Effects of advancing age on the central response of rat facial neurons to axotomy: Light microscope morphometry
✍ Scribed by Vaughan, Deborah W.
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 970 KB
- Volume
- 228
- Category
- Article
- ISSN
- 0003-276X
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✦ Synopsis
Following axotomy, the regrowth of peripheral axons takes longer in older individuals than in young ones. The present study compares central responses of facial motor neurons to a crush injury of the facial nerve in 3-monthold and 15-month-old male rats sampled through 28 days post-crush (dpc). Neuronal somata, nuclei, and nucleoli were measured in 30 pm brain stem sections within subdivisions of the facial nucleus that contain the cell bodies responsible for the movement of the vibrissae. The temporal patterns of change in the size of the three structures were interpreted with reference to the re-establishment of functional connections, i.e., the return of voluntary vibrissae activity, which is delayed by 4 days in the older animals relative to the younger ones. There was no agerelated difference in the pattern of soma1 swelling and recovery, nor was there a n age-related difference in the response of nuclei and nucleoli to axotomy through 4 dpc. Both nuclei and nucleoli increased in size in animals of both age groups, but after 4 dpc in the older animals nuclear enlargement was prolonged and the nucleolar increases were less robust compared to the younger animals. The greatest age difference appeared with the re-establishment of functional connections. In the 3-month-old animals, the resumption of whisker activity coincided with vigorous transient increases in the sizes of nuclei and nucleoli; in the 15-month-old animals, there was little nuclear response to functional recovery and a comparatively small increase in nuclear sizes. Given that signals from the periphery initiate central metabolic changes when the target is reached, this study suggests that the deteriorative effects of advancing may not simply reside in the neuron's decreased resiliency, but may reside in deficiencies in the signals derived from peripheral supporting cells, the target muscle, or in the reception of those signals.