Akademik Veri Yönetim Sistemi
GENERAL PHYSIOLOGY AND BIOPHYSICS, cilt.21, sa.2, ss.205-226, 2002 (SCI-Expanded)
Action potentials (APs) and impulse responses in the soma and axon of the rapidly and slowly adapting (SA) abdominal stretch receptor neurons of the crayfish (Astacus leptodactylus) were recorded with single microelectrode current-clamp technique. Impulse frequency response to constant current injection was almost constant in the SA neuron while the response decayed completely in the rapidly adapting (RA) neuron. Mean impulse frequency responses to current stimulations were similar in the receptor neuron pairs. In the RA neuron additional current steps evoked additional impulses while a sudden drop in the current amplitude caused adaptation. Impulse duration was dependent on the rate of rise when current ramps were used. Adaptation was facilitated when calculated receptor current was used. Exposing the neuron to 3 mmol/l TEA or scorpion venom resulted in partly elongated impulse responses. SA neuron could continuously convert the current input into impulse frequency irrespective of previous stimulation conditions. Exposing the SA neuron to 3 mmol/l TEA or 1 mmol/l Lidocaine reduced impulse duration to large current stimulations. The SA neuron fired spontaneously if it was exposed to 5-10 mmol/l Lidocaine or 10(-2) mg/ml Leiurus quinquestriatus venom. The action potential (AP) amplitudes in the RA soma, RA axon, SA soma, and SA axon were significantly different between components of all pairs. Duration of the AP in the axon of the RA neuron was significantly shorter than those in the RA soma, SA soma, and SA axon. Diameter of the RA axon was larger than that of the SA axon. Non-adapting impulse responses were promptly observed only in the SA axons. The results indicate that the RA neuron is a sort of rate receptor transducing the rapid length changes in the receptor muscle while the SA neuron is capable of transducing the maintained length changes in the receptor muscle. The differences in firing properties mainly originate from the differences in the active and passive properties of the receptor neurons.