Cerebral Composition and Function in Experimental Brain Injury in the Rat

Abstract

NEURONAL activity is dependent on the ability of nervous tissue to control the concentration of electrolytes across the nerve cell membrane. The most important component of this process is the active extrusion of sodium from the neuronal cytoplasm against an osmotic gradient. A nerve impulse is normally initiated by the production of an area of increased permeability on the cell surface which allows the outward flow of potassium ions and the inward flow of sodium ions¹. After the passage of the impulse, energy is required to restore the electrolyte distribution associated with the resting polarized state¹. Nerve impulses can also be initiated by altering the electrolyte content of the fluid surrounding the neurone. Electrolyte disturbances occur in oedematous brain following trauma and cold injury and have been studied in detail by Pappius and Gulati, but in such conditions the mechanism of water accumulation and other ionic changes are not known². The following experiments were carried out on anoxic-ischaemic brain damage in rats³ in order to investigate the role of changes in the electrolyte and water content of the brain in the production of the hemiplegia and convulsions which occur in this condition, and their relationship to cerebral protein synthesis and energy production.