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Article: Gene expression of synaptosomal-associated protein 25 (SNAP-25) in the prefrontal cortex of the spontaneously hypertensive rat (SHR)
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TitleGene expression of synaptosomal-associated protein 25 (SNAP-25) in the prefrontal cortex of the spontaneously hypertensive rat (SHR)
 
AuthorsLi, Q1
Wong, JH3
Lu, G2
Antonio, GE3
Yeung, DK3
Ng, TB3
Forster, LE3
Yew, DT3
 
Issue Date2009
 
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/bbadis
 
CitationBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2009, v. 1792 n. 8, p. 766-776 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.bbadis.2009.05.006
 
AbstractDopamine is believed to play an important role in the etiology of attention-deficit/hyperactivity disorder (ADHD). In our previous study, we showed that gene expression of dopamine D4 receptor decreased in the spontaneously hypertensive rat (SHR) in the prefrontal cortex (PFC). In the present study, we explored the potential causes of dysfunction in the dopamine system in ADHD. It is the first time that neuronal activities in both juvenile SHR and WKY rats have been measured by functional MRI (fMRI). Our results showed that in PFC the Blood Oxygenation Level Dependent (BOLD) signal response in SHR was much higher than WKY under stressful situations. We tested the effects of acute and repeated administration of amphetamine on behavioral changes in SHR combined with the expression of the neuronal activity marker, c-fos, in the PFC. Meanwhile dopamine-related gene expression was measured in the PFC after repeated administration of amphetamine. We found that potential neuronal damage occurred through deficit of D2-like receptor protective functions in the PFC of the SHR. We also measured the expression of synaptosomal-associated protein 25 (SNAP-25) in SHR in PFC. The results showed decreased expression of SNAP-25 mRNA in the PFC of SHR; this defect disappeared after repeated injection of D-AMP.
 
ISSN0925-4439
2012 Impact Factor: 4.91
2012 SCImago Journal Rankings: 2.016
 
DOIhttp://dx.doi.org/10.1016/j.bbadis.2009.05.006
 
ISI Accession Number IDWOS:000269112500004
 
DC FieldValue
dc.contributor.authorLi, Q
 
dc.contributor.authorWong, JH
 
dc.contributor.authorLu, G
 
dc.contributor.authorAntonio, GE
 
dc.contributor.authorYeung, DK
 
dc.contributor.authorNg, TB
 
dc.contributor.authorForster, LE
 
dc.contributor.authorYew, DT
 
dc.date.accessioned2011-02-08T06:46:53Z
 
dc.date.available2011-02-08T06:46:53Z
 
dc.date.issued2009
 
dc.description.abstractDopamine is believed to play an important role in the etiology of attention-deficit/hyperactivity disorder (ADHD). In our previous study, we showed that gene expression of dopamine D4 receptor decreased in the spontaneously hypertensive rat (SHR) in the prefrontal cortex (PFC). In the present study, we explored the potential causes of dysfunction in the dopamine system in ADHD. It is the first time that neuronal activities in both juvenile SHR and WKY rats have been measured by functional MRI (fMRI). Our results showed that in PFC the Blood Oxygenation Level Dependent (BOLD) signal response in SHR was much higher than WKY under stressful situations. We tested the effects of acute and repeated administration of amphetamine on behavioral changes in SHR combined with the expression of the neuronal activity marker, c-fos, in the PFC. Meanwhile dopamine-related gene expression was measured in the PFC after repeated administration of amphetamine. We found that potential neuronal damage occurred through deficit of D2-like receptor protective functions in the PFC of the SHR. We also measured the expression of synaptosomal-associated protein 25 (SNAP-25) in SHR in PFC. The results showed decreased expression of SNAP-25 mRNA in the PFC of SHR; this defect disappeared after repeated injection of D-AMP.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2009, v. 1792 n. 8, p. 766-776 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.bbadis.2009.05.006
 
dc.identifier.citeulike5348386
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.bbadis.2009.05.006
 
dc.identifier.epage776
 
dc.identifier.hkuros175858
 
dc.identifier.isiWOS:000269112500004
 
dc.identifier.issn0925-4439
2012 Impact Factor: 4.91
2012 SCImago Journal Rankings: 2.016
 
dc.identifier.issue8
 
dc.identifier.openurl
 
dc.identifier.pmid19482079
 
dc.identifier.scopuseid_2-s2.0-67651085288
 
dc.identifier.spage766
 
dc.identifier.urihttp://hdl.handle.net/10722/131756
 
dc.identifier.volume1792
 
dc.languageeng
 
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/bbadis
 
dc.relation.ispartofBiochimica et Biophysica Acta (BBA)
 
dc.subject.meshAmphetamines - pharmacology
 
dc.subject.meshAttention Deficit Disorder with Hyperactivity - metabolism - physiopathology
 
dc.subject.meshGene Expression Regulation
 
dc.subject.meshRats, Inbred SHR
 
dc.subject.meshSynaptosomal-Associated Protein 25 - genetics - metabolism
 
dc.titleGene expression of synaptosomal-associated protein 25 (SNAP-25) in the prefrontal cortex of the spontaneously hypertensive rat (SHR)
 
dc.typeArticle
 
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<contributor.author>Antonio, GE</contributor.author>
<contributor.author>Yeung, DK</contributor.author>
<contributor.author>Ng, TB</contributor.author>
<contributor.author>Forster, LE</contributor.author>
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Author Affiliations
  1. The University of Hong Kong
  2. Prince of Wales Hospital Hong Kong
  3. Chinese University of Hong Kong