Microtubule-associated protein 2 (MAP-2): a sensitive marker of seizure-related brain damage

Ballough, G.P.; Martin, Lee J.; Cann, Frank J.; Graham, John S.; Smith, Carl; Kling, Cathleen E.; Forster, Jeffry S.; Phann, Sorabe; Filbert, Margaret G.

doi:10.1016/0165-0270(95)00019-q

Cited by 53 publications

(40 citation statements)

References 23 publications

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“…Pronounced damage was seen in perirhinal cortex, amygdaloid complex, hippocampus and midline thalamic nuclei. This pattern of soman-induced seizure-related brain damage is consistent with previous reports (Ballough et al, 1995(Ballough et al, , 1998: McDonough et al, 1998).…”

Section: Resultssupporting

confidence: 81%

“…Control animals showed no evidence of MAP2 loss in any of the above brain regions. And the MAP2 immunostaining was consistent between individuals and exhibited the normal staining pattern described previously (Ballough et al, 1995(Ballough et al, , 1998 Treatment Groups Figure 2. Histogram depicting median lesion volumes of temporal lobe necrosis (mm 3 ).…”

Section: Resultsmentioning

confidence: 78%

“…MAP2 immunostaining was not observed in areas composed of white matter, except in small numbers of scattered neurons. The loss of the neuron-specific MAP2 marker indicates severe neuronal damage and provides clear demarcation of widespread neuronal necrosis (Ballough et al, 1995). In this study severely damaged brain regions were easily identified by an almost total absence of MAP2 immunostaining (Fig 1, soman).…”

Section: Resultsmentioning

confidence: 82%

“…The remaining hemispheres were paraffin processed, sectioned at 4 um and stained with hematoxylin and eosin (H&E). Morphometric image analysis of MAP2 stained sections was performed according to the procedure described by Ballough et al, (1995).…”

Section: Methodsmentioning

confidence: 99%

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Proceedings of the 2001 ECBC Scientific Conference on Chemical and Biological Defense Research, 6-8 March 2001, Marriott's Hunt Valley Inn, Hunt Valley, MD

Berg¹

2001

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Section: Resultssupporting

confidence: 81%

Section: Resultsmentioning

confidence: 78%

Section: Resultsmentioning

confidence: 82%

Section: Methodsmentioning

confidence: 99%

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Proceedings of the 2001 ECBC Scientific Conference on Chemical and Biological Defense Research, 6-8 March 2001, Marriott's Hunt Valley Inn, Hunt Valley, MD

Berg¹

2001

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“…For each rat, the average number of counts was obtained for six fields each of superficial, middle and deep thirds of cerebral cortex. For densitometric analysis, optical density of immunoreactivity in defined cortical areas was measured using Loats Inquiry Software (Loats Corporation, Westminster, MD, USA) as described (Ballough et al, 1995). The primary antibodies were used at concentrations that result in a slow, progressive DAB reaction to provide even staining of sections.…”

Section: Histology and Immunocytochemistrymentioning

confidence: 99%

Effect of glutamine synthetase inhibition on astrocyte swelling and altered astroglial protein expression during hyperammonemia in rats

