Sable Helen J K, Paige Nicholas B, Nalan Patricia A, Pace Rachel L, Hicks Carina B, Regan Samantha L, Williams Michael T, Vorhees Charles V, Lester Deranda B
University of Memphis, USA.
University of Memphis, USA.
Neuroscience. 2025 Feb 16;567:150-162. doi: 10.1016/j.neuroscience.2024.12.037. Epub 2025 Jan 3.
We examined DA activity in the medial prefrontal cortex (mPFC) and nucleus accumbens core (NAcc) in two Different Rat Models of Attention-Deficit/Hyperactivity Disorder: Spontaneously Hypertensive Rats (SHR) Versus Lphn3 Knockout Rats. We examined baseline stimulation-evoked phasic DA release, half-life, and DA autoreceptor (DAR) functioning in the mPFC and NAcc, as well as the response to nomifensine (10 mg/kg, IP), a DA transporter (DAT) blocker, on these measures in the NAcc. Both rat models were hypodopaminergic, with notable regional and mechanistic differences. The SHRs displayed decreased DA release in the NAcc compared to their control strain (i.e., WKY rats), with no differences in the mPFC, leading a much lower NAcc-to-PFC DA release ratio in SHRs compared to controls suggesting an imbalance in DA transmission between these regions. The Lphn3 KO rats were considered hypodopaminergic based on the reduced summed DA release in the mPFC and NAcc compared to WT controls, although differences were not observed when examining each site independently. Lphn3 KOs displayed increased DA half-life in the mPFC compared with Lphn3 WT rats, an indication of decreased DAT reuptake, with no differences in the NAcc. DAT blockade by nomifensine had a similar effect on DA release in the NAcc of SHRs and WKYs, but increased DA release in the NAcc of Lphn3 KOs to a greater extent than in WTs. These results suggest that the efficacy of pharmacotherapies used to treat externalizing disorders such as ADHD and/or SUD, likely differ between SHRs and Lphn3 KO rats.
我们在注意力缺陷多动障碍的两种不同大鼠模型中,即自发性高血压大鼠(SHR)与Lphn3基因敲除大鼠,检测了内侧前额叶皮质(mPFC)和伏隔核核心(NAcc)中的多巴胺(DA)活性。我们检测了基线刺激诱发的阶段性DA释放、半衰期以及mPFC和NAcc中DA自身受体(DAR)的功能,以及在NAcc中对DA转运体(DAT)阻滞剂诺米芬辛(10mg/kg,腹腔注射)的这些指标的反应。两种大鼠模型均为多巴胺能不足,存在显著的区域和机制差异。与对照品系(即WKY大鼠)相比,SHR在NAcc中的DA释放减少,mPFC中无差异,这导致SHR与对照相比,NAcc与PFC的DA释放比值低得多,表明这些区域之间的DA传递失衡。与野生型(WT)对照相比,Lphn3基因敲除大鼠由于mPFC和NAcc中DA释放总量减少而被认为多巴胺能不足,尽管单独检查每个部位时未观察到差异。与Lphn3野生型大鼠相比,Lphn3基因敲除大鼠在mPFC中的DA半衰期增加,这表明DAT再摄取减少,在NAcc中无差异。诺米芬辛对DAT的阻断对SHR和WKY大鼠NAcc中的DA释放有类似影响,但与WT相比,Lphn3基因敲除大鼠NAcc中的DA释放增加幅度更大。这些结果表明,用于治疗诸如注意力缺陷多动障碍和/或物质使用障碍等外化性疾病的药物疗法的疗效,在SHR和Lphn3基因敲除大鼠之间可能有所不同。