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

Calcium has been shown to play a major role in the regulation of endocytosi s and exocytosis of synaptic vesicles and retrograde axonal transport of pr oteins. The role of calcium in the regulation of neurotrophin retrograde ax onal transport is unknown. This study aimed to determine if calcium plays a role in the uptake and retrograde axonal transport of I-125-beta nerve gro wth factor (I-125-beta NGF) within sympathetic neurons innervating the iris by comparing it with I-125-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 I-125-anti-DB H retrograde axonal transport by 90 and 70%, respectively. In contrast, cad mium (200 nmol/eye) had no effect on I-125-beta NGF retrograde axonal trans port, while nickel (100 nmol/eye) caused a significant increase in the amou nt transported to the ganglia. The L-type VSCC antagonist nifedipine (10 nm ol/eye) and N-type VSCC antagonist omega-conotoxin (1.5 nmol/eye) both had no effect on I-125-anti-DBH retrograde axonal transport which suggests that these types of calcium channels are not involved in the exocytosis/endocyt osis of anti-DBH containing vesicles. Thapsigargin (0.2 nmol/eye), an inhib itor of sarcoplasmic reticulum Ca2+-ATPases also significantly inhibited I- 125-anti-DBH transport but had no effect on I-125-beta NGF retrograde trans port. This suggests that I-125-anti-DBH and I-125-beta NGF are internalized into different vesicle types and that the endocytosis and retrograde axona l transport of I-125-beta NGF are not dependent upon calcium. (C) 1999 Publ ished by Elsevier Science B.V. All rights reserved.