Activation of protein kinase C inhibits retrograde transport of neurotrophins in mice

Retrograde axonal transport of neurotrophins from nerve terminal to cell body requires a number of key processes, including internalization of the receptor‐neurotrophin complex into vesicles and formation of multivesicular bodies and their transport along the axon. Previous studies have shown that e...

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Veröffentlicht in:Journal of neuroscience research 2003-04, Vol.72 (2), p.203-210
Hauptverfasser: Ozsarac, Nesrin, Weible 2nd, Michael, Reynolds, Anna J., Hendry, Ian A.
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container_issue 2
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container_title Journal of neuroscience research
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creator Ozsarac, Nesrin
Weible 2nd, Michael
Reynolds, Anna J.
Hendry, Ian A.
description Retrograde axonal transport of neurotrophins from nerve terminal to cell body requires a number of key processes, including internalization of the receptor‐neurotrophin complex into vesicles and formation of multivesicular bodies and their transport along the axon. Previous studies have shown that each of these processes can be regulated by kinases. In this study, we looked at the role of protein kinase C (PKC) in retrograde transport by injecting labeled neurotrophins together with relevant pharmacological agents into the eye and measuring the accumulation of radioactivity in the trigeminal and superior cervical ganglia. Inhibitors of PKC, Ro‐31‐8220 and rottlerin, did not affect the retrograde transport of nerve growth factor (NGF); however, phorbol ester activation of classical and novel PKCs blocked retrograde transport. The effect of phorbol esters was partially reversed by rottlerin and Ro‐31‐8220. Activation of PKC has been shown to be involved in the disorganization of actin filaments. In this study, we show that Ro‐31‐8220 reverses growth cone collapse by phorbol 12‐myristate 13‐acetate and suggest that one of the effects of activating PKC on retrograde transport is to disrupt the actin filaments. © 2003 Wiley‐Liss, Inc.
doi_str_mv 10.1002/jnr.10568
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Neurosci. Res</addtitle><description>Retrograde axonal transport of neurotrophins from nerve terminal to cell body requires a number of key processes, including internalization of the receptor‐neurotrophin complex into vesicles and formation of multivesicular bodies and their transport along the axon. Previous studies have shown that each of these processes can be regulated by kinases. In this study, we looked at the role of protein kinase C (PKC) in retrograde transport by injecting labeled neurotrophins together with relevant pharmacological agents into the eye and measuring the accumulation of radioactivity in the trigeminal and superior cervical ganglia. Inhibitors of PKC, Ro‐31‐8220 and rottlerin, did not affect the retrograde transport of nerve growth factor (NGF); however, phorbol ester activation of classical and novel PKCs blocked retrograde transport. The effect of phorbol esters was partially reversed by rottlerin and Ro‐31‐8220. 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subjects Actin Cytoskeleton - drug effects
Animals
Axonal Transport - drug effects
Axonal Transport - physiology
Cell Survival - drug effects
Enzyme Activators - pharmacology
Enzyme Inhibitors - pharmacology
Eye - innervation
Eye - metabolism
Growth Cones - drug effects
Indoles - pharmacology
Male
Mice
Mice, Inbred BALB C
Nerve Growth Factors - drug effects
Nerve Growth Factors - metabolism
Neurons, Afferent - drug effects
Neurons, Afferent - metabolism
NGF
NT4
p75NTR
phorbol esters
Presynaptic Terminals - drug effects
Protein Kinase C - antagonists & inhibitors
Protein Kinase C - drug effects
Protein Kinase C - metabolism
Receptor, Nerve Growth Factor - metabolism
Receptor, trkA - metabolism
Superior Cervical Ganglion - metabolism
Sympathetic Nervous System - metabolism
Tetradecanoylphorbol Acetate - pharmacology
Trigeminal Ganglion - metabolism
TrkA
title Activation of protein kinase C inhibits retrograde transport of neurotrophins in mice
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