Stress-Induced Increase in Blood–Brain Barrier Permeability in Control and Monosodium Glutamate-Treated Rats

Abstract

Glutamate administration in neonatal rats causes reversible changes in blood–brain barrier (BBB) permeability and known neurotoxic lesions. This study was aimed to evaluate whether glutamate administered to neonatal rats influences properties of the developing BBB with consequences on adult BBB function. The vulnerability of the BBB was examined after short-lasting stress exposure by measurement of plasma albumin extravasation using immunoelectrophoresis. In control rats, 30 min of immobilization stress resulted in increased endogenous albumin extravasation in the hypothalamus, hippocampus, brain stem and cerebellum, but not in the cortex and striatum. Basal levels of albumin in adult glutamate-treated rats (4 mg monosodium glutamate/g BW, IP, five times during neonatal period) were significantly lower in the hypothalamus compared to that in controls. Stress-induced increase in albumin levels was lower in the brain stem, higher in the hypothalamus, and similar in other brain regions studied in glutamate-treated rats in comparison with controls. It is concluded that short-lasting immobilization stress increased BBB permeability in some but not all brain regions studied. Glutamate treatment of neonatal rats resulted in low basal albumin levels in the hypothalamus but did not exert a pronounced influence on adult BBB function. BBB vulnerability in glutamate-treated rats during stress exposure was increased in the hypothalamus and decreased in the brain stem.