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编 号：F307785
分子式：C9H9Cl2N3O
分子量：246.09
分子式：C9H9Cl2N3O
分子量：246.09
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CAS No: 29110-47-2
产品详情
生物活性：
Guanfacine is an orally active noradrenergic α2A agonist and has high selective for the α2A receptor subtype. Guanfacine has effects in producing hypotension and sedation. Guanfacine can be used for the research of a variety of prefrontal cortex (PFC) cognitive disorders, including tourette's syndrome and attention deficit hyperactivity disorder (ADHD).
体内研究：
Guanfacine enhances PFC working memory function in aged monkeys and improves impulse control in monkeys performing a delayed discounting task.Guanfacine improves cognitive performance when infused directly into the rat or monkey PFC.Guanfacine blocks 2A receptors in the monkey dIPFC markedly impairs working memory, behavioral inhibition and greatly reduces persistent neuronal firing.
体外研究：
Guanfacine increases the delay-related neuronal firing needed for working memory on dIPFC neurons at the cellular level.Guanfacine improves PFC cognitive function by inhibiting the production of CAMP, closing HCN channels, and strengthening the PFC networks.
Guanfacine is an orally active noradrenergic α2A agonist and has high selective for the α2A receptor subtype. Guanfacine has effects in producing hypotension and sedation. Guanfacine can be used for the research of a variety of prefrontal cortex (PFC) cognitive disorders, including tourette's syndrome and attention deficit hyperactivity disorder (ADHD).
体内研究：
Guanfacine enhances PFC working memory function in aged monkeys and improves impulse control in monkeys performing a delayed discounting task.Guanfacine improves cognitive performance when infused directly into the rat or monkey PFC.Guanfacine blocks 2A receptors in the monkey dIPFC markedly impairs working memory, behavioral inhibition and greatly reduces persistent neuronal firing.
体外研究：
Guanfacine increases the delay-related neuronal firing needed for working memory on dIPFC neurons at the cellular level.Guanfacine improves PFC cognitive function by inhibiting the production of CAMP, closing HCN channels, and strengthening the PFC networks.
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