The effect of different maternal deprivation paradigms on the expression of hippocampal glucocorticoid receptors, calretinin and calbindin-D28k in male and female adolescent rats

Neurochem Int. 2011 Nov;59(6):847-52. doi: 10.1016/j.neuint.2011.07.010. Epub 2011 Aug 3.

Abstract

Maternal deprivation (MD) is a well-established protocol used to investigate neurobiological changes that are associated with the etiology of and vulnerability to stress-related diseases in animal models. The resulting psychophysiological effects, the timing and duration of these adverse stimuli, and the method by which they exert their effects on the animals remain unclear. This study characterized differences in the hippocampal expression of glucocorticoid receptors (GRs) and the calcium-binding proteins calretinin (CALR) and calbindin-D28k (CALB) in male and female rats that underwent different MD paradigms during the stress hyporesponsive period (SHRP). Both GRs and the two calcium-binding proteins were much more abundant in females than in males. MD paradigms had a significant effect on CALR and CALB expression in both males and females but affected GR levels only in males. Additionally, expression of the two calcium-binding proteins in the hippocampus responded differently to MD-induced stress, especially in females. Taken together, these results indicate that females are able to modulate their response to stress better than males.

Publication types

  • Comparative Study

MeSH terms

  • Aging / physiology
  • Aging / psychology
  • Animals
  • Calbindin 1
  • Calbindin 2
  • Calbindins
  • Disease Models, Animal
  • Female
  • Hippocampus / growth & development
  • Hippocampus / metabolism*
  • Hippocampus / physiopathology
  • Male
  • Maternal Deprivation*
  • Pregnancy
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Glucocorticoid / biosynthesis*
  • Receptors, Glucocorticoid / metabolism
  • S100 Calcium Binding Protein G / biosynthesis*
  • Sex Characteristics*
  • Stress, Psychological / metabolism*
  • Stress, Psychological / physiopathology

Substances

  • Calb1 protein, rat
  • Calb2 protein, rat
  • Calbindin 1
  • Calbindin 2
  • Calbindins
  • Receptors, Glucocorticoid
  • S100 Calcium Binding Protein G