Journal
NEUROPSYCHOPHARMACOLOGY
Volume 36, Issue 1, Pages 274-293Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/npp.2010.88
Keywords
exposure therapy; fear; drug craving; drug withdrawal; PTSD; addiction
Categories
Funding
- National Institute on Drug Abuse [DA012736, DA027752]
- National Institute of Mental Health [MH047840, MH063266]
- Science and Technology Center (The Center for Behavioral Neuroscience of the National Science Foundation) [IBN-9876754]
- Yerkes Base Grant
- Astra-Zeneca Pharmaceuticals
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH063266, R01MH047840, R37MH047840] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [K01DA027752, R01DA012736] Funding Source: NIH RePORTER
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Some psychiatric illnesses involve a learned component. For example, in posttraumatic stress disorder, memories triggered by trauma-associated cues trigger fear and anxiety, and in addiction, drug-associated cues elicit drug craving and withdrawal. Clinical interventions to reduce the impact of conditioned cues in eliciting these maladaptive conditioned responses are likely to be beneficial. Extinction is a method of lessening conditioned responses and involves repeated exposures to a cue in the absence of the event it once predicted. We believe that an improved understanding of the behavioral and neurobiological mechanisms of extinction will allow extinction-like procedures in the clinic to become more effective. Research on the role of glutamate-the major excitatory neurotransmitter in the mammalian brain-in extinction has led to the development of pharmacotherapeutics to enhance the efficacy of extinction-based protocols in clinical populations. In this review, we describe what has been learned about glutamate actions at its three major receptor types (N-methyl-D-aspartate (NMDA) receptors, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, and metabotropic glutamate receptors) in the extinction of conditioned fear, drug craving, and withdrawal. We then discuss how these findings have been applied in clinical research. Neuropsychopharmacology Reviews (2011) 36, 274-293; doi: 10.1038/npp.2010.88; published online 14 July 2010
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