Removal of the cortical projections alters expression of NOS in the different cell types of the superficial layers of the superior colliculus in rats

Abstract

Nitric oxide has several biological roles and nitric oxide synthase (NOS) is expressed in the nervous system, and co-localizes with NADPH-diaphorase. The superficial layers of the superior colliculus (SC), which receive retinal and cortical inputs, present NADPH-d staining in a sub-population of neurons that include all cell types. We have previously shown, by NADPH-diaphorase, that eye enucleation alters the intracellular distribution of NOS. Here, we studied the effect of cortical ablation on NOS expression by neurons in collicular superficial layers. Our results show that cortical ablation alters the proportion of different NOS-positive cell types, but not the intracellular distribution of the enzyme.

Differential regulation of the neuronal isoform of nitric oxide synthase in the superior colliculus and dorsal lateral geniculate nucleus of the adult rat brain following eye enucleation

“…In the DLG, we observed a few, sparse nNOS‐positive cells, localized preferentially to the central part of the nucleus. The nNOS immunostaining found in this study agreed with data from previous immunohistochemical mapping studies (Nucci et al, 2003; Tenorio et al, 2002).…”

“…The present results on the post‐lesion nNOS protein levels agree well with data from a previous study in chicks, in which we demonstrated that nNOS is upregulated in the chick visual system, and actual NO production increases, after unilateral enucleation (Torrão and Britto, 2004). Also, there are some other published examples of possible upregulation of nNOS after lesions, including the visual cortex after potassium chloride‐induced neurodegeneration (Torrão et al, 2002), axotomized retinal ganglion cells (Lee et al, 2003) and mesencephalic neurons (Nemcova et al, 2000), and some particular types of collicular neurons after cortical ablation (Tenorio et al, 2002). There are, however, reports on nNOS down‐regulation after monocular enucleation in the rat (Batista et al, 2003; Zhang et al, 1996), and visual deprivation (Aoki et al, 1993) or inhibition of retinal activity (Wong‐Riley et al, 1998) in primates.…”

NMDA receptor blockade alters the intracellular distribution of neuronal nitric oxide synthase in the superficial layers of the rat superior colliculus

“…Previous investigations have reported the effects of retinal deafferentation on nNOS expression (14,17,18,20). We think it highly unlikely that MK-801 treatment resulted in atrophy of the dendritic tree for the following reasons: 1) it is well established that in the absence of retinal fibers the overall dendritic development is remarkably normal (31).…”

“…The observations of Tenorio and co-workers (20) showing that the lack of neural activity arising from the retina, but not from the cortex, is able to modify the intracellular pattern of NADPH-d without a morphological change in SC cells (17) stimulated us to identify which molecular components regulate changes in the intracellular distribution of nNOS. Given the close interaction between NMDAR and nNOS observed in the SC PSDs (21), we asked whether the NMDAR has a direct influence on the intracellular distribution of nNOS in the neurons of SC superficial layers.…”

A quantitative study of the neuronal nitric oxide synthase expression in the superficial layers of the adult rat superior colliculus after perinatal enucleation

“…Furthermore, expression of NOS in the chick opticum tectum coincides temporally with the innervation by retinal axons, and removal of this pathway reduces dramatically the expression of NOS in the superficial layers of the tectum (Williams et al, 1994). In rats, cortical ablation alters the proportion of different NOS-positive cell types in the SC (Tenório et al, 2002). On the other hand, as we have previously described, the removal of the retinocollicular projection at birth does not alter the temporal pattern of nNOS expression in the SC superficial layers, but changes the intracellular distribution of this enzyme (Tenório et al, 1998).…”