Source:http://linkedlifedata.com/resource/pubmed/id/19352591
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2009-5-26
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| 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.
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| 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 |
1435-1463
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
116
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
607-13
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:19352591-Adolescent,
pubmed-meshheading:19352591-Adult,
pubmed-meshheading:19352591-Brain Chemistry,
pubmed-meshheading:19352591-DNA Mutational Analysis,
pubmed-meshheading:19352591-Female,
pubmed-meshheading:19352591-Gene Frequency,
pubmed-meshheading:19352591-Genetic Predisposition to Disease,
pubmed-meshheading:19352591-Genetic Testing,
pubmed-meshheading:19352591-Genotype,
pubmed-meshheading:19352591-Humans,
pubmed-meshheading:19352591-Male,
pubmed-meshheading:19352591-Polymorphism, Genetic,
pubmed-meshheading:19352591-Receptor, Serotonin, 5-HT1A,
pubmed-meshheading:19352591-Receptor, Serotonin, 5-HT2A,
pubmed-meshheading:19352591-Schizophrenia,
pubmed-meshheading:19352591-Sensory Gating,
pubmed-meshheading:19352591-Serotonin,
pubmed-meshheading:19352591-Young Adult
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| pubmed:year |
2009
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| pubmed:articleTitle |
Genetic variation of serotonin receptor function affects prepulse inhibition of the startle.
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| pubmed:affiliation |
Personality and Individual Differences, Institute of Psychology II, Dresden University of Technology, Dresden, Germany. david.braeuer@gmail.com
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| pubmed:publicationType |
Journal Article
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