Long-term changes in the ipsilateral substantia nigra after transient focal cerebral ischaemia in rats.
Transient focal cerebral ischaemia can cause neuronal damage in remote areas, including the ipsilateral thalamus and subsutantia nigra, as well as in the ischaemic core. In the present study, we investigated long-term changes in the ipsilateral substantia nigra from 1 up to 20 weeks after 90 min of transient focal cerebral ischaemia in rats, using tyrosine hydroxylase (TH), neuronal nuclei (NeuN), Iba-1, glial fibrillary acidic protein (GFAP) and brain-derived neurotrophic factor (BDNF) immunostaining. These results show that transient focal cerebral ischaemia in rats can cause a severe and prolonged neuronal damage in the ipsilateral striatum. Our results with TH and NeuN immunostaining also demonstrate that the atrophy of the ipsilateral substantia nigra after transient focal cerebral ischaemia was not static but progressive. Furthermore, our double-labelled immunohistochemical study suggests that BDNF released by GFAP-positive astrocytes may play a key role in the survival of dopaminergic neurones in the ipsilateral substantia nigra at the chronic stage after transient focal cerebral ischaemia, although the areas of the ipsilateral substantia nigra are decreased progressively after ischaemia. Thus our study provides further valuable information for the pathogenesis of neuronal damage after transient focal cerebral ischaemia.
Uchida
Hiroto
H
Department of Neurobiology and Therapeutics, Graduate School and Faculty of Pharmaceutical Sciences, The University of Tokushima, Tokushima, Japan.
Yokoyama
Hironori
H
Kimoto
Hiroki
H
Kato
Hiroyuki
H
Araki
Tsutomu
T
D000818:Animals; D001284:Atrophy; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology*; D007839:Functional Laterality / Q000502:physiology*; D007150:Immunohistochemistry; D008297:Male; D009410:Nerve Degeneration / Q000473:pathology; D009474:Neurons / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013378:Substantia Nigra / Q000378:metabolism / Q000473:pathology*