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代谢型谷氨酸受体抑制大鼠纹状体中D-[3H]-天冬氨酸输出的药理学特性

Pharmacological characterization of the metabotropic glutamate receptor inhibiting D-[3H]-aspartate output in rat striatum.

作者信息

Lombardi G, Alesiani M, Leonardi P, Cherici G, Pellicciari R, Moroni F

机构信息

Dipartimento di Farmacologia Preclinica e Clinica Mario Aiazzi Mancini, Università di Firenze, Italy.

出版信息

Br J Pharmacol. 1993 Dec;110(4):1407-12. doi: 10.1111/j.1476-5381.1993.tb13977.x.

DOI:10.1111/j.1476-5381.1993.tb13977.x
PMID:8306080
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2175867/
Abstract
  1. The effects of several agonists of the metabotropic glutamate receptor (mGluR) were studied in adult rat striatal slices by measuring (i) KCl (30 mM)-induced output of previously taken up D-[3H]-aspartate (Asp), (ii) forskolin (30 microM)-induced adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation and (iii) phophoinositide (PI) hydrolysis. 2. K(+)-induced efflux of D-[3H]-Asp was inhibited by the following mGluR agonists: (1S,3S,4S)-(carboxycyclopropyl)glycine (L-CCG-I), (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) and quisqualic acid (Quis). 2-Amino-4-phosphonobutyrate (L-AP4) was inactive up to 300 microM. The maximal inhibition of D-[3H]-Asp output was 60 +/- 8%. The EC50s of mGluR agonists were: 0.5 microM for L-CCG-I, 100 microM for 1S,3R-ACPD and 100 microM for Quis. 3. Forskolin-induced cyclic AMP accumulation was also inhibited by mGluR agonists. The maximal inhibition was 50 +/- 4% and was obtained at a concentration of 10 microM for L-CCG-I and 100 microM for 1S,3R-ACPD. The EC50s for this inhibition were: 0.9 microM for L-CCG-I and 20 microM for 1S,3R-ACPD. Quis (300 microM) inhibited cyclic AMP accumulation by approximately 20%. L-AP4 slightly potentiated cyclic AMP accumulation. 4. PI hydrolysis was stimulated by mGluR agonists. The most potent compound was Quis (100 microM), which increased inositol phosphate formation up to 2.2 fold over control values. Its EC50 was 15 microM. L-CCG-I and 1S,3R-ACPD increased inositol phosphate formation by approximately 1.8 fold and their EC50 values were 30 and 25 microM, respectively. L-AP4 did not affect PI hydrolysis. 5. In conclusion, mGluR agonists that reduce D-[3H]-Asp output have a pharmacological profile similar to that of mGluR agonists inhibiting cyclic AMP accumulation. L-CCG-I appears to be a relatively selective agonist for the mGluR receptor which inhibits D-[3H]-Asp efflux and cyclic AMP accumulation,while Quis appears to act preferentially on the mGluR receptor linked to the metabolism of PIs.
摘要
  1. 通过测量以下指标，研究了几种代谢型谷氨酸受体（mGluR）激动剂对成年大鼠纹状体切片的影响：（i）30 mM氯化钾（KCl）诱导的预先摄取的D-[3H]-天冬氨酸（Asp）的释放；（ii）30 μM福斯高林诱导的腺苷3':5'-环磷酸（环磷酸腺苷，cAMP）积累；以及（iii）磷脂酰肌醇（PI）水解。2. 以下mGluR激动剂可抑制K⁺诱导的D-[3H]-Asp外流：（1S,3S,4S）-(羧基环丙基)甘氨酸（L-CCG-I）、（1S,3R）-1-氨基环戊烷-1,3-二羧酸（1S,3R-ACPD）和喹啉酸（Quis）。2-氨基-4-膦酰丁酸（L-AP4）在高达300 μM时无活性。D-[3H]-Asp释放的最大抑制率为60±8%。mGluR激动剂的半数有效浓度（EC50）分别为：L-CCG-I为0.5 μM，1S,3R-ACPD为100 μM，Quis为100 μM。3. mGluR激动剂也可抑制福斯高林诱导的环磷酸腺苷积累。最大抑制率为50±4%，L-CCG-I在10 μM浓度时达到此抑制率，1S,3R-ACPD在100 μM浓度时达到。这种抑制作用的EC50分别为：L-CCG-I为0.9 μM，1S,3R-ACPD为20 μM。300 μM的Quis可使环磷酸腺苷积累抑制约20%。L-AP4可轻微增强环磷酸腺苷积累。4. mGluR激动剂可刺激PI水解。最有效的化合物是Quis（100 μM），其使肌醇磷酸形成增加至对照值的2.2倍。其EC50为15 μM。L-CCG-I和1S,3R-ACPD使肌醇磷酸形成增加约1.8倍，其EC50值分别为30 μM和25 μM。L-AP4不影响PI水解。5. 总之，降低D-[3H]-Asp释放的mGluR激动剂具有与抑制环磷酸腺苷积累的mGluR激动剂相似的药理学特征。L-CCG-I似乎是一种相对选择性的mGluR受体激动剂，可抑制D-[3H]-Asp外流和环磷酸腺苷积累，而Quis似乎优先作用于与PI代谢相关的mGluR受体。