et al. 2005

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Inhibition of glutamine synthesis reduces astrocyte swelling and associated physiological abnormalities during acute ammonium acetate infusion in anesthetized rats. We tested the hypothesis that inhibition of glutamine accumulation during more prolonged ammonium acetate infusion in unanesthetized rats reduces cortical astrocyte swelling and immunohistochemical changes in astrocytic proteins. Rats received a continuous i.v. infusion of either sodium acetate or ammonium acetate for 24 h to increase plasma ammonia from about 30-400 μmol/l. Cohorts were pretreated with vehicle or L-methionine-S-sulfoximine (MSO; 0.83 mmol/kg). MSO reduced glutamine synthetase activity by 57% and glutamine synthetase immunopositive cell number by 69%, and attenuated cortical glutamine accumulation by 71%. Hyperammonemia increased the number of swollen astrocytes in cortex and MSO reduced this increase to control values. The number of glial fibrillary acidic protein immunopositive cells in cortex was greater in hyperammonemic rats and the increase in superficial cortical layers was attenuated by MSO. Immunoreactivity for the gap junction protein connexin-43 in the neuropil, assessed by optical density, was greater in the hyperammonemic group compared with controls, but this increase was not attenuated by MSO. No changes in the optical density of GLT1 glutamate transporter immunoreactivity in cortex were detected in any group. We conclude that glutamine synthetase inhibition reduces astrocyte swelling and ameliorates some of the reactive astroglial cytoskeletal alterations seen at 24 h of hyperammonemia, but that gap junction changes in astrocytes occur independently of glutamine accumulation and swelling. Keywords ammonia; astrocyte; connexin; cerebral edema; glial fibrillary acidic protein; glutamine Astrocyte swelling is a distinctive feature of the histological finding in humans who die from severe liver disease or urea cycle disorders. Experimental models of liver dysfunction and hyperammonemia are also marked by watery swelling of astrocytes and cellular hypertrophy of astrocyte cell bodies without necessarily presenting with overt neuronal pathology. Thus, hyperammonemia is considered to be a major factor contributing to the cellular changes seen in severe hepatic encephalopathy (Norenberg, 1998 Tracer studies reveal that blood-borne ammonia is rapidly incorporated into brain glutamine, and that this process is markedly slowed in vivo by inhibiting glutamine synthetase (GS) with methionine sulfoximine (MSO), thereby disrupting compartmentation of nitrogen metabolism (Cooper et al., 1979). Based on the observations 1) that increased brain glutamine concentration is one of the most consistent biochemical change seen both clinically and experimentally with liver disease, urea cycle disorders or pure hyperammonemia (Cooper, 2001), and 2) that GS is enriched in astrocytes (Norenberg and Martinez-Hernandez, 1979), we postulated that glutamine accumulated in astrocytes may act as an osmolyte that contributes to astrocyte swelli...

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Primary sensory and forebrain motor systems in the newborn brain are preferentially damaged by hypoxia-ischemia

et al. 1997

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Cerebral hypoxia-ischemia causes encephalopathy and neurologic disabilities in newborns by unclear mechanisms. We tested the hypothesis that hypoxia-ischemia causes brain damage in newborns that is system-preferential and related to regional oxidative metabolism. One-week-old piglets were subjected to 30 minutes of hypoxia and then seven minutes of airway occlusion, producing asphyxic cardiac arrest, followed by cardiopulmonary resuscitation and four-day recovery. Brain injury in hypoxic-ischemia piglets (n = 6) compared to controls (n = 5) was analyzed by hematoxylin-eosin, Nissl, and silver staining, relationships between regional vulnerability and oxidative metabolism were evaluated by cytochrome oxidase histochemistry. Profile counting-based estimates showed that 13% and 27% of neurons in layers II/III and layers of somatosensory cortex had ischemic cytopathology, respectively; CA1 neuronal perikarya appeared undamaged, and < 10% of CA3 and CA4 neurons were injured; and neuronal damage was 79% in putamen, 17% in caudate, but nucleus accumbens was undamaged. Injury was found preferentially in primary sensory neocortices (particularly somatosensory cortex), basal ganglia (predominantly putamen, subthalamic nucleus, and substantia nigra reticulata), ventral thalamus, geniculate nuclei, and tectal nuclei. In sham piglets, vulnerable region generally had higher cytochrome oxidase levels than less vulnerable areas. Postischemic alterations in cytochrome oxidase were regional and laminar, with reductions (31-66%) occurring in vulnerable regions and increases (20%) in less vulnerable areas. We conclude that neonatal hypoxia-ischemia causes highly organized, system-preferential and topographic encephalopathy, targeting regions that function in sensorimotor integration and movement control. This distribution of neonatal encephalopathy is dictated possibly by regional function, mitochondrial activity, and connectivity.

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Microtubule-associated protein 2 (MAP-2): a sensitive marker of seizure-related brain damage

Cited by 53 publications

References 23 publications

Proceedings of the 2001 ECBC Scientific Conference on Chemical and Biological Defense Research, 6-8 March 2001, Marriott's Hunt Valley Inn, Hunt Valley, MD

Proceedings of the 2001 ECBC Scientific Conference on Chemical and Biological Defense Research, 6-8 March 2001, Marriott's Hunt Valley Inn, Hunt Valley, MD

Effect of glutamine synthetase inhibition on astrocyte swelling and altered astroglial protein expression during hyperammonemia in rats

Primary sensory and forebrain motor systems in the newborn brain are preferentially damaged by hypoxia-ischemia

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