Synaptosomal glutamate uptake in a model of experimental cerebral ischemia.

In the present investigation we studied the synaptosomal uptake of glutamate in brain omogenate of Mongolian gerbils submitted to bilateral common carotid occlusion, with and without subsequent return of blood flow. The results show that glutamate uptake after ischemia is reduced by about 35% The damage appears to be persistent, since return of blood flow restores uptake only slightly. The membrane alterations occurring in ischemia could explain the persistence of glutamate transporter impairment. Besides the blockade of NMDA receptors, the stimulation and/or the protection of the uptake systems for glutamate could be of help in preventing neuronal ischemic damage

Substrate-stimulated oxygen consumption by isolated rat brain microvessels in the presence and absence of ATP.

We report here properties of isolated brain microvessels such as the rate of oxygen consumption with different substrates; the permeabilizing effect of added ATP is studied. With the isolation procedure presented the cerebral endothelium has a metabolic activity comparable to that reported in the literature. The respiratory rate of the microvessels is not affected by the addition of ATP, whereas it is significantly increased by addition of succinate and alpha-chetoglutarate. The exposure of the isolated brain capillaries to ATP, in a Ca2+-free medium, increases the uptake of 6-carboxyfluorescein. This may be due to pores opened by ATP in the endothelial cell membrane in the absence of divalent cations

Increasing Frequency of Multiple Sclerosis in Padova, Italy. A 30 year epidemiological survey

I.F.: 2,9