Nitric oxide synthase in the frog cerebellum: Response of Purkinje neurons to unilateral eighth nerve transection
Article first published online: 1 AUG 2002
Copyright © 2002 Wiley-Liss, Inc.
The Anatomical Record
Volume 268, Issue 1, pages 73–83, September 2002
How to Cite
Pisu, M. B., Conforti, E., Botta, L., Valli, P. and Bernocchi, G. (2002), Nitric oxide synthase in the frog cerebellum: Response of Purkinje neurons to unilateral eighth nerve transection. Anat. Rec., 268: 73–83. doi: 10.1002/ar.10138
- Issue published online: 1 AUG 2002
- Article first published online: 1 AUG 2002
- Manuscript Accepted: 14 MAY 2002
- Manuscript Received: 5 DEC 2001
- NADPH diaphorase activity;
- NOS immunoreactivity;
When vestibular damage occurs, nitric oxide synthase (NOS) expression in rat cerebellar flocculus is affected. Since compensation for postural symptoms occurs and Purkinje cells play an important role in movement coordination and motor learning, we analyzed in situ the induction of NOS in the Purkinje cell population of the cerebellum (corpus cerebelli) of frog after unilateral transection of the eighth statoacoustic nerve to gain insight into the role of NO in neural plasticity after injury. Three days after neurectomy, the early effects induced NADPH diaphorase reactivity in most of the Purkinje cells on the ipsilateral side, while on the contralateral side the highest labeling was observed at 15 days. This finding can give information on the dynamics of vestibular compensation, in which NOS involvement was investigated. At 30 days, NADPH diaphorase reactivity was present in a large number of Purkinje cells of the whole cerebellum, while at 60 days a down-regulation for NADPH diaphorase reactivity was evident. A similar trend was observed for NOS-immunoreactivity, which was still present at 60 days in a high percentage of Purkinje cells, mainly on the ipsilateral side. On the basis of cell density evaluations, it was proposed that the early induction of NOS after neurectomy was linked to the degeneration of a part of the Purkinje neurons, while the permanence of NOS labeling might be due to a neuroprotective role of NO in the restoration phase of the vestibular compensation process. Anat Rec 268:73–83, 2002. © 2002 Wiley-Liss, Inc.