(Q43678306)

25 November 2017

title

Electroconvulsive shock exposure prevents neuronal apoptosis after kainic acid-evoked status epilepticus (English)

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25 November 2017

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Kondratyev A

1

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25 November 2017

Sahibzada N

series ordinal

2

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25 November 2017

Gale K

series ordinal

3

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25 November 2017

publication date

1 July 2001

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25 November 2017

published in

Molecular Brain Research

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25 November 2017

volume

91

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25 November 2017

issue

1-2

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25 November 2017

page(s)

1-13

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Antiapoptotic herpesvirus Bcl-2 homologs escape caspase-mediated conversion to proapoptotic proteins

25 November 2017

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Regional and temporal pattern of expression of nerve growth factor and basic fibroblast growth factor mRNA in rat brain following electroconvulsive shock

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Kainate-induced apoptosis in cultured murine cerebellar granule cells elevates expression of the cell cycle gene cyclin D1.

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The rescuing effect of nerve growth factor is the result of up-regulation of bcl-2 in hyperoxia-induced apoptosis of a subclone of pheochromocytoma cells, PC12h

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Hippocampal kindling protects several structures from the neuronal damage resulting from kainic acid-induced status epilepticus

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Intracerebral injection of caspase-3 inhibitor prevents neuronal apoptosis after kainic acid-evoked status epilepticus

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Electroshock seizures protect against apoptotic hippocampal cell death induced by adrenalectomy.

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7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

Widespread patterns of neuronal damage following systemic or intracerebral injections of kainic acid: a histological study

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7 January 2021

Multiple Bcl-2 family members demonstrate selective dimerizations with Bax

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7 January 2021

Deep prepiriform cortex modulates kainate-induced hippocampal injury

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7 January 2021

Kainic acid induced seizures: neurochemical and histopathological changes

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7 January 2021

Roles of Bcl-2 and caspases in hypoxia-induced neuronal cell death: a possible neuroprotective mechanism of peptide growth factors

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7 January 2021

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7 January 2021

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7 January 2021

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7 January 2021

BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax.

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7 January 2021

Apoptosis of hippocampal neurons after amygdala kindled seizures.

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7 January 2021

10.1016/S0169-328X(01)00099-7

Identifiers

DOI

1 reference

25 November 2017

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