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  • Title: The effects of age on enzyme activities in the rat facial nucleus following axotomy: acetylcholinesterase and cytochrome oxidase.
    Author: Vaughan DW.
    Journal: Exp Neurol; 1990 Aug; 109(2):224-36. PubMed ID: 2165914.
    Abstract:
    Advancing age affects the ability of motor neurons to regrow axons after the facial nerve is crushed. In rats, it requires 14 days after injury for 3-month-old animals to resume normal whisker activity, compared to at least 19 days in 15-month-old animals. The present study examines central enzymatic responses of facial motor neurons to axotomy. During the postoperative period from 1 day through 8 weeks, alternate frozen sections of brain stem are histochemically reacted to demonstrate activities of acetylcholinesterase (AChE) or cytochrome oxidase (COX) and the reactions are quantified using computerized image analyzing densitometry. AChE activity is evaluated separately in perikaryal cytoplasm and neuropil, while COX is assayed in the facial nucleus as a whole. Coincident with the initiation of axon outgrowth the activities of these enzymes decrease in the neurons. For AChE the decrease is greater in the older animals; for COX the decrease is equivalent in both age groups. With regard to the perikaryal AChE and the neuropil AChE, the recovery patterns are different in the two locations. In the perikarya AChE activity begins to recover after 4 days in both age groups; however, AChE activity in the neuropil remains decreased until after functional recovery of whisker activity, when it recovers rapidly in the 3-month-old animals, but more gradually in the 15-month-old animals. In both age groups, COX activity gradually decreases in response to axotomy. In the 3-month-old animals it recovers rapidly following return of whisker activity, while in the 15-month animals COX activity is maintained at the decreased level through 28 days post-crush, before it begins its gradual recovery. The study demonstrates that age differences are most apparent after the reestablishment of functional connections. This age-related deficiency may be related to deficiencies in retrogradely transported signals arising from the reinnervated target or in the older neuron's ability to respond to such signals.
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