NGF AUGMENTATION RESCUES TRIGEMINAL GANGLION AND PRINCIPALIS NEURONS,BUT NOT BRAIN-STEM OR CORTICAL WHISKER PATTERNS, AFTER INFRAORBITAL NERVE INJURY AT BIRTH

Prior studies indicate that neonatal nerve injury kills many trigemina l (V) first- and second-order cells, and interrupts pattern formation in the brainstem and cerebral cortex. Yet it is not known whether effe cts upon cell survival and pattern formation are causally related. To determine whether axotomized V ganglion cells can be rescued by an exo genous trophic agent, rats received 5 mg/kg of nerve growth factor (NG F) prior to, and every day after, infraorbital nerve section on the da y of birth until sacrifice on postnatal day (PND) 1, 3, 5, 7, or 14. O ther animals received identical lesions without NGF. Ganglion cell num bers were significantly reduced by PND1 in pups not given NGF, while N GF-treated rats displayed no significant cell loss through PND7. Howev er, NGF did not permanently rescue V neurons because ganglion cell num bers were reliably reduced by PND14. Cell numbers in V nucleus princip alis were reduced by PND1 in pups not given NGF, while NGF-treated ani mals displayed no cell loss through PND14. NGF's rescue of second-orde r cells is probably an indirect effect of NGF actions upon V ganglion cells because, in other newborns, NGF failed to maintain principalis c ells after direct lesion of the left V ganglion. To determine whether preventing cell death permits whisker-related pattern formation, other rats also received NGF prior to and after infraorbital nerve section at birth. After 3-14 days, patterns were assessed in the brainstem and cortex with cytochrome oxidase histochemistry and serotonin immunocyt ochemistry. Whisker-related patterns failed to develop as in cases not given NGF. These data indicate that communication with the periphery is necessary for the maintenance of central whisker-related patterns. They also suggest that V ganglion cells can be rescued, albeit tempora rily, from rapid injury-induced death by NGF, thereby delaying injury- induced cell death in nucleus principalis. However, the mechanism(s) r esponsible for injury-induced pattern alterations in the developing V system remains to be elucidated. (C) 1993 Wiley-Liss, Inc.