Source:http://linkedlifedata.com/resource/pubmed/id/17537977
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
22
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pubmed:dateCreated |
2007-5-31
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pubmed:abstractText |
The dentate gyrus filters incoming activity into the hippocampus proper. It plays a role in learning and memory and in pathological states such as epilepsy. Some of hilar interneurons of the dentate gyrus express neuropeptide Y (NPY), which modulates granule cell activity. A subpopulation of the NPY-expressing inhibitory interneurons is sensitive to seizure-induced damage. Pretreatment with beta-estradiol in ovariectomized rats protects hilar interneurons against seizure-induced injury, including the NPY-containing damage-sensitive subpopulation. Here, we demonstrate that beta-estradiol enhances NPY expression within the hilar interneurons. In vitro paired-pulse stimulation of the mixed perforant path revealed beta-estradiol-induced augmentation of granule cell network inhibition, which at interstimulus intervals between 200 and 300 ms (corresponding to approximately 3-5 Hz) was NPY sensitive and involved Y1 receptors, whereas it was insensitive to GABA(B) or metabotropic glutamate receptor antagonists. Additionally, beta-estradiol pretreatment attenuated propagation of low-frequency (3.3 or 5 Hz) burst activity through the dentate gyrus. Scavenging endogenous NPY by intracerebroventricular administration of anti-NPY antibody accelerated kainic acid-induced seizure onset and increased seizure-induced neuronal damage in the hilus compared with rats treated with beta-estradiol alone. Together, we show that beta-estradiol upregulates hilar NPY and that this leads to enhancement in dentate gyrus inhibition of incoming frequencies between 3 and 5 Hz. Such frequencies are similar to the discharge frequencies recorded during seizure initiation in some patients with epilepsy. Thus, beta-estradiol-induced NPY-sensitive filtering of 3-5 Hz frequencies may be an important regulator of incoming seizure activity, but it could also serve a physiological purpose in modulating information flow into the hippocampus proper.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1529-2401
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
30
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pubmed:volume |
27
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6054-63
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pubmed:dateRevised |
2007-12-3
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pubmed:meshHeading |
pubmed-meshheading:17537977-Animals,
pubmed-meshheading:17537977-Dentate Gyrus,
pubmed-meshheading:17537977-Estradiol,
pubmed-meshheading:17537977-Female,
pubmed-meshheading:17537977-Neural Inhibition,
pubmed-meshheading:17537977-Neuropeptide Y,
pubmed-meshheading:17537977-Rats,
pubmed-meshheading:17537977-Rats, Sprague-Dawley,
pubmed-meshheading:17537977-Seizures
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pubmed:year |
2007
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pubmed:articleTitle |
Beta-estradiol increases dentate gyrus inhibition in female rats via augmentation of hilar neuropeptide Y.
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pubmed:affiliation |
Saul R. Korey Department of Neurology, Laboratory of Developmental Epilepsy, Albert Einstein College of Medicine and the Einstein/Montefiore Comprehensive Epilepsy Management Center, Bronx, New York 10461, USA. jvelisko@aecom.yu.edu
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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