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Energy expenditure during stress ulcer formation in vulnerable rats

D Greenberg1, S H Ackerman

  • 1Department of Psychiatry, Cornell University Medical College, White Plains, New York.

Insights

Early life stress in rat pups leads to hypothermia and reduced oxidative metabolism when food-deprived. This impaired thermogenesis is not reversed by norepinephrine, suggesting a link to stress ulcer susceptibility.

Area of Science:

  • Physiology
  • Neuroendocrinology
  • Developmental Biology

Background:

  • Early life maternal separation in rat pups (postnatal day 15) induces vulnerability to hypothermia and gastric erosion under stress.
  • This vulnerability is hypothesized to be linked to decreased oxidative metabolism and impaired thermogenesis.

Purpose of the Study:

  • To investigate the association between early life stress (maternal separation) and oxidative metabolism in rat pups.
  • To determine if impaired thermogenesis, potentially mediated by norepinephrine (NE), contributes to hypothermia in stressed rat pups.

Main Methods:

  • Measured oxygen (O2) consumption in 30-day-old rat pups subjected to maternal separation at postnatal day 15 (15w) or day 21 (21w).
  • Assessed O2 consumption during conditions of food availability, food deprivation, and food deprivation with restraint.
  • Administered exogenous norepinephrine (NE) to evaluate its effect on O2 consumption in separated and non-separated rats.

Main Results:

  • Rat pups separated at day 15 (15w) exhibited significantly lower O2 consumption than controls (21w) when food-deprived or food-deprived and restrained, indicating reduced heat production.
  • Administration of exogenous NE failed to restore O2 consumption in 15w rats during food deprivation or restraint, suggesting the issue is not solely due to insufficient NE.
  • Oxidative metabolism was decreased in 15w rats under stress, leading to hypothermia.

Conclusions:

  • Early life maternal separation in rats impairs oxidative metabolism during stress, resulting in hypothermia.
  • The observed hypothermia and reduced oxidative metabolism are not corrected by exogenous norepinephrine, indicating a mechanism beyond simple NE deficiency.
  • Decreased oxidative metabolism may underlie the susceptibility to stress ulcers observed in various experimental models following early life stress.

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