Duration Of Slow Potentials Research Articles

Slow active potentials in ventral inhibitory motor neurons of the nematode Ascaris.

The ability of ventral inhibitory motor neurons of the nematode Ascaris to generate slow depolarizing potentials was investigated using intracellular recording and current injection. In quiescent cells, regenerative depolarizations with peak amplitudes of approximately 20 mV and durations of several 100 ms were evoked in response to brief depolarizing current pulses. Repetitive slow potentials were produced in response to sustained depolarizing currents in a threshold-dependent manner. Repetitive slow potentials also occurred spontaneously, exhibiting cycle periods of about 700 ms. The ability of inhibitory motor neurons to generate slow potentials was blocked by addition of Co++, Cd++, or other Ca-channel blockers to the saline but not by TTX or substitution of Na+ with Tris. The amplitude and duration of slow potentials were increased in the presence of Ba++, Sr++, and TEA. Spontaneous slow potentials exhibited characteristics expected of intrinsically generated oscillations, including frequency modulation by injection of prolonged offset currents, phase resetting by brief current pulses, and suppression by strong hyperpolarization. Slow potentials appear to be generated in the ventral nerve cord processes and/or cell body of the motor neuron, and they produce rhythmic inhibitory postsynaptic potentials in ventral muscle cells. Slow potentials may therefore contribute to locomotory or other motor behaviors of the animal.

Temperature acclimation in the central nervous system of rainbow trout ( Salmo gairdnerii)

1. 1. The midbrain response to direct electrical stimulation of the retina was measured in rainbow trout acclimated to 10°C and following transfer and acclimation to 4 and 16°C. The evoked midbrain potential consisted first of a positive deflection upon which was superimposed two negative spikes of supposed pre-synaptic origin, and secondly of a slow negative potential, interpreted as post-synaptic in origin. 2. 2. Transfer of 10° acclimated trout to 4° caused an average 39 per cent protraction of the entire midbrain response pattern. After 21 days' acclimation to 4°, the negative spike latencies had decreased to 18 and 19 per cent above the 10° controls and the duration of the slow potential had decreased to 16 per cent above the 10° controls. 3. 3. Transfer of 10° acclimated trout to 16° caused an initial shortening of the negative spike latencies and slow potential duration. These values lengthened somewhat during acclimation to 16° but, since a similar lengthening occurred int he 10° controls, the change was judged noncompensatory. 4. 4. Thus, significant compensation occurred in response to low temperature acclimation (4°) but not to high temperature acclimation (16°). These results contrast with brain tissue respiration measurements that show that metabolic compensation is much more complete between 10 and 16° than between 4 and 10°.