Changes in extracellular potassium and calcium concentration and neural activity during prolonged electrical stimulation of the cat cerebral cortex at defined charge densities

In cats anesthetized with nitrous oxide and halothane, ion-selecting microelectrodes were used to monitor changes in the concentration of potassium [K+]0 and calcium [Ca2+]0 in the extracellular compartment of the cerebral cortex during as long as 4 h of continuous stimulation of the cortical surface. At stimulus charge densities shown to induce only minimal localized histologic changes [20 microC/cm2 . ph at 50 pulses per second (pps)], [K+]0 at a depth of about 750 micrometers underwent only a transient increase at the beginning of stimulation, followed by a rapid return to the prestimulus concentration. [Ca2+]0 was unaffected. At a higher charge density (100 microC/cm2 . ph at 20 pps) there was a rapid transient increase in [K+]0, followed by a more gradual return to a plateau about 1 mM above the prestimulus value. [Ca+]0 usually underwent an initial increase followed by a slow decrease to a plateau value above 0.5 mM. At a charge density of 100 microC/cm2 . ph and 50 pps (shown in histological studies to induce significant neural damage), [Ca2+]0 slowly decreased to near or below 0.5 mM in the middle layers of the cortex. After 30 to 40 min of stimulation, [K+]0 underwent episodic fluctuations about a plateau value 0.5 to 1 mM above the prestimulus concentration. Simultaneous recordings of the compound action potential in the ipsilateral pyramidal tract indicated that these fluctuations were due to local changes in the excitability of intracortical circuitry conditioned by the intense stimulation. The results have implications for the possible interrelation of the changes in extracellular ionic concentrations and the early stages of stimulation-induced neural damage.     

Permeability of Brain Capillaries to Hexoses and Pentoses in the Rabbit

The initial loss in the rabbit brain of non-electrolytes injected into the carotid artery was measured with ‘Indicator Diffusion’ technique, 3–0–methyl-D-glucose shared with D-glucose the ability to pass into the brain by a mediated transport mechanism. The rate of transport of the following substances could not be distinguished: D-mannose, D-galactose, D-arabinose and 1)-ribose. They all penetrated more slowly than D-glucose. D-mannitol was also lost from the blood during the passage through the brain. This observation, together with the known inability of D-mannitol to pass the blood-brain barrier, suggests that the loss takes place into the endothelial cytoplasma. Thus the basal plasma membrane of the endothrlial cells together with the basal membrane proper may define blood-brain barrier chararteristirs.