Immunohistochemical study of glial reaction and serum-protein extravasation in relation to neuronal damage in rat hippocampus after ischemia

Schmidt‐Kastner, Rainald; Szymaś, J; Hossmann, K.‐A.

doi:10.1016/0306-4522(90)90048-9

Cited by 180 publications

(65 citation statements)

References 63 publications

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“…In contrast, the delayed component of torsinA increase includes prominent expression in reactive astrocytes in regions of hippocampus (e.g., CA1) known to undergo neuron loss and synaptic reorganization after ischemia (Arabadzisz and Freund, 1999;Briones et al, 2004). In agreement with previous work, astrocytic and microglial markers showed the most prominent post-ischemic response in the CA1 region (Schmidt-Kastner et al, 1990;Morioka et al, 1991;Gottlieb and Matute, 1999). Although not specifically evaluated in this study, the persistent modest increase in torsinA expression noted in cerebellum (Fig.…”

Section: Post-ischemic Torsina Expression In the Cnssupporting

confidence: 77%

Glial elements contribute to stress-induced torsinA expression in the CNS and peripheral nervous system

et al. 2008

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DYT1 dystonia is caused by a single GAG deletion in Exon 5 of TOR1A, the gene encoding torsinA, a putative chaperone protein. In this study, central and peripheral nervous system perturbations (transient forebrain ischemia and sciatic nerve transection, respectively) were used to examine the systems biology of torsinA. After forebrain ischemia, quantitative real-time RT-PCR identified increased torsinA transcript levels in hippocampus, cerebral cortex, thalamus, striatum, and cerebellum at 24 h and 7 d. Expression declined toward sham values by 14 d in striatum, thalamus and cortex, and by 21 d in cerebellum and hippocampus. TorsinA transcripts were localized to dentate granule cells and pyramidal neurons in control hippocampus and were moderately elevated in these cell populations at 24 h after ischemia, after which CA1 expression was reduced, consistent with the loss of this vulnerable neuronal population. Increased in situ hybridization signal in CA1 stratum radiatum, stratum lacunosum-moleculare, and stratum oriens at 7 d after ischemia was correlated with the detection of torsinA immunoreactivity in interneurons and reactive astrocytes at 7 and 14 days. Sciatic nerve transection increased torsinA transcript levels between 24 h and 7 days in both ipsilateral and contralateral dorsal root ganglia (DRG). However, increased torsinA immunoreactivity was localized to both ganglion cells and satellite cells in ipsilateral DRG but was restricted to satellite cells contralaterally. These results suggest that torsinA participates in the response of neural tissue to central and peripheral insults and its sustained up-regulation indicates that torsinA may contribute to remodeling of neuronal circuitry. The striking induction of torsinA in astrocytes and satellite cells points to the potential involvement of glial elements in the pathobiology of DYT1 dystonia. KeywordsDYT1; dystonia; reactive astrocytes; hippocampus; satellite cells; dorsal root ganglia DYT1 dystonia obeys an autosomal dominant inheritance pattern with reduced penetrance, usually begins in childhood and frequently generalizes. The causal mutation is a GAG deletion in the TOR1A gene that removes a single glutamic acid residue near the carboxy terminus of the encoded protein torsinA (Ozelius et al., 1997;Ozelius et al., 1999 Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Neuwald et al., 1999;Kamm et al., 2004;Callan et al., 2007). Members of the AAA+ family function as molecular chaperones for protein quality control (protein complex assembly, operation, disassembly, protein folding, unfolding, and degrad...

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Section: Post-ischemic Torsina Expression In the Cnssupporting

confidence: 77%

Glial elements contribute to stress-induced torsinA expression in the CNS and peripheral nervous system

et al. 2008

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“…In addition, the hypertrophy of astrocytes, as re flected by an increase in the GF AP immunoreactiv ity, and the degradation of MAP2 have been con sidered to be sensitive and reliable markers of sub tle and morphologically undetectable neuronal damage during the early stages of cerebral ischemia (Kuwai et aI., 1989;Inuzuka et a!., 1990;Schmidt Kastner et a!., 1990;Rischke and Krieglstein, 1991). In our study, neither the degradation of MAP2 nor the increase in the GF AP immunoreactivity could be observed in the ipsilateral hippocampal CA 1 field from the cognitively impaired rats.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Spatial Cognitive Impairment after Middle Cerebral Artery Occlusion in Rats: No Involvement of the Hippocampus

