Hypoxia-
ischemia during the perinatal period causes excitotoxic lesions in sensitive brain areas, such as the striatum. The impact of
hypoxia-
ischemia on nigral neurons is less well known.
Hypoxia alone, a less traumatic event without overt histological sequelae, has neuroprotective properties when used as a preconditioning stimulus. In some pathologies, injured neurons of the nigrostriatal system in the adult may be the result of neurodegenerative processes that originated at early stages of life. The effects of
hypoxia on the immunoreactivity to
tyrosine hydroxylase of the dopaminergic neurons of the substantia nigra pars compacta and the effects of a period of
hypoxia previous to an excitotoxic lesion were examined by means of histological and Western blot methods, at immediate and late periods of the episode. By counting the number of
tyrosine hydroxylase-stained neurons and c-fos-positive nuclei a short period after injection of
quinolinic acid into the striatum, we observed that
hypoxia induced a more marked decrease in the number of
tyrosine hydroxylase-stained neurons. On the contrary, c-fos-positive profiles decreased in the substantia nigra pars reticulata of the
quinolinic acid-injected animals after the preconditioning
hypoxia.
Hypoxia alone did not affect the number of
tyrosine hydroxylase-positive neurons in the pars compacta nor did
hypoxia induce c-fos expression in the pars reticulata. More sensitive Western blot analysis of tissue blocks that included the whole substantia nigra demonstrated the same trend as the immunohistochemical results. We conclude that the responses of the substantia nigra neurons to
hypoxia are regionalized and potential
neuroprotective effects may depend on the vulnerability of each neuronal type.