Non-rapid eye movement sleep is suppressed in transgenic mice with a deficiency in the somatotropic system

Neurosci Lett. 1996 Dec 13;220(2):97-100. doi: 10.1016/s0304-3940(96)13232-8.


Sleep-wake activity was studied in a transgenic mouse model (TH-hGH) with a deficiency in the somatotropic axis (growth hormone (GH)-releasing hormone (GHRH)-GH-insulin-like growth factor-I (IGF-I)). This dwarf transgenic mouse strain expresses a human GH (hGH) reporter gene linked to 4.8 kb of the rat tyrosine hydroxylase flanking sequence, targeting the production of hGH to sites of tyrosine hydroxylase synthesis in the brain. Endogenous GH and IGF-I are suppressed in these mice, as well as GHRH. Sleep-wake activity (EEG and EMG) was recorded for 2 to 3 days in nine transgenic mice and nine wild-type littermates. Non-rapid eye movement sleep (NREMS) was significantly suppressed during both the light and the dark period in the transgenic mice; rapid eye movement sleep (REMS) was not altered. The results provide evidence that the somatotropic axis contributes to normal sleep regulation.

Publication types

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

MeSH terms

  • Animals
  • Brain / metabolism*
  • Brain / physiology
  • Growth Hormone-Releasing Hormone / deficiency*
  • Growth Hormone-Releasing Hormone / genetics
  • Insulin-Like Growth Factor I / deficiency*
  • Insulin-Like Growth Factor I / genetics
  • Mice
  • Mice, Transgenic
  • Rats
  • Sleep / physiology*
  • Tyrosine 3-Monooxygenase / biosynthesis


  • Insulin-Like Growth Factor I
  • Growth Hormone-Releasing Hormone
  • Tyrosine 3-Monooxygenase