PMID- 23727437
OWN - NLM
STAT- MEDLINE
DCOM- 20140729
LR  - 20211021
IS  - 1873-7064 (Electronic)
IS  - 0028-3908 (Print)
IS  - 0028-3908 (Linking)
VI  - 76 Pt B
IP  - 0 0
DP  - 2014 Jan
TI  - Adaptations in AMPA receptor transmission in the nucleus accumbens contributing 
      to incubation of cocaine craving.
PG  - 287-300
LID - S0028-3908(13)00233-5 [pii]
LID - 10.1016/j.neuropharm.2013.04.061 [doi]
AB  - Cue-induced cocaine craving in rodents intensifies or "incubates" during the 
      first months of withdrawal from long access cocaine self-administration. This 
      incubation phenomenon is relevant to human users who achieve abstinence but 
      exhibit persistent vulnerability to cue-induced relapse. It is well established 
      that incubation of cocaine craving involves complex neuronal circuits. Here we 
      will focus on neuroadaptations in the nucleus accumbens (NAc), a region of 
      convergence for pathways that control cocaine seeking. A key adaptation is a 
      delayed (~3-4 weeks) accumulation of Ca(2+)-permeable AMPAR receptors (CP-AMPARs) 
      in synapses on medium spiny neurons (MSN) of the NAc. These CP-AMPARs mediate the 
      expression of incubation after prolonged withdrawal, although different 
      mechanisms must be responsible during the first weeks of withdrawal, prior to 
      CP-AMPAR accumulation. The cascade of events leading to CP-AMPAR accumulation is 
      still unclear. However, several candidate mechanisms have been identified. First, 
      mGluR1 has been shown to negatively regulate CP-AMPAR levels in NAc synapses, and 
      it is possible that a withdrawal-dependent decrease in this effect may help 
      explain CP-AMPAR accumulation during incubation. Second, an increase in 
      phosphorylation of GluA1 subunits (at the protein kinase A site) within 
      extrasynaptic homomeric GluA1 receptors (CP-AMPARs) may promote their synaptic 
      insertion and oppose their removal. Finally, elevation of brain-derived 
      neurotrophic factor (BDNF) levels in the NAc may contribute to maintenance of 
      incubation after months of withdrawal, although incubation-related increases in 
      BDNF accumulation do not account for CP-AMPAR accumulation. Receptors and 
      pathways that negatively regulate incubation, such as mGluR1, are promising 
      targets for the development of therapeutic strategies to help recovering addicts 
      maintain abstinence. This article is part of a Special Issue entitled 'NIDA 40th 
      Anniversary Issue'.
CI  - Copyright (c) 2013 Elsevier Ltd. All rights reserved.
FAU - Loweth, Jessica A
AU  - Loweth JA
AD  - Department of Neuroscience, The Chicago Medical School at Rosalind Franklin 
      University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL 60064, 
      USA.
FAU - Tseng, Kuei Y
AU  - Tseng KY
FAU - Wolf, Marina E
AU  - Wolf ME
LA  - eng
GR  - R01 DA009621/DA/NIDA NIH HHS/United States
GR  - DA009621/DA/NIDA NIH HHS/United States
GR  - F32 DA030844/DA/NIDA NIH HHS/United States
GR  - DA0015835/DA/NIDA NIH HHS/United States
GR  - K05 DA029099/DA/NIDA NIH HHS/United States
GR  - R01 DA015835/DA/NIDA NIH HHS/United States
GR  - R37 DA015835/DA/NIDA NIH HHS/United States
GR  - DA029099/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20130530
PL  - England
TA  - Neuropharmacology
JT  - Neuropharmacology
JID - 0236217
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Receptors, AMPA)
SB  - IM
MH  - Adaptation, Physiological/*physiology
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cocaine-Related Disorders/*physiopathology
MH  - Drug-Seeking Behavior/*physiology
MH  - Humans
MH  - Nucleus Accumbens/*metabolism
MH  - Receptors, AMPA/*metabolism
PMC - PMC3836860
MID - NIHMS487257
OTO - NOTNLM
OT  - BDNF
OT  - Cocaine
OT  - Incubation
OT  - Metabotropic glutamate receptor
OT  - Nucleus accumbens
OT  - Protein kinase A
EDAT- 2013/06/04 06:00
MHDA- 2014/07/30 06:00
PMCR- 2015/01/01
CRDT- 2013/06/04 06:00
PHST- 2013/02/25 00:00 [received]
PHST- 2013/04/29 00:00 [revised]
PHST- 2013/04/30 00:00 [accepted]
PHST- 2013/06/04 06:00 [entrez]
PHST- 2013/06/04 06:00 [pubmed]
PHST- 2014/07/30 06:00 [medline]
PHST- 2015/01/01 00:00 [pmc-release]
AID - S0028-3908(13)00233-5 [pii]
AID - 10.1016/j.neuropharm.2013.04.061 [doi]
PST - ppublish
SO  - Neuropharmacology. 2014 Jan;76 Pt B(0 0):287-300. doi: 
      10.1016/j.neuropharm.2013.04.061. Epub 2013 May 30.