Transient changes in the presence of nitric oxide synthases and nitrotyrosine immunoreactivity after focal cortical lesions

Bidmon, Hans‐Jürgen; Wu, Jang‐Yen; Buchkremer-Ratzmann, Irmgard; Mayer, Bernd; Witte, Otto W.; Zilles, Karl

doi:10.1016/s0306-4522(97)00275-3

Cited by 48 publications

(14 citation statements)

References 102 publications

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“…Also radical-induced, pathological, intravascular changes are restricted to the ipsilateral hemisphere in this lesion model. 41 Keeping in mind that antibodies bind to proteins that appear only after transcription and translation of mRNA have taken place, induction of Mn-SOD seems to occur very early. The increase in the number of Mn-SOD-positive cells seen between days 2 to 7, as well as the astrocytic responses, may have been induced by further damage due to peroxynitrite, as observed in other studies.…”

Section: 35mentioning

confidence: 99%

“…Therefore, it is not clear to what extent certain effects are model dependent, and it seems more likely that the detection of diaschisis depends on the markers or tracers and their concentrations studied (optimal concentrations may be different for the penumbra and the remote regions) as well as on the time after injury, because diaschisis is a transient phenomenon. 35,41,44 Noteworthy, Szele et al 52 reported that remote changes in GAP43, synaptophysin, and certain growth factors differ according to the methods used to induce the cortical lesions. Compared with cortical photothrombosis, subcortical injury and related edema are certainly different in MCAO, and changes of Mn-SOD and CuZn-SOD differ partly in both models.…”

Section: 35mentioning

confidence: 99%

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Transient Increase of Manganese–Superoxide Dismutase in Remote Brain Areas After Focal Photothrombotic Cortical Lesion

Bidmon

Kato

Schleicher

et al. 1998

Stroke

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Background and Purpose-Free radicals including superoxide are responsible for postlesional cytotoxicity. In contrast to the constitutive CuZn-superoxide dismutases (SODs), manganese-superoxide dismutase (Mn-SOD) is inducible and has the potential to protect neurons by its superoxide dismutating activity. Therefore, we studied the presence and the regional changes in Mn-SOD within the brain after focal cortical ischemia. Methods-Focal cortical photothrombotic lesions were produced in the hindlimb region of rat brains. Animals were anesthetized and transcardially perfused with Zamboni's fixative. Mn-SOD was immunohistochemically localized using an antiserum against rat-Mn-SOD. Changes in Mn-SOD immunoreactivity were quantified by image analysis. Results-Focal photothrombosis caused a perilesional increase in Mn-SOD after 24 hours, followed by a further significant increase at 48 hours in perilesional cortex, ipsilateral corpus callosum, hippocampus, and thalamus, as well as in a homotopic cortical area within the nonlesioned hemisphere. At day 2, Mn-SOD was present in neurons and astrocytes. Up to day 7, Mn-SOD increased in the entire ipsilateral and contralateral cortex but remained higher elevated in the ipsilateral hippocampus and thalamus. Thereafter, Mn-SOD decreased globally but remained elevated in some cortical neurons up to day 60. Conclusions-The early transient increase of Mn-SOD in distinct brain regions, which are functionally connected via afferents and efferents, suggests that these regions are affected by the injury. It suggests that Mn-SOD protects the cells in these regions from superoxide-induced damage and therefore may limit the retrograde and anterograde spread of neurotoxicity. (Stroke. 1998;29:203-211.)

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Section: 35mentioning

confidence: 99%

Section: 35mentioning

confidence: 99%

Transient Increase of Manganese–Superoxide Dismutase in Remote Brain Areas After Focal Photothrombotic Cortical Lesion

Bidmon

Kato

Schleicher

et al. 1998

Stroke

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“…In addition, focal cerebral ische-mia was induced by photothrombosis of the temporoparietal cortex, which is known to produce a pure cortical lesion. 14 Neuronal damage and glial reactions were studied in the VPN and RTN up to 14 days after induction of ischemia.…”

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confidence: 99%

Different Mechanisms of Secondary Neuronal Damage in Thalamic Nuclei After Focal Cerebral Ischemia in Rats

Dihné

Grommes

Lutzenburg

et al. 2002

Stroke

117

106

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Background and Purpose-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.

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“…Interestingly, enriched environmental conditions were not able to reverse the degenerative alterations in the neurons. Accordingly, to explain our contradictory results regarding COX-2 and 3-NT on the one hand and dMBP on the other, we suggest that COX-2 and 3-NT may indicate oxidative stress [45] . dMBP expression is assumed to be a result of degeneration processes that are not reversible in enriched environmental conditions.…”

Section: Discussionmentioning

confidence: 78%

Enriched Environmental Conditions Ameliorate Age-Dependent Alterations in the Somatosensory System, but Do Not Affect the Motor System of the Rat Spinal Cord

et al. 2006

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At the behavioral level, old rats are known to show a number of age-related changes such as characteristic impairments in the sensorimotor system, which is most strikingly expressed in a walking impairment involving the hind limbs. We have previously shown that sensorimotor impairments involving the hind limbs are in part reversible following housing in an enriched environment. The question arises as to whether these effects are accompanied by cytological alterations in the spinal cord. During aging, we found an increase in cyclooxygenase with nitrotyrosine in the fasciculus gracilis and lateral funiculus. The somatosensory tracts and dorsal horn were more affected by myelin-degrading processes than the other parts of the spinal cord. The accumulation of lipofuscin seemed to depend on age, but independent of the environment. In contrast, the age-related calretinin immunoreactivity loss in the substantia gelatinosa from both the cervical and the lumbar enlargements was significantly reduced in stimulating environmental conditions. Morphologically, the lectin binding sites of the perineuronal nets seemed to be decreased. The results provide evidence that the somatosensory system of the spinal cord is affected by age-dependent alterations independently of the motor system.

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Transient changes in the presence of nitric oxide synthases and nitrotyrosine immunoreactivity after focal cortical lesions

Cited by 48 publications

References 102 publications

Transient Increase of Manganese–Superoxide Dismutase in Remote Brain Areas After Focal Photothrombotic Cortical Lesion

Transient Increase of Manganese–Superoxide Dismutase in Remote Brain Areas After Focal Photothrombotic Cortical Lesion

Different Mechanisms of Secondary Neuronal Damage in Thalamic Nuclei After Focal Cerebral Ischemia in Rats

Enriched Environmental Conditions Ameliorate Age-Dependent Alterations in the Somatosensory System, but Do Not Affect the Motor System of the Rat Spinal Cord

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