Changes in Dendrites of Adult Rat Ganglion Cells Regenerating Axons into Peripheral Grafts

Abstract

Axotomized neurons in the retina and other regions of the central nervous system (CNS) of adult rodents can regenerate long axons into segments of peripheral nerve (PN) grafted near their cell somata (Leoz and Arcante 1914; So and Aguayo 1985; Ramon y Cajal 1928; Aguayo 1985; Politis and Spencer 1986; Vidal-Sanz et al. 1987). When such PN grafts are used as “bridges” to replace the optic nerve (ON) and join again the eye and the superior colliculus (SC), some of the retinofugal fibers regrow along the graft and re-enter the SC where they can form synaptic contacts (Vidal-Sanz et al. 1987). However, since axonal regeneration into PN grafts requires that both the axotomy and the graft be near the somata of the retinal ganglion cells (RGC’s) (Aguayo et al. 1983; Aguayo 1985), the grafting procedure also results in the rapid or protracted death of a large number of RGC’s (Richardson et al. 1982; Villegas-Perez et al. 1988). Because axotomy to neurons other than RGC’s is known to also cause a spectrum of functional and anatomical alterations that affect the cell body (Misantone et al. 1984) and dendrites of surviving cells (James 1933; Watson 1974; Mendell 1984; Nja and Purves 1978; Villegas-Perez et al. 1988), we have studied anatomic changes in somata and dendritic arbors of RGC’s from 1 to 4 months after axotomy and grafting of a segment of PN whose most distal end was left blind-ended under the scalp, unconnected to the SC. The studies reported here are an early attempt to investigate the severity and duration of retrograde responses of injured RGC’s during periods of rapid regrowth — 1 and 2 months after PN grafting — and at 4 months after the insertion of the graft, when most axons can be assumed to have stopped extending actively along these blind-ended grafts (Aguayo et al. 1986; Trecarten et al. 1986).