Chapter 2 Glucocorticoids, hippocampal damage and the glutamatergic synapse

In an approach meant to decrease the total lifetime exposure to GCs, the chapter demonstrates that a neonatal behavioral intervention that reduces adult basal GC concentrations in the rat prevents some neuron loss and spatial learning deficits that characterize aging in the rats.

Abstract

This chapter reviews the present knowledge concerning the cell biology of how glucocorticoids (GCs) damage hippocampal neurons. It presents studies that suggest that GCs leave hippocampal neurons in a state of metabolic vulnerability. In the absence of a coincident metabolic challenge, this vulnerability is survived readily. However, when co-incident insults occur, neuronal viability is compromised, at least in part via exacerbation of the EAA cascade of damage. These observations are of some potential relevance, in that they suggest that exogenous GCs, in the aftermath of some insults, can potentially exacerbate hippocampal damage, and should be avoided if possible. It has been shown that inhibiting the GC stress response in the aftermath of status epilepticus seizures, by administering the adrenal steroidogenesis inhibitor metyrapone, diminish hippocampal damage. In an approach meant to decrease the total lifetime exposure to GCs, the chapter demonstrates that a neonatal behavioral intervention that reduces adult basal GC concentrations in the rat prevents some neuron loss and spatial learning deficits that characterize aging in the rat.