Department of Pharmacology and Toxicolog, Medical College of Georgia, Augusta, Georgia, USA.
J Pharmacol Exp Ther. 2011 Mar;336(3):751-66. doi: 10.1124/jpet.110.175422. Epub 2010 Nov 24.
This study was designed to evaluate further a prototypical ranitidine analog, JWS-USC-75-IX, [(3-[[[2-[[(5-dimethylaminomethyl)-2-furanyl]methyl]thio]ethyl]amino]-4-nitropyridazine, JWS], for neuropharmacologic properties that would theoretically be useful for treating cognitive and noncognitive behavioral symptoms of neuropsychiatric disorders. JWS was previously found to inhibit acetylcholinesterase (AChE) activity, serve as a potent ligand at muscarinic M₂ acetylcholine receptors, and elicit positive effects on spatial learning, passive avoidance, and working memory in rodents. In the current study, JWS was evaluated for binding activity at more than 60 neurotransmitter receptors, transporters, and ion channels, as well as for inhibitory activity at AChE and butyrylcholinesterase (BChE). The results indicate that JWS inhibits AChE and BChE at low (micromolar) concentrations and that it is a functional antagonist at M₂ receptors (K(B) = 320 nM). JWS was subsequently evaluated orally across additional behavioral assays in rodents (dose range, 0.03-10.0 mg/kg) as well as nonhuman primates (dose range, 0.05-2.0 mg/kg). In rats, JWS improved prepulse inhibition (PPI) of the acoustic startle response in nonimpaired rats and attenuated PPI deficits in three pharmacologic impairment models. JWS also attenuated scopolamine and (-)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801)-related impairments in a spontaneous novel object recognition task and a five-choice serial reaction time task, respectively. In monkeys, JWS elicited dose-dependent improvements of a delayed match-to-sample task as well as an attention-related version of the task where randomly presented (task-relevant) distractors were presented. Thus, JWS (potentially via effects at several drug targets) improves information processing, attention, and memory in animal models and could potentially treat the cognitive and behavioral symptoms of some neuropsychiatric illnesses.
本研究旨在进一步评估一种原型雷尼替丁类似物 JWS-USC-75-IX[(3-[[[2-[[(5-二甲基氨基甲酰基)-2-呋喃基]甲基]硫基]乙基]氨基]-4-硝基嘧啶嗪,JWS],因其具有神经药理学特性而受到理论上用于治疗神经精神疾病的认知和非认知行为症状。JWS 先前被发现抑制乙酰胆碱酯酶 (AChE) 活性,作为毒蕈碱 M₂ 乙酰胆碱受体的有效配体,并在啮齿动物中对空间学习、被动回避和工作记忆产生积极影响。在本研究中,JWS 被评估了对 60 多种神经递质受体、转运体和离子通道的结合活性,以及对 AChE 和丁酰胆碱酯酶 (BChE) 的抑制活性。结果表明,JWS 在低浓度(微摩尔)下抑制 AChE 和 BChE,并且是 M₂ 受体的功能性拮抗剂(K(B)=320 nM)。随后,JWS 在啮齿动物(剂量范围为 0.03-10.0 mg/kg)和非人类灵长类动物(剂量范围为 0.05-2.0 mg/kg)的其他行为测定中进行了口服评估。在大鼠中,JWS 改善了正常大鼠的听觉起始反应的预脉冲抑制 (PPI),并减轻了三种药物损伤模型中的 PPI 缺陷。JWS 还分别减轻了东莨菪碱和(-)-5-甲基-10,11-二氢-5H-二苯并[a,d]环庚烯-5,10-亚胺马来酸盐 (MK-801) 相关的自发新物体识别任务和 5 选择连续反应时间任务中的损伤。在猴子中,JWS 引起了延迟匹配样本任务的剂量依赖性改善,以及任务相关的随机呈现的(任务相关的)分心物的注意力相关版本的任务。因此,JWS(可能通过几种药物靶点的作用)改善了动物模型中的信息处理、注意力和记忆,并且可能治疗某些神经精神疾病的认知和行为症状。