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S100b counteracts neurodegeneration of rat cholinergic neurons in brain slices after oxygen-glucose deprivation.

Serbinek D, Ullrich C, Pirchl M, Hochstrasser T, Schmidt-Kastner R, Humpel C - Cardiovasc Psychiatry Neurol (2010)

Bottom Line: Our data showed that 3 days of OGD induced a marked decrease of cholinergic neurons (60% of control), which could be counteracted by 50 mug/mL recombinant S100b.The effect was dose and time dependent.We conclude that S100b is a potent neuroprotective factor for cholinergic neurons during ischemic events.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Psychiatry and Exp. Alzheimer's Research, Department of Psychiatry and Psychotherapy, Innsbruck Medical University, Anichstra beta e 35, 6020 Innsbruck, Austria.

ABSTRACT
Alzheimer's disease is a severe chronic neurodegenerative disorder characterized by beta-amyloid plaques, tau pathology, cerebrovascular damage, inflammation, reactive gliosis, and cell death of cholinergic neurons. The aim of the present study is to test whether the glia-derived molecule S100b can counteract neurodegeneration of cholinergic neurons after oxygen-glucose deprivation (OGD) in organotypic brain slices of basal nucleus of Meynert. Our data showed that 3 days of OGD induced a marked decrease of cholinergic neurons (60% of control), which could be counteracted by 50 mug/mL recombinant S100b. The effect was dose and time dependent. Application of nerve growth factor or fibroblast growth factor-2 was less protective. C-fos-like immunoreactivity was enhanced 3 hours after OGD indicating metabolic stress. We conclude that S100b is a potent neuroprotective factor for cholinergic neurons during ischemic events.

No MeSH data available.


Related in: MedlinePlus

Immunohistochemistry for cholinergic choline acetyltransferase (ChAT) positive neurons (a)–(c) and c-fos immunoreactive nuclei (d)–(f) in organotypic brain slices of the basal nucleus of Meynert. Slices show control stainings before ((a), (c), (d)), or 3 days (ChAT+, (b)) or 3 hours (c-fos+, (e) and (f)) after oxygen-glucose deprivation. Scale bar in A = 300 μm ((a), (b), (d), and (e)) and 75 μm ((c) and (f)).
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fig1: Immunohistochemistry for cholinergic choline acetyltransferase (ChAT) positive neurons (a)–(c) and c-fos immunoreactive nuclei (d)–(f) in organotypic brain slices of the basal nucleus of Meynert. Slices show control stainings before ((a), (c), (d)), or 3 days (ChAT+, (b)) or 3 hours (c-fos+, (e) and (f)) after oxygen-glucose deprivation. Scale bar in A = 300 μm ((a), (b), (d), and (e)) and 75 μm ((c) and (f)).

Mentions: When brain slices were cultured for 2 weeks in medium with normal glucose levels containing 10 ng/mL NGF, approximately 140 cholinergic nBM neurons/slice were detectable (Table 1; Figures 1(a) and 1(c)). This number did not change when slices were incubated without NGF for further 3 days (Table 1). Reduction of glucose to 6 mM (glucose deprivation) did not significantly change the number of cholinergic neurons after 1-2-3 days of incubation (Table 1). Slices exposed to hypoxia at normal (high) glucose did not show a reduced number of ChAT+ neurons after 1-2-3 days of incubation (Table 1). However, when slices were incubated in low glucose and hypoxia (oxygen-glucose deprivation, OGD), the number of ChAT+ neurons significantly decreased to about 70 neurons/slice after 3 days but not after 1 or 2 days of incubation (Table 1; Figure 1(b)).


S100b counteracts neurodegeneration of rat cholinergic neurons in brain slices after oxygen-glucose deprivation.

Serbinek D, Ullrich C, Pirchl M, Hochstrasser T, Schmidt-Kastner R, Humpel C - Cardiovasc Psychiatry Neurol (2010)

Immunohistochemistry for cholinergic choline acetyltransferase (ChAT) positive neurons (a)–(c) and c-fos immunoreactive nuclei (d)–(f) in organotypic brain slices of the basal nucleus of Meynert. Slices show control stainings before ((a), (c), (d)), or 3 days (ChAT+, (b)) or 3 hours (c-fos+, (e) and (f)) after oxygen-glucose deprivation. Scale bar in A = 300 μm ((a), (b), (d), and (e)) and 75 μm ((c) and (f)).
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2875695&req=5

fig1: Immunohistochemistry for cholinergic choline acetyltransferase (ChAT) positive neurons (a)–(c) and c-fos immunoreactive nuclei (d)–(f) in organotypic brain slices of the basal nucleus of Meynert. Slices show control stainings before ((a), (c), (d)), or 3 days (ChAT+, (b)) or 3 hours (c-fos+, (e) and (f)) after oxygen-glucose deprivation. Scale bar in A = 300 μm ((a), (b), (d), and (e)) and 75 μm ((c) and (f)).
Mentions: When brain slices were cultured for 2 weeks in medium with normal glucose levels containing 10 ng/mL NGF, approximately 140 cholinergic nBM neurons/slice were detectable (Table 1; Figures 1(a) and 1(c)). This number did not change when slices were incubated without NGF for further 3 days (Table 1). Reduction of glucose to 6 mM (glucose deprivation) did not significantly change the number of cholinergic neurons after 1-2-3 days of incubation (Table 1). Slices exposed to hypoxia at normal (high) glucose did not show a reduced number of ChAT+ neurons after 1-2-3 days of incubation (Table 1). However, when slices were incubated in low glucose and hypoxia (oxygen-glucose deprivation, OGD), the number of ChAT+ neurons significantly decreased to about 70 neurons/slice after 3 days but not after 1 or 2 days of incubation (Table 1; Figure 1(b)).

Bottom Line: Our data showed that 3 days of OGD induced a marked decrease of cholinergic neurons (60% of control), which could be counteracted by 50 mug/mL recombinant S100b.The effect was dose and time dependent.We conclude that S100b is a potent neuroprotective factor for cholinergic neurons during ischemic events.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Psychiatry and Exp. Alzheimer's Research, Department of Psychiatry and Psychotherapy, Innsbruck Medical University, Anichstra beta e 35, 6020 Innsbruck, Austria.

ABSTRACT
Alzheimer's disease is a severe chronic neurodegenerative disorder characterized by beta-amyloid plaques, tau pathology, cerebrovascular damage, inflammation, reactive gliosis, and cell death of cholinergic neurons. The aim of the present study is to test whether the glia-derived molecule S100b can counteract neurodegeneration of cholinergic neurons after oxygen-glucose deprivation (OGD) in organotypic brain slices of basal nucleus of Meynert. Our data showed that 3 days of OGD induced a marked decrease of cholinergic neurons (60% of control), which could be counteracted by 50 mug/mL recombinant S100b. The effect was dose and time dependent. Application of nerve growth factor or fibroblast growth factor-2 was less protective. C-fos-like immunoreactivity was enhanced 3 hours after OGD indicating metabolic stress. We conclude that S100b is a potent neuroprotective factor for cholinergic neurons during ischemic events.

No MeSH data available.


Related in: MedlinePlus