HEAT-SHOCK PROTEINS (HSP-72 KD) IN THERMOTOLERANT RAT SCIATIC-NERVES

Localized heating of the rat sciatic nerve over a length of 5 mm for 3 0 min at 43-degrees-C resulted in the production of heat shock protein 72 kd in every nucleated cell and in the induction of thermotolerance in the heated area. HSP-72 kd was never detected in axons. Heat treat ment (30 min, 45-degrees-C) of thermotolerant nerves, 24 h after pretr eatment, led to histopathological changes in the nerve, similar to tho se in nonthermotolerant nerves after a less strong treatment, i.e. hea ting for 30 min at 44-degrees-C. Although axons did not contain HSPs a fter treatment at 43-degrees-C, these structures tolerated treatment a t 45-degrees-C. Therefore we conclude that axons in the rat sciatic ne rve are relatively heat-resistant and therefore we assume that axons d o not need protection by HSPs; this is in contrast to endothelial cell s and Schwann cells. Axons can be damaged indirectly as a consequence of vascular damage leading to ischaemia. Development of thermotoleranc e of the vasculature. ensuring a sufficient blood flow in the heated a rea, prevents this indirect damage.