Krieger P, Grillner S, El Manira A
The Nobel Institute for Neurophysiology, Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Eur J Neurosci. 1998 Nov;10(11):3333-42. doi: 10.1046/j.1460-9568.1998.00337.x.
The effect of metabotropic glutamate receptor (mGluR) agonists and antagonists on the spinal cord network underlying locomotion in the lamprey has been analysed. The specific group I mGluR agonist (R,S)-3,5-dihydroxyphenylglycine (DHPG) and the broad-spectrum mGluR agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) both increased the burst frequency of N-methyl-D-aspartic acid (NMDA)-induced fictive locomotion and depolarized grey matter neurons. The burst frequency increase induced by the mGluR agonists was counteracted by the mGluR antagonists (+)-alpha-methyl-4-carboxyphenylglycine ((+)-MCPG), cyclopropan[b]chromen-1a-carboxylic acid ethylester (CPCCOEt) and (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA). Application of CPCCOEt alone reduced the locomotor burst frequency, indicating that mGluRs are endogenously activated during fictive locomotion. The mGluR antagonist CPCCOEt had no effect on NMDA-, or (S)-alpha-amino-3-hydroxy-5-methyl-4-isoazolepropionic acid (AMPA)-induced depolarizations. The mGluR agonists 1S,3R-ACPD and DHPG increased the amplitude of NMDA-induced depolarizations, a mechanism which could account for the increase in burst frequency. The group III mGluR agonist L-2-amino-4-phosphonobutyric acid reduced intraspinal synaptic transmission and burst frequency.
已经分析了代谢型谷氨酸受体（mGluR）激动剂和拮抗剂对七鳃鳗运动背后脊髓网络的影响。特异性I组mGluR激动剂（R，S）-3,5-二羟基苯甘氨酸（DHPG）和广谱mGluR激动剂（1S，3R）-1-氨基环戊烷-1,3-二羧酸（1S，3R-ACPD）均增加了N-甲基-D-天冬氨酸（NMDA）诱导的虚拟运动的爆发频率，并使灰质神经元去极化。mGluR激动剂诱导的爆发频率增加被mGluR拮抗剂（+）-α-甲基-4-羧基苯甘氨酸（（+）-MCPG）、环丙烷[b]色烯-1a-羧酸乙酯（CPCCOEt）和（RS）-1-氨基茚满-1,5-二羧酸（AIDA）抵消。单独应用CPCCOEt可降低运动爆发频率，表明mGluRs在虚拟运动期间被内源性激活。mGluR拮抗剂CPCCOEt对NMDA或（S）-α-氨基-3-羟基-5-甲基-4-异唑丙酸（AMPA）诱导的去极化没有影响。mGluR激动剂1S，3R-ACPD和DHPG增加了NMDA诱导的去极化幅度，这一机制可以解释爆发频率的增加。III组mGluR激动剂L-2-氨基-4-膦酰丁酸降低了脊髓内突触传递和爆发频率。
