The degeneration-regeneration process induced by bupivacaine injection has been studied in rat extensor digitorum longus (EDL) muscle in the presence or absence of nerve, the presence of tetrodotoxin (TTX)-induced block of nerve impulse conduction, and the presence of vinblastine- induced block of nerve axoplasmic flow associated to TTX block. Seven and 14 days after bupivacaine injection, myosin heavy chain (MHC) expression was analysed by immunohistochemistry and Western blot. Type 1 MHC isoform expression was almost completely dependent on nerve impulse discharge. Expression of the type 2A showed a zonal distribution in denervated muscles, and a marked down-regulation in the TTX-paralysed, but not in TTXvinblastine- treated muscles. These results show that expression of type 2A isoform in innervated- regenerated fast muscle is mainly due to neuromotor activity. They also suggest that 2A isoform expression is inhibited by a chemical factor carried by axoplasmic flow.
Nerve influence on rat fast-twitch skeletal muscle regeneration
DANIELI, DANIELA;GERMINARIO, ELENA;MEGIGHIAN, ARAM;MIDRIO, MENOTTI
2002
Abstract
The degeneration-regeneration process induced by bupivacaine injection has been studied in rat extensor digitorum longus (EDL) muscle in the presence or absence of nerve, the presence of tetrodotoxin (TTX)-induced block of nerve impulse conduction, and the presence of vinblastine- induced block of nerve axoplasmic flow associated to TTX block. Seven and 14 days after bupivacaine injection, myosin heavy chain (MHC) expression was analysed by immunohistochemistry and Western blot. Type 1 MHC isoform expression was almost completely dependent on nerve impulse discharge. Expression of the type 2A showed a zonal distribution in denervated muscles, and a marked down-regulation in the TTX-paralysed, but not in TTXvinblastine- treated muscles. These results show that expression of type 2A isoform in innervated- regenerated fast muscle is mainly due to neuromotor activity. They also suggest that 2A isoform expression is inhibited by a chemical factor carried by axoplasmic flow.Pubblicazioni consigliate
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