Modulation of impulse conduction through axonal branchpoint by physiological, chemical and physical factors.
The impulse conduction capability of a crustacean bifurcating motor axon was studied under various physiological and physical conditions, and effects of several pharmacological agents were tested. The passive and active membrane properties were measured by intra- and extracellular recording, macropatch clamp and vaseline gap voltage clamp. Block of condition after high-frequency stimulation is caused by accumulation of K+ in the extracellular space, while its differential nature is attributed to early activation of the Na+-K+ electrogenic pump and increased intracellular Ca2+ in the thinner branch. Decreased Na+ and K+ conductance, or increased K+ conductance induced by various drugs, largely reduced the maximal following frequency of the branchpoint. High pressure initially increased the neuron excitability, and later decreased, to below control levels, the axon ability to conduct at high frequency. Cooling had a similar effect on the delayed effects of high pressure. The physiological significance of the frequency-dependent block and its possible role in anesthesia, epilepsy, high-pressure nervous syndrome and behavior are discussed.
D000818:Animals; D001274:Atmospheric Pressure; D001369:Axons / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D003080:Cold Temperature; D007477:Ions; D009046:Motor Neurons / Q000502:physiology*; D009132:Muscles / Q000294:innervation; D008121:Nephropidae; D009431:Neural Conduction / Q000187:drug effects; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D007477:Ions; D012964:Sodium; D011188:Potassium; D002118:Calcium