Journal
BIOCHEMICAL PHARMACOLOGY
Volume 78, Issue 7, Pages 658-667Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bcp.2009.04.019
Keywords
Cognition enhancers; Cue detection; Schizophrenia; Cognitive disorders
Categories
Funding
- NIDA NIH HHS [T32 DA007267] Funding Source: Medline
- NIMH NIH HHS [MH080332, MH080426, R21 MH080426, R21 MH080426-02, R01 MH080332-03, R01 MH080332] Funding Source: Medline
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The identification and characterization of drugs for the treatment of cognitive disorders has been hampered by the absence of comprehensive hypotheses. Such hypotheses consist of (a) a precisely defined cognitive operation that fundamentally underlies a range of cognitive abilities and capacities and, if impaired, contributes to the manifestation of diverse cognitive symptoms: (b) defined neuronal mechanisms proposed to mediate the cognitive operation of interest; (c) evidence indicating that the putative cognition enhancer facilitates these neuronal mechanisms; (d) and evidence indicating that the cognition enhancer facilitates cognitive performance by modulating these underlying neuronal mechanisms. The evidence on the neuronal and attentional effects of nAChR agonists, specifically agonists selective for alpha 4 beta 2* nAChRs, has begun to support such a hypothesis. nAChR agonists facilitate the detection of signals by augmenting the transient increases in prefrontal cholinergic activity that are necessary for a signal to gain control over behavior in attentional contexts. The prefrontal microcircuitry mediating these effects include alpha 4 beta 2* nAChRs situated on the terminals of thalamic inputs and the glutamatergic stimulation of cholinergic terminals via ionotropic glutamate receptors. Collectively, this evidence forms the basis for hypothesis-guided development and characterization of cognition enhancers. (C) 2009 Elsevier Inc. All rights reserved
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