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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.

SUBMITTER: Calipari ES 

PROVIDER: S-EPMC5770429 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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

Calipari Erin S ES   Godino Arthur A   Peck Emily G EG   Salery Marine M   Mervosh Nicholas L NL   Landry Joseph A JA   Russo Scott J SJ   Hurd Yasmin L YL   Nestler Eric J EJ   Kiraly Drew D DD  

Nature communications 20180116 1


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 accum  ...[more]

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