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The Journal of Neurophysiology Vol. 81 No. 2 February 1999, pp. 795-802
Copyright ©1999 by the American Physiological Society
1Department of Organismal Biology and Anatomy, The University of Chicago, Chicago, Illinois 60637; and 2Department of Biology, Queens University, Kingston, Ontario K7L 3N6, Canada
Long-term effects of prior heat shock on neuronal potassium currents
recorded in a novel insect ganglion slice preparation. Brief
exposure to high temperatures (heat shock) induces long-lasting adaptive changes in the molecular biology of protein interactions and
behavior of poikilotherms. However, little is known about heat shock
effects on neuronal properties. To investigate how heat shock affects
neuronal properties we developed an insect ganglion slice from locusts.
The functional integrity of neuronal circuits in slices was
demonstrated by recordings from rhythmically active respiratory neurons
and by the ability to induce rhythmic population activity with
octopamine. Under these "functional" in vitro conditions we
recorded outward potassium currents from neurons of the ventral midline
of the A1 metathoracic neuromere. In control neurons, voltage steps to
40 mV from a holding potential of 
60 mV evoked in control neurons
potassium currents with a peak current of 10.0 ± 2.5 nA and a
large steady state current of 8.5 ± 2.6 nA, which was still
activated from a holding potential of 40 mV. After heat shock most of
the outward current inactivated rapidly (peak amplitude: 8.4 ± 2.4 nA; steady state: 3.6 ± 2.0 nA). This current was inactivated
at a holding potential of 40 mV. The response to temperature changes
was also significantly different. After changing the temperature from
38 to 42°C the amplitude of the peak and steady-state current was
significantly lower in neurons obtained from heat-shocked animals than
those obtained from controls. Our study indicates that not only heat shock can alter neuronal properties, but also that it is possible to
investigate ion currents in insect ganglion slices.
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