Effects of Acute Temperature Change and Acclimation Temperature on Neuromuscular Function and Lethality in Crayfish

Abstract

Times for 50% lethality (LD50) at temperatures of 35–40 C were two to three times longer for crayfish acclimated at 25 C than for those acclimated at 10 C. Nerveevoked excitatory postsynaptic potentials (EPSPs) and iontophoresed glutamateevoked postsynaptic potentials G-PSPs from the dactyl abductor of the first walking leg of Procambarus clarkii decreased in amplitude when the temperature was raised from 0 to 35 C. Reduction in EPSPs by stimulation of inhibitory axons and in G-PSPs by iontophoresis of gamma amino butyric acid (GABA) paralleled the excitatory potentials on warming. Preparations from crayfish acclimated to 10 C showed heatinduced neuromuscular block at 32.8 C for excitatory junctions and at 29.8 for inhibitory junctions. After acclimation at 25 C, the heat block temperature for excitation was 38.1 C and for inhibition was 34.8 C. Cold-induced neuromuscular block occurred at 5.5 C for inhibitory junctions of animals acclimated at 25 C. Cold block could not be induced at temperatures as low as −1 C for inhibitory junctions of animals acclimated at 10 C or for excitatory junctions of animals from either acclimation group. Inhibitory junctions are, therefore, more sensitive to heat and cold than excitatory ones. Focal extracellular recordings from excitatory junctions indicated that the principal mechanism for heat block is presynaptic. Quantal release of transmitter increased as temperature rose to a critical point where it decreased sharply from m-values 2.2–6.5 to less than 1. As temperature increased from 0 C to 15 C there was a sharp decrease in G-PSP duration; above 15 C, G-PSP duration declined with a lower slope. Warming from 10 C to 35 C increased the muscle membrane resting potential from 75–85 mV to 100–110 mV, an effect greater than predicted by Nernst relations. Part of the head-induced hyperpolarization in the high-temperature range was sensitive to ouabain (1 x 10⁻⁴ M). At 18 C, hyperpolarization of the muscle fiber membrane from −70 to −85 mV by injected current decreased the amplitude of G-PSPs; depolarization from −70 mV to −60 mV increased G-PSP amplitude, and further depolarization decreased it. The voltage-current (V-I) relations showed anomalous rectification in the hyperpolarized region. Depolarization of preparations held at above 30 C increased the amplitude of G-PSPs. Specific membrane resistance (Rm) decreased as temperature increased, with a high coefficient below 8–16 C and a low one above these temperatures. It is concluded that with rising temperature PSP amplitude is decreased mainly by shunting caused by decreases in muscle membrane resistance. Membrane resistance changes result from a direct effect of temperature on the membrane "leak" conductance and an indirect effect mediated via membrane hyperpolarization.