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5-HT2A receptor blockade and 5-HT2C receptor activation interact to reduce cocaine hyperlocomotion and Fos protein expression in the caudate-putamen

机译：5-HT2A受体阻滞和5-HT2C受体激活相互作用以减少Cocaine HyperCOCONION和FOS蛋白表达在凯特 - 腐败中

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Both the 5-HT2A receptor (R) antagonist M100907 and the 5-HT2CR agonist MK212 attenuate cocaine-induced dopamine release and hyperlocomotion. This study examined whether these drugs interact to reduce cocaine hyperlocomotion and Fos expression in the striatum and prefrontal cortex. We first determined from dose-effect functions a low dose of both M100907 and MK212 that failed to alter cocaine (15 mg/kg, i.p.) hyperlocomotion. Subsequently we examined whether these subthreshold doses given together would attenuate cocaine hyperlocomotion, consistent with a 5-HT2A/5-HT2CR interaction. Separate groups of rats received two sequential drug injections 5 min apart immediately before a 1-h locomotion test as follows: 1) saline + saline, 2) saline + cocaine, 3) 0.025 mg/kg M100907 + cocaine, 4) 0.125 mg/kg MK212 + cocaine, or 5) cocktail combination of 0.025 mg/kg M100907 and 0.125 mg/kg MK212 + cocaine. Brains were extracted for Fos immunohistochemistry 90 min after the second injection. We next examined the effects of 0.025 mg/kg M100907 and 0.125 mg/kg MK212, alone and in combination, on spontaneous locomotor activity. While neither drug given alone produced any effects, the M100907/MK212 cocktail attenuated cocaine hyperlocomotion as well as cocaine-induced Fos expression in the dorsolateral caudate-putamen (CPu), but had no effect on spontaneous locomotion. The findings suggest that 5-HT2ARs and 5-HT2CRs interact to attenuate cocaine hyperlocomotion and Fos expression in the CPu, and that the CPu is a potential locus of the interactive effects between these 5-HT2R subtypes on behavior. Further research investigating combined 5-HT2AR antagonism and 5-HT2CR agonism as a treatment for cocaine dependence is warranted.
机译：5-HT2A受体拮抗剂M100907和5-HT2CR激动剂MK212均可减弱可卡因诱导的多巴胺释放和运动过度。这项研究检查了这些药物是否相互作用，以减少纹状体和前额叶皮层中的可卡因运动过度和Fos表达。我们首先从剂量效应功能中确定了低剂量的M100907和MK212，它们都不能改变可卡因（15 mg / kg，i.p.）的过度运动。随后，我们检查了一起使用这些亚阈值剂量是否会减弱可卡因的超运动，这与5-HT2A / 5-HT2CR相互作用相一致。单独的大鼠组在进行1小时运动测试之前立即相隔5分钟进行两次连续药物注射，如下所示：1）生理盐水+生理盐水，2）生理盐水+可卡因，3）0.025 mg / kg M100907 +可卡因，4）0.125 mg / kg kg MK212 +可卡因，或5）0.025 mg / kg M100907和0.125 mg / kg MK212 +可卡因的混合物。第二次注射后90分钟提取大脑进行Fos免疫组化。接下来，我们检查了0.025 mg / kg M100907和0.125 mg / kg MK212单独或组合对自发运动活性的影响。虽然两种药物都不单独产生任何作用，但M100907 / MK212鸡尾酒减弱了可卡因的过度运动以及可卡因诱导的Fos在背侧尾状丘脑（CPu）中的表达，但对自发运动没有影响。研究结果表明5-HT2ARs和5-HT2CRs相互作用以减弱可卡因超运动和Fos表达在CPu中，并且CPu是这些5-HT2R亚型之间行为相互作用的潜在作用源。值得进一步研究，研究联合5-HT2AR拮抗作用和5-HT2CR激动作为可卡因依赖的治疗方法。

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