Department of Neuropsychopharmacology, Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, PL 31-343 Kraków, Poland.
Pharmacol Rep. 2013;65(5):1194-203. doi: 10.1016/s1734-1140(13)71477-4.
Metabotropic glutamate receptors (mGluRs) have been shown to be potential targets for numerous neurological diseases, including Parkinson's disease (PD). We previously reported that ACPT-1, a non-selective group III mGluRs agonist, injected locally into the globus pallidus, striatum or substantia nigra pars reticulata (SNr), significantly attenuated the haloperidol-induced catalepsy in rats. N,N'-dibenzhydryl-ethane-1,2-diamine dihydrochloride (AMN082) is a potent, brain penetrating mGluR7 agonist, selective over other mGluRs.
The aim of the present study was to determine whether (1) activation of mGluR7 by systemic administration of AMN082 may produce antiparkinsonian-like effects in the haloperidol-induced catalepsy and reserpine-induced akinesia models in rats; (2) striatal and nigral mGluR7 is likely to contribute to such an effect.
We found that AMN082 (1 and 3 mg/kg) decreased the haloperidol (0.25 mg/kg)-induced catalepsy, but was not efficient in attenuating the reserpine (2.5 mg/kg)-induced akinesia. When given locally, AMN082 also significantly diminished catalepsy in rats; however, its effective striatal doses were 10-fold lower than those used in the SNr (2.5 and 7.5 pmol/0.5 μl/ side vs. 25 and 75 pmol/0.5 μl/side, respectively).
The above findings support the idea that the activation of mGluR7 can produce antiparkinsonian-like effects in rats. Furthermore, our results indicate contribution of both striatal and nigral mGluR7 to the anticataleptic effects of AMN082.
代谢型谷氨酸受体(mGluRs)已被证明是许多神经疾病的潜在靶点,包括帕金森病(PD)。我们之前报道过,局部注射到苍白球、纹状体或黑质网状部(SNr)的非选择性 mGluR3 激动剂 ACPT-1 可显著减轻大鼠的氟哌啶醇诱导的僵住。N,N'-二苄基乙二胺二盐酸盐(AMN082)是一种有效的、可穿透血脑屏障的 mGluR7 激动剂,对其他 mGluRs 具有选择性。
本研究旨在确定(1)全身给予 AMN082 激活 mGluR7 是否会在氟哌啶醇诱导的僵住和利血平诱导的运动不能模型中产生类似帕金森病的效应;(2)纹状体和黑质 mGluR7 是否有助于这种效应。
我们发现 AMN082(1 和 3 mg/kg)可降低氟哌啶醇(0.25 mg/kg)诱导的僵住,但对利血平(2.5 mg/kg)诱导的运动不能没有效果。局部给予 AMN082 也显著减轻了大鼠的僵住;然而,其在纹状体中的有效剂量比在 SNr 中的低 10 倍(2.5 和 7.5 pmol/0.5 μl/侧与 25 和 75 pmol/0.5 μl/侧,分别)。
上述发现支持这样的观点,即激活 mGluR7 可以在大鼠中产生类似帕金森病的效应。此外,我们的结果表明,纹状体和黑质 mGluR7 都有助于 AMN082 的抗僵住作用。