Protein Synthesis and Calcium Uptake Following Complete Cerebral Ischemia of Rat Brain

Summary

The possible involvement of neuroexcitatory pathomechanisms in the development of postischemic neuron injury was examined in rats subjected to 10-min cardiac arrest for the induction of complete cerebral ischemia of the central nervous system. In vivo 45Ca uptake and cerebral protein synthesis were studied by means of a double-tracer autoradiographic approach following increasing intervals after postischemic recirculation. In the pyramidal layer of the hippocampal CA1 subfield, protein synthesis was permanently inhibited for 4 days postischemia at an unchanged number of intact neurons whereas the in vivo 45Ca uptake started to increase significantly after 2 days postischemia. After 7 days postischemia, however, a 50% loss of CA1 neurons was observed. Conversely, rates of protein synthesis of the reticular and ventral thalamic nucleus, the colliculus inferior, and the caudate nucleus were suppressed for 1 day postischemia paralleled by an enormous in vivo 45Ca uptake in the reticular thalamic nucleus but a moderate one in the other brain regions. Metabolic changes were accompanied by a definite loss of neurons of the reticular thalamic nucleus whereas cell alterations in the other mentioned brain regions which were devoid of their GABAergic input were of a “chronic” and principally reversible type of neuron injury. Our results, in consequence, indicate that the magnitude of in vivo 45Ca uptake is a good indicator for the severity of neuronal injury and that the duration and degree of suppressed protein synthesis possibly induced by hyperexcitability and/or loss of inhibition determine the extent of postischemic neuronal injury.