Different mechanisms of secondary XXXX in thalamic nuclei after focal @entity2806 in rats.

@entity10747 @entity2806 @entity63 @entity2500 @entity4 @entity16 @entity9479 @entity1188 @entity528
BACKGROUND AND PURPOSE: After focal @entity2806 , depending on its localization and extent, secondary @entity528 may occur that is remote from the initial lesion. In this study differences in secondary damage of the ventroposterior thalamic nucleus (VPN) and the @entity9479 ( @entity9479 ) were investigated with the use of different @entity63 models. METHODS: Transient @entity2500 ( @entity2500 ) leads to cortical @entity1188 , including parts of the basal ganglia such as the globus pallidus, and to @entity4 . @entity63 generates pure cortical @entity1188 sparing the basal ganglia and with only minor @entity4 . @entity528 was quantified within the ipsilateral @entity9479 and VPN 14 days after @entity63 . Glial reactions were studied with the use of immunohistochemistry. RESULTS: @entity2500 resulted in delayed neuronal cell loss of the ipsilateral VPN and @entity9479 . Glial activation occurred in both nuclei beginning after 24 hours. @entity63 resulted in delayed neuronal cell loss only within the VPN. Even 2 weeks after @entity63 , glial activation could only be seen within the VPN. CONCLUSIONS: Pure cortical @entity1188 after @entity63 , without major @entity4 and without effects on the globus pallidus of the basal ganglia, only lead to secondary VPN damage that is possibly due to @entity10747 . @entity2500 , which results in @entity1188 and which causes @entity4 , leads to secondary damage in the VPN and @entity9479 . Thus, additional @entity16 may be due to loss of protective GABAergic input from the globus pallidus to the @entity9479 or due to the extensive @entity4 . @entity10747 is not possible because the @entity9479 , in contrast to the VPN, has no efferents to the cortex.
