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Granulocyte-colony stimulating factor controls neural and behavioral plasticity in response to cocaine.

Abstract Cocaine addiction is characterized by dysfunction in reward-related brain circuits, leading to maladaptive motivation to seek and take the drug. There are currently no clinically available pharmacotherapies to treat cocaine addiction. Through a broad screen of innate immune mediators, we identify granulocyte-colony stimulating factor (G-CSF) as a potent mediator of cocaine-induced adaptations. Here we report that G-CSF potentiates cocaine-induced increases in neural activity in the nucleus accumbens (NAc) and prefrontal cortex. In addition, G-CSF injections potentiate cocaine place preference and enhance motivation to self-administer cocaine, while not affecting responses to natural rewards. Infusion of G-CSF neutralizing antibody into NAc blocks the ability of G-CSF to modulate cocaine's behavioral effects, providing a direct link between central G-CSF action in NAc and cocaine reward. These results demonstrate that manipulating G-CSF is sufficient to alter the motivation for cocaine, but not natural rewards, providing a pharmacotherapeutic avenue to manipulate addictive behaviors without abuse potential.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title nature communications
Publication Year Start




PMID- 29339724
OWN - NLM
STAT- In-Process
LR  - 20180123
IS  - 2041-1723 (Electronic)
IS  - 2041-1723 (Linking)
VI  - 9
IP  - 1
DP  - 2018 Jan 16
TI  - Granulocyte-colony stimulating factor controls neural and behavioral plasticity
      in response to cocaine.
PG  - 9
LID - 10.1038/s41467-017-01881-x [doi]
AB  - Cocaine addiction is characterized by dysfunction in reward-related brain
      circuits, leading to maladaptive motivation to seek and take the drug. There are 
      currently no clinically available pharmacotherapies to treat cocaine addiction.
      Through a broad screen of innate immune mediators, we identify granulocyte-colony
      stimulating factor (G-CSF) as a potent mediator of cocaine-induced adaptations.
      Here we report that G-CSF potentiates cocaine-induced increases in neural
      activity in the nucleus accumbens (NAc) and prefrontal cortex. In addition, G-CSF
      injections potentiate cocaine place preference and enhance motivation to
      self-administer cocaine, while not affecting responses to natural rewards.
      Infusion of G-CSF neutralizing antibody into NAc blocks the ability of G-CSF to
      modulate cocaine's behavioral effects, providing a direct link between central
      G-CSF action in NAc and cocaine reward. These results demonstrate that
      manipulating G-CSF is sufficient to alter the motivation for cocaine, but not
      natural rewards, providing a pharmacotherapeutic avenue to manipulate addictive
      behaviors without abuse potential.
FAU - Calipari, Erin S
AU  - Calipari ES
AD  - Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of
      Medicine at Mount Sinai, New York, NY, USA.
AD  - Department of Pharmacology, Vanderbilt Center for Addiction Research, Vanderbilt 
      University School of Medicine, Nashville, TN, 37232, USA.
FAU - Godino, Arthur
AU  - Godino A
AD  - Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of
      Medicine at Mount Sinai, New York, NY, USA.
AD  - Department of Biology, Ecole Normale Superieure de Lyon, Lyon, France.
FAU - Peck, Emily G
AU  - Peck EG
AD  - Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of
      Medicine at Mount Sinai, New York, NY, USA.
FAU - Salery, Marine
AU  - Salery M
AD  - Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of
      Medicine at Mount Sinai, New York, NY, USA.
FAU - Mervosh, Nicholas L
AU  - Mervosh NL
AD  - Department of Psychiatry, Friedman Brain Institute, Icahn School of Medicine at
      Mount Sinai, New York, NY, USA.
FAU - Landry, Joseph A
AU  - Landry JA
AD  - Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of
      Medicine at Mount Sinai, New York, NY, USA.
AD  - Department of Psychiatry, Friedman Brain Institute, Icahn School of Medicine at
      Mount Sinai, New York, NY, USA.
FAU - Russo, Scott J
AU  - Russo SJ
AUID- ORCID: 0000-0002-6470-1805
AD  - Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of
      Medicine at Mount Sinai, New York, NY, USA.
FAU - Hurd, Yasmin L
AU  - Hurd YL
AD  - Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of
      Medicine at Mount Sinai, New York, NY, USA.
AD  - Department of Psychiatry, Friedman Brain Institute, Icahn School of Medicine at
      Mount Sinai, New York, NY, USA.
FAU - Nestler, Eric J
AU  - Nestler EJ
AD  - Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of
      Medicine at Mount Sinai, New York, NY, USA.
AD  - Department of Psychiatry, Friedman Brain Institute, Icahn School of Medicine at
      Mount Sinai, New York, NY, USA.
FAU - Kiraly, Drew D
AU  - Kiraly DD
AUID- ORCID: 0000-0002-4818-5169
AD  - Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of
      Medicine at Mount Sinai, New York, NY, USA. [email protected]
AD  - Department of Psychiatry, Friedman Brain Institute, Icahn School of Medicine at
      Mount Sinai, New York, NY, USA. [email protected]
AD  - Seaver Autism Center for Research and Treatment, Icahn School of Medicine at
      Mount Sinai, New York, NY, USA. [email protected]
LA  - eng
GR  - K08 DA044308/DA/NIDA NIH HHS/United States
GR  - P01 DA008227/DA/NIDA NIH HHS/United States
GR  - K99 DA042111/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20180116
PL  - England
TA  - Nat Commun
JT  - Nature communications
JID - 101528555
PMC - PMC5770429
EDAT- 2018/01/18 06:00
MHDA- 2018/01/18 06:00
CRDT- 2018/01/18 06:00
PHST- 2017/04/19 00:00 [received]
PHST- 2017/10/20 00:00 [accepted]
PHST- 2018/01/18 06:00 [entrez]
PHST- 2018/01/18 06:00 [pubmed]
PHST- 2018/01/18 06:00 [medline]
AID - 10.1038/s41467-017-01881-x [doi]
AID - 10.1038/s41467-017-01881-x [pii]
PST - epublish
SO  - Nat Commun. 2018 Jan 16;9(1):9. doi: 10.1038/s41467-017-01881-x.