Hypothermia-induced changes in rat short latency somatosensory evoked potentials.

Under general anesthesia, rats were gradually cooled from 37 degrees C to 24 degrees C, Slowly cooling avoided large temperature gradients between central and peripheral nervous systems. Short latency somatosensory potentials were evoked by forepaw stimulation and recorded from skull and depth structures. Cooling progressively increased onset and peak latencies and duration of all potentials. Amplitude of surface and depth recorded potentials decreased with decreasing temperatures except amplitude of surface component I increased. The response of surface and depth components to different rates of stimulation and cooling clearly indicates that cooling slows synaptic transmission much more than fiber conduction. The response of surface and depth recorded potentials to hypothermia suggests that evoked activity in cervical dorsal column and cuneate nucleus contributes to surface component I, that activity in cuneate nucleus, medial lemniscus, and inferior cerebellar peduncle contributes to surface component II, and that activity in thalamocortical fibers and probably cerebellum contributes to surface component III. These conclusions agree with our previous thoughts about the origin of short latency, surface recorded somatosensory evoked potentials.