The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.
Glutamate Receptors in Extinction and Extinction-Based Therapies for Psychiatric Illness
Open accessAbstract
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--aspartate (NMDA) receptors, α-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.
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Cites
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“Single units within IL fire selectively to presentations of a previously fear conditioned cue during an extinction retention test 24 h after extinction training but not during the extinction training session itself (Milad and Quirk, 2002).”
BackgroundNeural Mechanisms of Extinction Learning and Retrieval
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“Electrolytic lesions (Quirk et al, 2000) or localized inactivation (Sierra-Mercado et al, 2006) of the infralimbic (IL) region of mPFC impair extinction retention while having little to no effect on acquisition or within-session extinction, suggesting a role for this region specifically in…”
BackgroundSwitching on and off fear by distinct neuronal circuits
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Cited by
Fear Extinction as a Model for Translational Neuroscience: Ten Years of Progress
Milad, M. R., & Quirk, G. J. (2012) · Annual Review of Psychology · doi:10.1146/annurev.psych.121208.131631 · Cited by 1,466
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Scofield, M. D., Heinsbroek, J. A., Gipson, C. D., Kupchik, Y. M., Spencer, S., Smith, A. C. W., Roberts-Wolfe, D., & Kalivas, P. W. (2016) · Pharmacological Reviews · doi:10.1124/pr.116.012484 · Cited by 598
Pharmacotherapy of Anxiety Disorders: Current and Emerging Treatment Options
Garakani, A., Murrough, J. W., Freire, R. C., Thom, R. P., Larkin, K., Buono, F. D., & Iosifescu, D. V. (2020) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2020.595584 · Cited by 440
Singewald, N., Schmuckermair, C., Whittle, N., Holmes, A., & Ressler, K. J. (2015) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2014.12.004 · Cited by 390
“As shown in Table 4, systemic administration of ligands on this binding site, D-serine or D-cycloserine (DCS), augments extinction consolidation [see (Bukalo et al., 2014;Myers et al., 2011) for recent detailed reviews].”
Influential
Metadata
- Authors
- Myers, K. M., Carlezon, W. A., & Davis, M.
- Venue
- Neuropsychopharmacology
- Published
- 2010-07-14
- Volume
- 36
- Issue
- 1
- Pages
- 274-293
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- OpenAlex
- W2080574895
- Cited by
- 173
- References
- 49
- FWCI
- 11.04
- Type
- journal article
- Language
- en
- Open access
- bronze
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