Robert A. Ratcheson

Human Motor Cortex: Sensory Input Data from Single Neuron Recordings

Recordings were made from single neurons in the hand area of the human motor cortex while peripheral physiologic stimuli were applied. Such cells responded only to active and passive hand movements. Tactile and autditory (click) stimuli were itneffective. The majority of cells were activated only by movements of the contralateral hand, but a significant number (4 of 16) could be excited if a given movement was made by either hand. Of the cells responding to active movement, some showed an increased discharge before onset of the voluntary action. Such cells were excited by the same movement executed passively, a result that indicates sensory feedback from receptors activated by that movement.

Regionally Selective Metabolic Effects of Hypoglycemia in Brain

Abstract: Regional CNS levels of glucose reserves, glycolytic intermediates, and high‐energy phosphate reserves were measured in insulin‐treated, hypoglycemic rats and correlated with EEG activity. Intravenous administration of insulin to paralyzed, ventilated animals causes concomitant reduction of blood glucose levels and progressive abnormality and eventual loss of EEG activity. In all regions of brain examined, glucose and glycogen levels decrease until they are essentially depleted, and glucose‐6‐phosphate and fructose‐1,6‐biphosphate fall approximately 80%. Pyruvate levels decrease 50% in cerebral cortex and brain stem and a lesser amount in striatum, hippocampus, thalamus, and cerebellum. Lactate levels fall 50–60% in all regions except cerebellum, where no change is observed. ATP and phosphocreatine levels remain normal until the EEG is isoelectric, and then decrease in all regions except cerebellum. These results demonstrate that hypoglycemia does not have a uniform effect on brain glucose and energy metabolism, and cerebellum seems to be relatively protected.

Effect of nitrous oxide anesthesia upon cerebral energy metabolism

RAPID inactivation of cerebral tissue for measurement of labile cerebral metabolites in unanesthetized animals is most often obtained using techniques of whole body immersion (PONTEN et al., 1973a, b) or decapitation (LOWRY et al., 1964; FERRENDELLI et al., 1972) into a liquid nitrogen bath, ‘freeze-blowing’ (VEECH et al., 1973), or microwave irradiation (MEDINA et al., 1975). These techniques are limited to animals of less than 500 g body weight and are frequently unsatisfactory for chronic experiments which require physiologic and/or surgical manipulation. Techniques permitting the introduction of physiologic and surgical variables (PONTEN et d., 1973b), or those used for the evaluation of cerebral energy metabolism in large animals (RATCHESON & FERRENDELLI, in preparation) require the use of anesthetic agents. A combination of 70% nitrous oxide with 30% oxygen is usually employed. Whether this anesthetic itself alters cerebral metabolism, thus artifactually altering CNS neurochemical processes, has not been resolved. Both an increase and decrease in cerebral metabolic rate of oxygen utilization (CMRO,) has been attributed to nitrous oxide anesthesia (WOLLMAN et ~ l . , 1975; THEYE & MICHENFELDER, 1968). Anesthetics have been implicated in raising the levels of high energy compounds (GATFIELD et al., 1966), but this elevation may be due to the method of rapid inactivation of cerebral tissue employed (MINARD & DAVIS, 1962; NILSSON & BUSTO, 1973; NILSSON & SIESJO, 1970; PONTEN et a[., 1973a, b). NILSSON & BUSTO (1973) reported no effect of N 2 0 on organic phosphate compounds in rats, but found changes in brain tissue glucose and lactate concentration. The purpose of this study is to compare the levels of labile cerebral metabolites in mice exposed to air and in mice exposed to 70% nitrous oxide and 30% oxygen to determine if this anesthetic mixture alters CNS levels of high energy compounds, carbohydrate substrates, or rate of high energy phosphate ( P) utilization.