Heat shock proteins (HSP-72 kd) in thermotolerant rat sciatic nerves

Abstract

Localized heating of the rat sciatic nerve over a length of 5 mm for 30 min at 43°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 treatment (30 min, 45°C) of thermotolerant nerves, 24 h after pre-treatment, led to histopathological changes in the nerve, similar to those in non-thermotolerant nerves after a less strong treatment, i.e. heating for 30 min at 44°C. Although axons did not contain HSPs after treatment at 43°C, these structures tolerated treatment at 45 °C. Therefore we conclude that axons in the rat sciatic nerve are. relatively heat-resistant and therefore we assume that axons do not need protection by HSPs; this is in contrast to endothelid cells and Schwann cells. Axons can be damaged indirectly as a consequence of vascular damage leading to ischaemia. Development of thermotolerance of the vasculature, ensuring a sufficient blood flow in the heated area, prevents this indirect damage.

Key Words:

• Heat shock proteins
• hyperthermia
• neuropathy
• sciatic nerve
• thermotolerance