title: Can fear extinction be enhanced? A review of pharmacological and behavioral findings.
abstract: There is considerable interest, from both a basic and clinical standpoint, in gaining a greater understanding of how pharmaceutical or behavioral manipulations alter fear extinction in animals. Not only does fear extinction in rodents model exposure therapy in humans, where the latter is a cornerstone of behavioral intervention for anxiety disorders such as post-traumatic stress disorder and specific phobias, but also understanding more about extinction provides basic information into learning and memory processes and their underlying circuitry. In this paper, we briefly review three principal approaches that have been used to modulate extinction processes in animals and humans: a purely pharmacological approach, the more widespread approach of combining pharmacology with behavior, and a purely behavioral approach. The pharmacological studies comprise modulation by: brain derived neurotrophic factor (BDNF), d-cycloserine, serotonergic and noradrenergic drugs, neuropeptides, endocannabinoids, glucocorticoids, histone deacetylase (HDAC) inhibitors, and others. These studies strongly suggest that extinction can be modulated by drugs, behavioral interventions, or their combination, although not always in a lasting manner. We suggest that pharmacotherapeutic manipulations provide considerable promise for promoting effective and lasting fear reduction in individuals with anxiety disorders. This article is part of a Special Issue entitled 'Memory enhancement'.
authors.affiliation: Department of Psychology, Texas A&M University, College Station, TX 77843-4235, United States.
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Fitzgerald
authors.affiliation: Institute for Neuroscience, Texas A&M University, College Station, TX 77843-4235, United States.
authors.forename: Jocelyn R
authors.initials: JR
authors.lastname: Seemann
authors.affiliation: Department of Psychology, Texas A&M University, College Station, TX 77843-4235, United States; Institute for Neuroscience, Texas A&M University, College Station, TX 77843-4235, United States. Electronic address: maren@tamu.edu.
authors.forename: Stephen
authors.initials: S
authors.lastname: Maren
mesh_terms: D000818:Animals; D003214:Conditioning, Classical / Q000187:drug effects / Q000502:physiology; D005108:Extinction, Psychological / Q000187:drug effects / Q000502:physiology*; D005239:Fear / Q000187:drug effects* / Q000502:physiology*; D005473:Fluoxetine / Q000494:pharmacology; D006801:Humans; D007980:Levodopa / Q000494:pharmacology; D018377:Neurotransmitter Agents / Q000494:pharmacology*; D011433:Propranolol / Q000494:pharmacology; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D018377:Neurotransmitter Agents; D005473:Fluoxetine; D015016:Yohimbine; D007980:Levodopa; D011433:Propranolol
keywords: Context; Fluoxetine; Massed extinction; Propranolol; Yohimbine; l-Dopa