[Synthesis and release of N-acetylaspartyl glutamate (NAAG) in medial giant axons in crayfish]. / Sintez i osvobozhdenie N-acetylaspartylglutamate (NAAG) v sredinnykh gigantskikh aksonakh raka.

Studies of crayfish Medial Giant nerve Fiber suggested that glutamate (GLU) released from the axon during action potential generation initiates metabolic and electrical responses of periaxonal glia. This investigation sought to elucidate the mechanism of GLU appearance extracellularly following axon stimulation. Axoplasm and periaxonal glial sheath from nerve fibers incubated with radiolabelled L-GLU contained radiolabeled GLU, glutamine (GLN), GABA, aspartate (ASP), and NAAG. Total radiolabel release was not altered by electrical stimulation of nerve cord loaded with [14C]-GLU by bath application or loaded with [14C]-GLU, [3H]-D-ASP, or [3H]-NAAG by axonal injection. However, radioactivity distribution among GLU and its metabolic products in the superfusate was changed, with NAAG accounting for the largest fraction. In axons incubated with radiolabeled GLU, the stimulated increase in radioactive NAAG in the superfusate coincided with the virtual clearance of radioactive NAAG from the axon. The increase in [3H]-GLU in the superfusion solution that was seen upon stimulation of nerve bathloaded with [3H]-NAAG was reduced when beta-NAAG, a competitive NAALADase inhibitor, was present. Together, these results suggest that some GLU is metabolized to NAAG in the giant axon and its periaxonal glia and that, upon stimulation, NAAG is released and converted to GLU by NAALADase. A quisqualate-, beta-NAAG-sensitive NAALADase activity was detected in nerve cord homogenates. Stimulation or NAAG administration in the presence of NAALADase inhibitor caused a transient hyperpolarization of the periaxonal glia comparable to that produced by L-GLU. The results implicate N-acetylaspartylglutamate (NAAG) and GLU as potential mediators. of the axon-glia interactions.

[Kinetics of nerve ending ion currents with nonhomogeneous distribution of ion channel density]. / Issledovanie kinetiki ionnykh tokov nervnogo okanchaniia pri neodnorodnom raspredelenii plotnostei ionnykh kanalov.

The Hodgkin-Huxley's equations of unmyelinated nerve fiber's electric behaviour has been used to create model of nerve endings electrogenesis. The Eler's integration method has been applied to solve the partial differential equation system which describes the spread of excitation in nerve ending. The effect of nonhomogeneous distribution densities of ionic channels along nerve ending on the ionic currents were simulated. The comparison of computed curves with nerve ending responses recorded by extracellular electrodes was performed. It was shown that the better match between simulated and recorded responses observes during densities' decrease potential-dependent sodium, potassium and calcium-activated potassium channels according to exponent along the nerve ending without changes of calcium channels density. As the result the amplitude and time-course of spread action potential, calcium current and transmitter release along the nerve ending appear to be changed.