The regulation of the retrograde axonal transport of (125)I-beta nerve growth factor is independent of calcium.

Calcium has been shown to play a major role in the regulation of endocytosis and exocytosis of synaptic vesicles and retrograde axonal transport of proteins. The role of calcium in the regulation of neurotrophin retrograde axonal transport is unknown. This study aimed to determine if calcium plays a role in the uptake and retrograde axonal transport of (125)I-beta nerve growth factor ((125)I-betaNGF) within sympathetic neurons innervating the iris by comparing it with (125)I-anti-dopamine beta hydroxylase (anti-DBH). The nonspecific voltage-sensitive calcium channel (VSCC) antagonists, cadmium (200 nmol/eye) and nickel (100 nmol/eye) reduced the amount of (125)I-anti-DBH retrograde axonal transport by 90 and 70%, respectively. In contrast, cadmium (200 nmol/eye) had no effect on (125)I-betaNGF retrograde axonal transport, while nickel (100 nmol/eye) caused a significant increase in the amount transported to the ganglia. The L-type VSCC antagonist nifedipine (10 nmol/eye) and N-type VSCC antagonist omega-conotoxin (1.5 nmol/eye) both had no effect on (125)I-anti-DBH retrograde axonal transport which suggests that these types of calcium channels are not involved in the exocytosis/endocytosis of anti-DBH containing vesicles. Thapsigargin (0.2 nmol/eye), an inhibitor of sarcoplasmic reticulum Ca(2+)-ATPases also significantly inhibited (125)I-anti-DBH transport but had no effect on (125)I-betaNGF retrograde transport. This suggests that (125)I-anti-DBH and (125)I-betaNGF are internalized into different vesicle types and that the endocytosis and retrograde axonal transport of (125)I-betaNGF are not dependent upon calcium.