Biophysical and metabolic bases of cooling effects on cortical membrane potentials in the cat

Neuronal and silent cell membrane potentials were recorded in cat cortex during focal cooling by 5–6 C, either transiently for 1–2 min or for 10–15 min. Effects were compared between locally anesthetized, immobilized preparations and those under pentobarbital general anesthesia. The findings suggest actions at common membrane sites in effects of cooling and general anesthesia. In immobilized animals, transient cooling depolarized neurons by 1–2 mv/C. Silent cells responded similarly but with a slower onset. Intraneuronal wave activity and neuronal firing patterns showed related changes during the cooling cycle. Increased cell firing during transient cooling was not confined to depolarizing shifts but also occurred during hyperpolarizing shifts. Raising topical Ca²⁺ levels to 20 mM blocked depolarization by transient cooling, but 7.5 mM solutions were without effect. Repeated transient cooling or continuous cooling for 10–15 min produced almost complete depolarization of neurons and silent cells for periods extending considerably beyond recovery of brain temperature. Moreover, these cumulative effects beyond the cooling period were potentiated by the weaker 7.5 mM Ca²⁺ solutions. Pentobarbital anesthesia blocked the effects of sustained cooling on neuronal and silent cell membrane potentials and on unit firing activity. Also, topical 7.5-mM Ca²⁺ solutions failed to potentiate effects of cooling during barbiturate anesthesia. The effects of transient cooling are discussed in terms of membrane leakage currents that may be blocked by Ca²⁺. Cumulative effects with prolonged cooling suggest interference with membrane metabolism, and the possible role of cooperative binding and release of cations from membrane surface glycoproteins in these responses is considered.