Abstract
Raising the temperature from 22 to 32°C induced a marked hyperpolarization (15-30mV) associated with an increase in membrane conductance of Aplysia neurons, whereas lowering the temperature from 22 to 12°C caused a significant depolarization (10-20mV) with a decrease in conductance. These temperature effects were far greater than those expected from the Nernst equation. The reversal potentials of these temperature responses corresponded with the equilibrium potential of K+, suggesting these responses were produced by opening or closing of K+ channels. Ouabain (5×10-4M) did not affect these temperature responses though it depolarized all cells examined (5-25mV). Intracellularly injected guanosine 5′-O-(2-thiodiphosphate) (GDPβS) selectively depressed the response to warming without affecting the response to cooling. Intracellular application of guanosine 5′-O-(3-thiotriphosphate) (GTPγS) produced a gradual increase in K+ conductance of the resting membrane and apparently depressed the response to warming while it markedly augmented the response to cooling. These results suggest that GTP-binding protein can be activated thermally to open K+ channels without receptor stimulation. It is significant that the resting membrane potential of the neuron in the central nervous system may be regulated not only by Na+ pump but also by spontaneous activation of a certain GTP-binding protein, at least in Aplysia.
