The effect of nerve growth factor (NGF) upon axoplasmic transport in sympathetic neurons of the mouse

To study a possible agent which controls axoplasmic transport, the rates of transport were examined in postganglionic sympathetic neurons in adult mice which had been treated with nerve growth factor (NGF). Rates were measured by observing the movement along the nerve of a front of radioactive material after a prior intraganglionic injection ofL-[4,5-³H]leucine. The faster of two rates observed in female mice increased from a control value of1.22 ± 0.48mm/h (N= 15) to an experimental value of 1.83 ± 0.53mm/h (N= 6; P < 0.005)following the intramuscular injection of a total of 34 μg NGF/g body weight. In contrast, the same treatment caused the slower of the two rates to decrease from a control value of2.32 ± 0.81mm/day (N = 12) to an experimental value of 1.63 ± 0.70mm/day (N= 12; P < 0.05). The rate of slow transport was also examined in male animals. Untreated male mice exhibit a lower rate of slow transport (1.08 ± 0.38mm/day (N= 9) than do untreated females of equal age (P < 0.001). The result that nerve growth factor increases the rate of the faster phase of transport, and decreases the rate of the slower phase, indicates that this protein exerts a selective effect on transport.To obtain an independent measure of the influence of NGF, the extent of incorporation ofL-[4,5-³H]leucine into tissue proteins of excised stellate ganglia was assessed after 1 h in organ culture. Animals treated with NGF showed increased incorporation of tritiated leucine. Incorporation of radioactive leucine was correlated with the rateof transport in both control animals (r = 0.61) animals treaetd with NGF (r = 0.67). Within the framework of normal biological function, NGF may exert a controlling influence on both phases of axoplasmic transport in sympathetic postganglionic neurons.     

A comparison of the inhibitory effects of disodium pyrophosphate and disodium ethane-hydroxy-1, 1-diphosphonate on simple calcergy.

Both disodium pyrophosphate and disodium ethane-hydroxy-1, 1-diphosphate inhibit the reaction of simple calcergy induced in the mouse by lead acetate. The pyrophosphate is effective only by a direct interaction with the lead salt and the disphosphonate is effective only before the occurrence of histochemically demonstrable calcification.