PMID- 18345022
OWN - NLM
STAT- MEDLINE
DCOM- 20080619
LR  - 20240316
IS  - 0007-1188 (Print)
IS  - 1476-5381 (Electronic)
IS  - 0007-1188 (Linking)
VI  - 154
IP  - 2
DP  - 2008 May
TI  - Neuroplasticity in the mesolimbic dopamine system and cocaine addiction.
PG  - 327-42
LID - 10.1038/bjp.2008.77 [doi]
AB  - The main characteristics of cocaine addiction are compulsive drug use despite 
      adverse consequences and high rates of relapse during periods of abstinence. A 
      current popular hypothesis is that compulsive cocaine use and cocaine relapse is 
      due to drug-induced neuroadaptations in reward-related learning and memory 
      processes, which cause hypersensitivity to cocaine-associated cues, impulsive 
      decision making and abnormal habit-like learned behaviours that are insensitive 
      to adverse consequences. Here, we review results from studies on the effect of 
      cocaine exposure on selected signalling cascades, growth factors and 
      physiological processes previously implicated in neuroplasticity underlying 
      normal learning and memory. These include the extracellular signal-regulated 
      kinase (ERK) signalling pathway, brain-derived neurotrophic factor (BDNF), 
      glutamate transmission, and synaptic plasticity (primarily in the form of 
      long-term potentiation and depression, LTP and LTD). We also discuss the degree 
      to which these cocaine-induced neuroplasticity changes in the mesolimbic dopamine 
      system mediate cocaine psychomotor sensitization and cocaine-seeking behaviours, 
      as assessed in animal models of drug addiction. Finally, we speculate on how 
      these factors may interact to initiate and sustain cocaine psychomotor 
      sensitization and cocaine seeking.
FAU - Thomas, M J
AU  - Thomas MJ
AD  - Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA. 
      tmhomas@umn.edu
FAU - Kalivas, P W
AU  - Kalivas PW
FAU - Shaham, Y
AU  - Shaham Y
LA  - eng
GR  - P50 DA015369/DA/NIDA NIH HHS/United States
GR  - R01 DA019666/DA/NIDA NIH HHS/United States
GR  - DA12513/DA/NIDA NIH HHS/United States
GR  - R01 DA003906/DA/NIDA NIH HHS/United States
GR  - DA019666/DA/NIDA NIH HHS/United States
GR  - ImNIH/Intramural NIH HHS/United States
GR  - R37 DA003906/DA/NIDA NIH HHS/United States
GR  - DA015369/DA/NIDA NIH HHS/United States
GR  - DA03906/DA/NIDA NIH HHS/United States
GR  - R01 DA012513/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, N.I.H., Intramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20080317
PL  - England
TA  - Br J Pharmacol
JT  - British journal of pharmacology
JID - 7502536
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
CIN - Br J Pharmacol. 2008 May;154(2):259-60. PMID: 18414384
MH  - Animals
MH  - Behavior, Addictive/drug therapy/*metabolism/physiopathology
MH  - Behavior, Animal
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cocaine-Related Disorders/drug therapy/*metabolism/physiopathology/psychology
MH  - Dopamine/*metabolism
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Glutamic Acid/metabolism
MH  - Humans
MH  - Limbic System/enzymology/*metabolism
MH  - Models, Animal
MH  - Neural Pathways/metabolism/physiopathology
MH  - *Neuronal Plasticity
MH  - Psychomotor Performance
MH  - Recurrence
MH  - *Synaptic Transmission
PMC - PMC2442442
EDAT- 2008/03/18 09:00
MHDA- 2008/06/20 09:00
PMCR- 2009/05/01
CRDT- 2008/03/18 09:00
PHST- 2008/03/18 09:00 [pubmed]
PHST- 2008/06/20 09:00 [medline]
PHST- 2008/03/18 09:00 [entrez]
PHST- 2009/05/01 00:00 [pmc-release]
AID - bjp200877 [pii]
AID - 10.1038/bjp.2008.77 [doi]
PST - ppublish
SO  - Br J Pharmacol. 2008 May;154(2):327-42. doi: 10.1038/bjp.2008.77. Epub 2008 Mar 
      17.