pubmed-article:19352591 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19352591 | lifeskim:mentions | umls-concept:C0034838 | lld:lifeskim |
pubmed-article:19352591 | lifeskim:mentions | umls-concept:C0001721 | lld:lifeskim |
pubmed-article:19352591 | lifeskim:mentions | umls-concept:C0042333 | lld:lifeskim |
pubmed-article:19352591 | lifeskim:mentions | umls-concept:C0871125 | lld:lifeskim |
pubmed-article:19352591 | lifeskim:mentions | umls-concept:C0920644 | lld:lifeskim |
pubmed-article:19352591 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:19352591 | pubmed:dateCreated | 2009-5-26 | lld:pubmed |
pubmed-article:19352591 | pubmed:abstractText | Prepulse inhibition (PPI) is the attenuation of the startle response towards an instantaneous and intense stimulus when preceded by a weaker non-startling stimulus. Deficits in this sensorimotor gating process have been associated with the pathophysiology of schizophrenia and other psychiatric disorders. Among the neurotransmitters involved in PPI modulation, serotonin (5-HT) has so far received comparably little attention. While a recent pharmacological study suggests an important role of different 5-HT receptor (5-HTR) subtypes in PPI modulation, the mechanisms by which 5-HTR impact on PPI remain to be further elucidated. Therefore, we employed a molecular genetic approach in order to examine whether PPI is associated with two functional 5-HTR gene polymorphisms, 5-HTR1A C-1019G and 5-HTR2A T102C. In a sample of 81 healthy volunteers, we found no significant main effects of the polymorphisms, but a significant interaction effect on PPI at short (50 ms) and mid-long (150 ms) pulse-prepulse intervals. The presence of the 5-HTR2A T allele (reported to result in higher 5-HTR2A expression) led to attenuated PPI only in the absence of the 5-HTR1A G allele (reported to result in reduced 5-HTR1A autoreceptor expression). Our results may indicate that a higher 5-HTR2A expression together with a reduced 5-HTR1A autoreceptor expression and consequently, elevated firing rates of serotonergic neurons results in elevated 5-HTR2A activation by serotonin which could potently attenuate PPI. While further research into the molecular mechanisms underlying this interaction is needed, our results underscore the role of 5-HTR in PPI modulation and further implicate the 5-HTR1A G-1019C and the 5-HTR2A T102C polymorphisms in the pathophysiology of schizophrenia. | lld:pubmed |
pubmed-article:19352591 | pubmed:language | eng | lld:pubmed |
pubmed-article:19352591 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19352591 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:19352591 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19352591 | pubmed:month | May | lld:pubmed |
pubmed-article:19352591 | pubmed:issn | 1435-1463 | lld:pubmed |
pubmed-article:19352591 | pubmed:author | pubmed-author:StrobelAlexan... | lld:pubmed |
pubmed-article:19352591 | pubmed:author | pubmed-author:BrockeBurkhar... | lld:pubmed |
pubmed-article:19352591 | pubmed:author | pubmed-author:LeschKlaus-Pe... | lld:pubmed |
pubmed-article:19352591 | pubmed:author | pubmed-author:HenschTilmanT | lld:pubmed |
pubmed-article:19352591 | pubmed:author | pubmed-author:BräuerDavidD | lld:pubmed |
pubmed-article:19352591 | pubmed:author | pubmed-author:DiersKerstenK | lld:pubmed |
pubmed-article:19352591 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19352591 | pubmed:volume | 116 | lld:pubmed |
pubmed-article:19352591 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19352591 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19352591 | pubmed:pagination | 607-13 | lld:pubmed |
pubmed-article:19352591 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:19352591 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19352591 | pubmed:articleTitle | Genetic variation of serotonin receptor function affects prepulse inhibition of the startle. | lld:pubmed |
pubmed-article:19352591 | pubmed:affiliation | Personality and Individual Differences, Institute of Psychology II, Dresden University of Technology, Dresden, Germany. david.braeuer@gmail.com | lld:pubmed |
pubmed-article:19352591 | pubmed:publicationType | Journal Article | lld:pubmed |
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