TEMPERATURE DEPENDENCY OF BASAL AND EVOKED RELEASE OF AMINO-ACIDS ANDCALCITONIN-GENE-RELATED PEPTIDE FROM RAT DORSAL SPINAL-CORD

Moderate hypothermia significantly diminishes consequences of spinal a nd cerebral anoxia. One component of this neuroprotection has been hyp othesized to be suppression of excitotoxic transmitter release. Whethe r this suppression is attributable to reduced hypoxic injury that indu ces release or an alteration of the release process itself is unclear. We sought to characterize the temperature sensitivity (Q(10)) of basa l and evoked calcitonin gene-related peptide (CGRP) and amino acid rel ease from dorsal horn slices of rat spinal cord over a range of temper atures from 40 to 8 degrees C. At 40 degrees C, potassium (60 mM) and capsaicin (10 mu M) evoked a 21- and 32-fold increase in basal CGRP co ncentrations, respectively. Capsaicin had no effect on glutamate relea se, but potassium evoked a 2.7-fold increase. Release evoked by either potassium or capsaicin was reduced in a biphasic fashion with declini ng temperature. Over the range of 40 to 34 degrees C, the Q(10) values for evoked release for CGRP were 11.3 (potassium) and 39.7 (capsaicin ) and for glutamate, 5.5 (potassium). Over the range of 34 to 8 degree s C, Q(10) values were near unity for all evoked release (0.8 and 1.3 for CGRP and 1.2 for glutamate). Although serine, glycine, glutamine, taurine, and citrulline showed no evoked release, basal levels were re duced at temperatures below 34 degrees C. The pronounced temperature d ependency of evoked transmitter release between 40 and 34 degrees C is consistent with the profound cerebral protection observed with mild h ypothermia in which metabolic activity is only slightly depressed.