Neuropsychopharmacology reports · 2018
Chemokine CXCL1 is responsible for cocaine-induced reward in mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Saika Fumihiro, Matsuzaki Shinsuke, Kobayashi Daichi, Kiguchi Norikazu, Kishioka Shiroh
Аннотация
AIM: We have previously demonstrated that upregulation of CC chemokines through dopamine receptor signaling in the prefrontal cortex (PFC) underlies methamphetamine (Meth)-induced reward. Given the common pharmacological property of Meth and cocaine (Coca), which are highly addictive psychostimulants, we hypothesized that chemokines may also contribute to Coca-induced reward. The aim of this study was to identify a key chemokine-mediating Coca-induced reward in mice.
METHODS: The mRNA expression levels of chemokines were measured by reverse transcription-quantitative polymerase chain reaction. Coca-induced reward was evaluated by conditioned place preference test.
RESULTS: We found that mRNA expression levels of CC chemokine ligand 2 (CCL2), CCL7, and CXC chemokine ligand 1 (CXCL1) were upregulated in the PFC after a single administration of Coca (20 mg/kg, s.c.). Upregulation of CXCL1, but not CCL2 and CCL7, mRNA in the PFC was also observed after repeated administration of Coca. A single administration of dopamine D1 receptor agonist SKF 81297 (10 mg/kg, s.c.), but not D2 receptor agonist sumanirole, upregulated CXCL1 mRNA in the PFC. Coca-induced reward was attenuated by the pretreatment of SB 225002 (5 mg/kg, s.c.), a selective antagonist of CXC chemokine receptor 2 (CXCR2, cognate receptor for CXCL1).
CONCLUSIONS: Collectively, we identified CXCL1 as a key regulator in Coca-induced reward and propose that pharmacological approach targeting CXCL1 could be a novel pharmacotherapy for Coca-induced reward.
METHODS: The mRNA expression levels of chemokines were measured by reverse transcription-quantitative polymerase chain reaction. Coca-induced reward was evaluated by conditioned place preference test.
RESULTS: We found that mRNA expression levels of CC chemokine ligand 2 (CCL2), CCL7, and CXC chemokine ligand 1 (CXCL1) were upregulated in the PFC after a single administration of Coca (20 mg/kg, s.c.). Upregulation of CXCL1, but not CCL2 and CCL7, mRNA in the PFC was also observed after repeated administration of Coca. A single administration of dopamine D1 receptor agonist SKF 81297 (10 mg/kg, s.c.), but not D2 receptor agonist sumanirole, upregulated CXCL1 mRNA in the PFC. Coca-induced reward was attenuated by the pretreatment of SB 225002 (5 mg/kg, s.c.), a selective antagonist of CXC chemokine receptor 2 (CXCR2, cognate receptor for CXCL1).
CONCLUSIONS: Collectively, we identified CXCL1 as a key regulator in Coca-induced reward and propose that pharmacological approach targeting CXCL1 could be a novel pharmacotherapy for Coca-induced reward.