Adenosine Kinase Expression in the Frontal Cortex in Schizophrenia.
The adenosine hypothesis of schizophrenia posits that reduced availability of the neuromodulator adenosine contributes to dysregulation of dopamine and glutamate transmission and the symptoms associated with schizophrenia. It has been proposed that increased expression of the enzyme adenosine kinase...
| Publicado en: | Schizophrenia Bulletin Vol. 46; no. 3; pp. 690 - 699 |
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| Autores principales: | , , , , , , |
| Formato: | pictorial research tables/charts Journal Article |
| Publicado: |
Oxford University Press / USA
May2020
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| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=142688496&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 142688496 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 05867614 2CZ jtl: Schizophrenia Bulletin issn: 05867614 maglogo: N pubinfo: dt: May2020 vid: 46 iid: 3 pid: 622 pub: Oxford University Press / USA artinfo: ui: 142688496 142688496 142688496 10.1093/schbul/sbz086 142688496 ppf: 690 ppct: 9 formats: tig: atl: Adenosine Kinase Expression in the Frontal Cortex in Schizophrenia. aug: au: Moody, Cassidy L Funk, Adam J Devine, Emily Homan, Ryan C Devore Boison, Detlev McCullumsmith, Robert E O'Donovan, Sinead M affil: Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, Cincinnati, OH sug: subj: Schizophrenia Physiopathology Transferases Metabolism Frontal Lobe Metabolism Gene Expression Human Animal Studies Rats Haloperidol Therapeutic Use Fatty Acids Therapeutic Use Schizophrenia Drug Therapy Limbic System Metabolism Autopsy ab: The adenosine hypothesis of schizophrenia posits that reduced availability of the neuromodulator adenosine contributes to dysregulation of dopamine and glutamate transmission and the symptoms associated with schizophrenia. It has been proposed that increased expression of the enzyme adenosine kinase (ADK) may drive hypofunction of the adenosine system. While animal models of ADK overexpression support such a role for altered ADK, the expression of ADK in schizophrenia has yet to be examined. In this study, we assayed ADK gene and protein expression in frontocortical tissue from schizophrenia subjects. In the dorsolateral prefrontal cortex (DLPFC), ADK-long and -short splice variant expression was not significantly altered in schizophrenia compared to controls. There was also no significant difference in ADK splice variant expression in the frontal cortex of rats treated chronically with haloperidol-decanoate, in a study to identify the effect of antipsychotics on ADK gene expression. ADK protein expression was not significantly altered in the DLPFC or anterior cingulate cortex (ACC). There was no significant effect of antipsychotic medication on ADK protein expression in the DLPFC or ACC. Overall, our results suggest that increased ADK expression does not contribute to hypofunction of the adenosine system in schizophrenia and that alternative mechanisms are involved in dysregulation of this system in schizophrenia. pubtype: Academic Journal doctype: pictorial research tables/charts Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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