PMID- 24374101
OWN - NLM
STAT- MEDLINE
DCOM- 20150107
LR  - 20231110
IS  - 1873-2747 (Electronic)
IS  - 0361-9230 (Print)
IS  - 0361-9230 (Linking)
VI  - 105
DP  - 2014 Jun
TI  - Can fear extinction be enhanced? A review of pharmacological and behavioral 
      findings.
PG  - 46-60
LID - S0361-9230(13)00196-2 [pii]
LID - 10.1016/j.brainresbull.2013.12.007 [doi]
AB  - 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'.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Fitzgerald, Paul J
AU  - Fitzgerald PJ
AD  - Department of Psychology, Texas A&M University, College Station, TX 77843-4235, 
      United States.
FAU - Seemann, Jocelyn R
AU  - Seemann JR
AD  - Institute for Neuroscience, Texas A&M University, College Station, TX 77843-4235, 
      United States.
FAU - Maren, Stephen
AU  - Maren S
AD  - 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.
LA  - eng
GR  - R01 MH065961/MH/NIMH NIH HHS/United States
GR  - R01MH065961/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20131225
PL  - United States
TA  - Brain Res Bull
JT  - Brain research bulletin
JID - 7605818
RN  - 0 (Neurotransmitter Agents)
RN  - 01K63SUP8D (Fluoxetine)
RN  - 2Y49VWD90Q (Yohimbine)
RN  - 46627O600J (Levodopa)
RN  - 9Y8NXQ24VQ (Propranolol)
SB  - IM
MH  - Animals
MH  - Conditioning, Classical/drug effects/physiology
MH  - Extinction, Psychological/drug effects/*physiology
MH  - Fear/*drug effects/*physiology
MH  - Fluoxetine/pharmacology
MH  - Humans
MH  - Levodopa/pharmacology
MH  - Neurotransmitter Agents/*pharmacology
MH  - Propranolol/pharmacology
MH  - Yohimbine/pharmacology
PMC - PMC4039692
MID - NIHMS558856
OTO - NOTNLM
OT  - Context
OT  - Fluoxetine
OT  - Massed extinction
OT  - Propranolol
OT  - Yohimbine
OT  - l-Dopa
EDAT- 2014/01/01 06:00
MHDA- 2015/01/08 06:00
PMCR- 2015/06/01
CRDT- 2013/12/31 06:00
PHST- 2013/09/10 00:00 [received]
PHST- 2013/12/10 00:00 [revised]
PHST- 2013/12/11 00:00 [accepted]
PHST- 2013/12/31 06:00 [entrez]
PHST- 2014/01/01 06:00 [pubmed]
PHST- 2015/01/08 06:00 [medline]
PHST- 2015/06/01 00:00 [pmc-release]
AID - S0361-9230(13)00196-2 [pii]
AID - 10.1016/j.brainresbull.2013.12.007 [doi]
PST - ppublish
SO  - Brain Res Bull. 2014 Jun;105:46-60. doi: 10.1016/j.brainresbull.2013.12.007. Epub 
      2013 Dec 25.