTP was observed. These data support the idea that besides the glutamatergic system, the synergistic activation of dopaminergic synapses is necessary for LTP maintenance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Benzazepines / metabolism
  • Cell Membrane / metabolism
  • Corpus Striatum / metabolism*
  • Dopamine / physiology
  • Electric Stimulation
  • Genotype
  • Hippocampus / physiology*
  • Long-Term Potentiation / physiology*
  • Mice
  • Mice, Knockout
  • Neurons / physiology*
  • Receptors, Dopamine D1 / deficiency*
  • Receptors, Dopamine D1 / genetics
  • Receptors, Dopamine D1 / physiology
  • Synapses / physiology
  • Time Factors


  • Benzazepines
  • Receptors, Dopamine D1
  • Dopamine