Abstract：
:The molecular mechanisms regulating the retrograde axonal transport of nerve growth factor (NGF) are currently unknown. This study identifies some of the signalling events involved. The phosphoinositide 3-kinase (PI3-kinase) inhibitor wortmannin (1 nmol/eye) irreversibly inhibits the amount of 125I-betaNGF retrogradely transported in both sensory and sympathetic neurons. Another PI3-kinase inhibitor LY294002 (100 nmol/eye) also inhibited 125I-betaNGF retrograde transport in sensory neurons. The pp70S6K inhibitor rapamycin (1 micromol/eye) had the same effect, inhibiting 125I-betaNGF transport only in sensory neurons. The cPLA2 inhibitor AACOCF3 (10 nmol/eye) had no effect on 125I-betaNGF transport in either sensory or sympathetic neurons. The TrkA receptor tyrosine kinase inhibitor AG-879 (10 nmol/eye) reduced 125I-betaNGF transport by approximately 50% in both sensory and sympathetic neurons. Cytochalasin D (2 nmol/eye), a disruptor of actin filaments and the dynein ATPase inhibitor erythro-9-[3-(2-hydroxynonyl)]adenine (EHNA) both inhibited 125I-betaNGF retrograde transport. These results demonstrate that in vivo TrkA tyrosine kinase activity, actin filaments and dynein are involved in the retrograde transport of NGF. In addition, different PI3-kinase isoforms may be recruited within different neuronal populations to regulate the retrograde transport of NGF. Potentially, these isoforms could activate alternative signalling pathways, such as pp70S6K in sensory neurons.
journal_name
Brain Resjournal_title
Brain researchauthors
Reynolds AJ,Bartlett SE,Hendry IAdoi
10.1016/s0006-8993(98)00396-5subject
Has Abstractpub_date
1998-07-06 00:00:00pages
67-74issue
1-2eissn
0006-8993issn
1872-6240pii
S0006-8993(98)00396-5journal_volume
798pub_type
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