Glutamatergic Excitation of Cortical Neurons Depending on the Point of Origin on the Membrane and Cholinergic Regulation in Hypothermia

Abstract

Experiments on guinea pig sensorimotor cortex slices with cooling of the incubation medium from 34°C to 21–22°C showed that hypothermia had no effect on evoked spike responses to application of glutamate to cell bodies, while application of glutamate to dendritic loci induced spike responses in the body with a short latent period with a hypothermic increase in the level of spontaneous activity and a longer latent period with a hypothermic decrease. Low-frequency neurons mainly showed increases in spontaneous activity on cooling, while high-frequency neurons (activity greater than 4 spikes/sec) responded with decreases in spike activity. The level of spontaneous sensorimotor cortex neuron activity started to change when the temperature dropped below 30°C. At this temperature, responses to iontophoretic delivery of acetylcholine to nerve cells decreased and there was a reduction in spike amplitude, which became greater with increasing cooling. These data provide evidence that hypothermic changes in the level of spontaneous activity evoked by altered influences on cell bodies of glutamatergic excitation of the dendrites, along with impairment to ion homeostasis, leading to decreases in spike amplitude are associated with temperature-dependent limiting of the rate of the M-cholinergic process over the temperature range 27–29°C. Neurons with different functional properties had different sensitivities to hypothermia.