Different mechanisms of secondary neuronal damage in thalamic nuclei after focal cerebral ischemia in rats.
OBJECTIVE
After focal cerebral ischemia, depending on its localization and extent, secondary neuronal damage may occur that is remote from the initial lesion. In this study differences in secondary damage of the ventroposterior thalamic nucleus (VPN) and the reticular thalamic nucleus (RTN) were investigated with the use of different ischemia models.


METHODS
Transient middle cerebral artery occlusion (MCAO) leads to cortical infarction, including parts of the basal ganglia such as the globus pallidus, and to widespread edema. Photothrombotic ischemia generates pure cortical infarcts sparing the basal ganglia and with only minor edema. Neuronal degeneration was quantified within the ipsilateral RTN and VPN 14 days after ischemia. Glial reactions were studied with the use of immunohistochemistry.


RESULTS
MCAO resulted in delayed neuronal cell loss of the ipsilateral VPN and RTN. Glial activation occurred in both nuclei beginning after 24 hours. Photothrombotic ischemia resulted in delayed neuronal cell loss only within the VPN. Even 2 weeks after photothrombotic ischemia, glial activation could only be seen within the VPN.


CONCLUSIONS
Pure cortical infarcts after photothrombotic ischemia, without major edema and without effects on the globus pallidus of the basal ganglia, only lead to secondary VPN damage that is possibly due to retrograde degeneration. MCAO, which results in infarction of cortex and globus pallidus and which causes widespread edema, leads to secondary damage in the VPN and RTN. Thus, additional RTN damage may be due to loss of protective GABAergic input from the globus pallidus to the RTN or due to the extensive edema. Retrograde degeneration is not possible because the RTN, in contrast to the VPN, has no efferents to the cortex.
Dihné
Marcel
M
Department of Neurology, Rheinisch Westfälische Technische Hochschule-Aachen, Aachen, Germany.
Grommes
Christian
C
Lutzenburg
Michael
M
Witte
Otto W
OW
Block
Frank
F
D000818:Animals; D001479:Basal Ganglia / Q000098:blood supply / Q000473:pathology; D002545:Brain Ischemia / Q000209:etiology / Q000473:pathology*; D002452:Cell Count; D016923:Cell Death; D002540:Cerebral Cortex / Q000098:blood supply / Q000473:pathology; D004195:Disease Models, Animal; D018450:Disease Progression; D007150:Immunohistochemistry; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000473:pathology*; D008028:Light Coagulation; D008297:Male; D009457:Neuroglia / Q000473:pathology; D009474:Neurons / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013787:Thalamic Nuclei / Q000098:blood supply* / Q000473:pathology*; D013788:Thalamus / Q000098:blood supply / Q000473:pathology; D013997:Time Factors