The non-impulsive stretch-receptor complex of the crab: a study of depolarization--release coupling at a tonic sensorimotor synapse
Blight, A.R.; Llinás, R.
Proceedings of the Clinical Dialysis and Transplant Forum 290(1039): 219-276
1980
ISSN/ISBN: 0094-6044 PMID: 6252555 Document Number: 156290
A new preparation for the study of synaptic transmission from the thoracic ganglion of the crab C. sapidus is described. The central anatomy of the nonimpulsive stretch-receptor neurons of the thoracic-coxal joint, and that of the promotor motoneurons with which they form synaptic junctions, was studied, using intracellular Co staining and light and electron microscopy. Attention was centered on the interaction of the stretch-receptor T-fiber and the 4 large motoneurons supplying the promoter muscle, which have their cell-bodies on the dorsal surface of the ganglion. The presynaptic terminal region of the T-fiber appeared to be a simple cylinder in form with a diameter of 40-60 .mu.m, containing large stores of synaptic vesicles at its periphery opposite the complex of motoneuron dendrites. Depolarization-release coupling in the T-fiber has similar properties to those observed in the squid giant synapse: same values for threshold, peak release and suppression potential. The crab synapses differ from that of the squid in that they normally transmit prolonged, graded depolarizations (i.e., receptor potentials) which are decrementally conducted from the periphery. The junctions were capable of continuous tonic transmission over many seconds without the strong depletion seen in more phasic synapses. Some of the time- and amplitude-dependent behavior of the overall reflex can be encoded at the level of the synaptic transmission, largely through the parameter of transmitter availability. Conduction of electrical signals in the proximal and presynaptic part of the sensory fiber was also investigated. Transient responses to step depolarizing currents in the fiber indicate the existence of a mechanism for the partial compensation of capacitative distortion in the decrementally-conducted receptor potential.