There is increasing evidence that heat shock (HS) has long-term effects on
electrophysiological properties of neurons and synapses. Prior HS protects
neural circuitry from a subsequent heat stress but little is known about th
e mechanisms that mediate this plasticity and induce thermotolerance. Expos
ure of Locusta migratoria to HS conditions of 45 degreesC for 3 h results i
n thermotolerance to hitherto lethal temperatures. Locust flight motor patt
erns were recorded during tethered flight at room temperature, before and a
fter HS. In addition, intracellular action potentials (APs) were recorded f
rom control and HS motoneurons in a semi-intact preparation during a heat s
tress. HS did not alter the timing of representative depressor or elevator
muscle activity, nor did it affect the ability of the locust to generate a
steering motor pattern in response to a stimulus. However, HS did increase
the duration of APs recorded from neuropil segments of depressor motoneuron
s. Increases in AP duration were associated with protection of AP generatio
n against failure at subsequent elevated temperatures. Failure of AP genera
tion at high temperatures was preceded by a concomitant burst of APs and de
polarization of the membrane. The protective effects of HS were mimicked by
pharmacological blockade of IK+ with tetraethylammonium (TEA). Taken toget
her, these findings are consistent with a hypothesis that HS protects neuro
nal survival and function via K+ channel modulation. (C) 2001 John Wiley &
Sons. Inc.