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[Mechanism of calcium channel operation in the neuronal membranes of rat spinal ganglia].

A model of the calcium channel functioning is developed which provides a satisfactory description for the results of the experiments with intracellular injection of 3.5-cycloadenosine monophosphate (cAMP) into neurons of rat dorsal root ganglions. According to the model, the value of the intracellular concentration of cAMP necessary for keeping the calcium channels in the functioning state is equal to 10(-4)-10(-5)M. It is also shown that the neurons investigated contain a high-molecular factor whose interaction with cAMP molecules predetermines the active state of calcium channels.

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[Development of satellite-neuron relations in the spinal ganglia of the rat].

Cerebrospinal ganglia of 11-, 13-, 15-, 18- and 20-day-old embryos have been studied light- and electron-microscopically. On the 11th day of anlage the ganglia are presented exclusively as neuroblasts: the satellite-cells are formed later from lemmoblasts that install into the ganglion on the 13th-15th days both from the surrounding mesenchyme and from the developing roots and trunklets of the cerebrospinal nerves. In the ganglion they undergo proliferation and further differentiation. On the 15th day simple satellite-neuron interrelationships are formed: one satellite-cell is tightly connected with perikaryons of some neuroblasts and young neurons. On the 18th day around some neurons a double layered capsule is formed from the satellite-cells. Multilayered tunics are formed only on the 10th-15th day after birth. During the process of the capsule formation an unusual reactive character of the satellite-neuron interrelationships is revealed, it is manifested as, performed by the satellite-cells, an active microphagocytosis of the perikaryon cytoplasmic processes and the initial segment of the sensitive neuron main process. In embryogenesis the lemmocyte-axon interrelationships develop earlier than the satellite-neuronal ones.

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Reduction of experimentally induced neuronal death in spinal ganglia of the chick embryo by nerve growth factor.

Extirpation of the wing bud in 2-day chick embryos results in a conspicuous degeneration of neurons in both populations of brachial dorsal root ganglia (DRG). Daily injections of 1 to 6 micrograms of nerve growth factor (NGF), beginning at 4 1/2 days of incubation, rescued all small, late differentiating (DM) neurons and approximately 50% of large, early differentiating (VL) neurons, which would have died otherwise. The fact that NGF is an effective substitute for the hypothetical trophic maintenance factor for DRG which is normally produced by limb tissues strengthens our belief that NGF is identical with this factor. The control experiment, i.e., wing extirpation without NGF injections, revealed an inconsistency with previous data. Experiments on a number of different neuronal units had shown rather consistently that the period of experimentally induced neuron degeneration, caused by removal of the target, is synchronous with the period of normally occurring neuronal death in the same neuronal unit. This synchrony rule is violated by the VL population of brachial DRG. In this unit, the peak of degeneration resulting from wing bud extirpation occurs considerably earlier than the peak of normally occurring neuronal death. The competition hypothesis for the explanation of neuronal death had been based, in part, on the synchrony rule. We discuss the question of whether the deviation from the synchrony rule observed in our material represents a serious challenge to the competition hypothesis.

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