Okada

Nakanishi

Tamura

et al. 1995

J Cereb Blood Flow Metab

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Summary:The behavioral and neurochemical changes in the chronic phase of permanent occlusion of the right middle cerebral artery (MCA) in rats were investigated. One month after MCA occlusion, 23 rats were unable to solve a radial eight-arm maze task during an entire I-month period, whereas seven rats were able to solve this task. Three months after occlusion, 19 MCA-oc cluded rats failed to solve the task successfully again for at least I month (the cognitively impaired rats), whereas II MCA-occluded rats were able to solve it (the cogni tively unimpaired rats). The rats that underwent behav ioral testing were examined for any changes in the ace tylcholine (ACh) levels in the hippocampus using HPLC with electrochemical detection or the formation of long term potentiation (L TP) in the population spike of the hippocampal CAl field. The immunohistochemical distriPermanent unilateral middle cerebral artery (MCA) occlusion in rats is widely used as a model of focal cerebral ischemia. In the acute phase, this model selectively causes infarction in the ipsilateral cerebral cortex and caudate nucleus-putamen com plex (Tamura et aI., 1981 a; lizuka et aI., 1989). Af ter the infarction in the territory of the MCA, �2 weeks after MCA occlusion, progressive shrinkage occurs in the ipsilateral thalamus (Fujie et aI., 1990) Received March 31, 1994; final revision received October 14, 1995; accepted February 27, 1995. Address correspondence and reprint requests to Dr. Michihiro Fujiwara, Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka 814-01, Japan.Abbreviations used: MeA, middle cerebral artery; LTP, long term potentiation; MAP2, microtubule-associated protein 2; GFAP, glial fibrillary acidic protein. 1012bution of either the microtubule-associated protein 2 (MAP2) or glial fibrillary acidic protein (GF AP) in the hippocampus of the cognitively impaired rats was also studied. In the cognitively impaired rats, neither the sup pression of the induction of L TP, nor the degradation of MAP2, nor the increase in the GFAP immunoreactivity was observed in the hippocampus. The levels of ACh in the hippocampus did not change significantly among the cognitively impaired, unimpaired, and the sham-operated rats. These results suggest that MCA occlusion is capable of producing long-term spatial cognitive disturbance in rats without any evidence of neurobiological damage in the hippocampus. Key Words: Focal cerebral ischemia Memory-Long-term potentiation-Microtubule-asso ciated protein 2-Glial fibrillary acidic protein.

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“…The brains were removed, post-fixed, placed in sucrose, and sectioned on a cryostat. Immunocytochemistry of tissue sections with antibodies against GFAP, S100, and BrdU was done as described (25)(26)(27).…”

Section: Methodsmentioning

confidence: 99%

Neural cell adhesion molecule (N-CAM) inhibits astrocyte proliferation after injury to different regions of the adult rat brain.

Krushel

Sporns

Cunningham

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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N-CAM or one of the N-CAM-related molecules was infused than on the opposite side. The inhibition was greatest in the cortical lesion sites ('50%) and was less pronounced in the hippocampus (-25%) and striatum ("20%). Two weeks after the lesion, the cerebral cortical sites infused with N-CAM continued to exhibit a significantly smaller population of dividing astrocytes than the sites on the opposite side. When N-CAM and basic fibroblast growth factor, which is known to stimulate astrocyte division in vitro, were coinfused into cortical lesion sites, astrocyte proliferation was still inhibited. These results suggest the hypothesis that, by reducing glial proliferation, N-CAM or its peptides may help create an environment that is more suitable for neuronal regeneration.

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Immunohistochemical study of glial reaction and serum-protein extravasation in relation to neuronal damage in rat hippocampus after ischemia

Cited by 180 publications

References 63 publications

Glial elements contribute to stress-induced torsinA expression in the CNS and peripheral nervous system

Glial elements contribute to stress-induced torsinA expression in the CNS and peripheral nervous system

Long-Term Spatial Cognitive Impairment after Middle Cerebral Artery Occlusion in Rats: No Involvement of the Hippocampus

Neural cell adhesion molecule (N-CAM) inhibits astrocyte proliferation after injury to different regions of the adult rat brain.

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