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Research article summary:

GABAergic inhibitory mechanisms for repetition-adaptivity in large-scale brain systems.

Abstract Extract:
Molecular mechanisms for systems level adaptivity of brain activation are largely unknown but a key role for active inhibition by gamma-aminobutyric acid (GABA) is plausible. We used functional magnetic resonance imaging to contrast the modulatory ... (Full abstract text below)

Published 2003Aug in Journal: Neuroimage (Language : eng)

Full Pubmed Extract

This information was retrieved, real-time, on your behalf from the public area of the Pubmed website:

1. Neuroimage. 2003 Aug;19(4):1578-88

GABAergic inhibitory mechanisms for repetition-adaptivity in large-scale brain systems.

Stephenson CM, Suckling J, Dirckx SG, Ooi C, McKenna PJ, Bisbrown-Chippendale R, Kerwin RW, Pickard JD, Bullmore ET

Brain Mapping Unit, Department of Psychiatry, University of Cambridge, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK.

Molecular mechanisms for systems level adaptivity of brain activation are largely unknown but a key role for active inhibition by gamma-aminobutyric acid (GABA) is plausible. We used functional magnetic resonance imaging to contrast the modulatory effects on brain adaptivity to task repetition and task difficulty of two GABAergic drugs, lorazepam and flumazenil. In a working memory paradigm, occipitotemporal regions clearly demonstrated attenuation of activation as a function of within-session task repetition or practice in data acquired following placebo, but this spatiotemporal pattern of repetition adaptivity was abolished by both lorazepam and flumazenil. However, in other brain systems flumazenil enhanced repetition adaptivity compared to placebo: in frontal cortex, flumzenil induced attenuation of signal related to task repetition and in hippocampus it exaggerated normal enhancement of signal with repetition. In contrast, there were no significant effects of either flumazenil or lorazepam on areas of frontal cortex which normally demonstrated significant neurocognitive load response or adaptivity to task difficulty. We argue that repetition adaptivity of large-scale brain systems is regulated by GABAergic inhibitory mechanisms and that expression of repetition adaptivity in a given brain system may show an "inverted-U" form of relationship with pharmacologically manipulable levels of GABAergic inhibitory tone.

PMID : 12948713 [PubMed - Indexed for MEDLINE]


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Full Author Information

First NameLastNameInitials
C M EStephensonCM
JSucklingJ
S GDirckxSG
COoiC
P JMcKennaPJ
RBisbrown-ChippendaleR
R WKerwinRW
J DPickardJD
E TBullmoreET

Affiliation: Brain Mapping Unit, Department of Psychiatry, University of Cambridge, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK.

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MESH categories and related page links

This article was linked to the MESH categories shown on the left below. The links on the right are related Memletics pages.

Category links from this article:

  • Adult
  • Arousal - drug effects, physiology
  • Brain Mapping
  • Cerebral Cortex - drug effects, physiology
  • Double-Blind Method
  • Female
  • Flumazenil - pharmacology
  • GABA Agonists - pharmacology
  • Habituation, Psychophysiologic - drug effects, physiology
  • Humans
  • Image Enhancement
  • Image Processing, Computer-Assisted
  • Lorazepam - pharmacology
  • Magnetic Resonance Imaging
  • Male
  • Memory, Short-Term - drug effects, physiology
  • Middle Aged
  • Neural Inhibition - drug effects, physiology
  • gamma-Aminobutyric Acid - physiology
   

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