对II型代谢型谷氨酸受体的引发刺激会抑制随后在体外诱导大鼠海马体长期抑郁。

Priming stimulation of group II metabotropic glutamate receptors inhibits the subsequent induction of rat hippocampal long-term depression in vitro.

作者信息

Mellentin C, Abraham W C

机构信息

Department of Psychology, Neuroscience Research Centre, University of Otago, Box 56, Dunedin, New Zealand.

出版信息

Neurosci Lett. 2001 Jul 6;307(1):13-6. doi: 10.1016/s0304-3940(01)01915-2.

DOI:10.1016/s0304-3940(01)01915-2

PMID:11516563

Abstract

The ability of priming activation of metabotropic glutamate receptors (mGluRs) to regulate long-term depression (LTD) was studied in area CA1 of hippocampal slices taken from young adult male rats. Pharmacological activation of Group I mGluRs 30-40 min prior to low-frequency stimulation at 3 Hz failed to affect LTD. Activation of Group II mGluRs, however, significantly inhibited the LTD by >50%, while activation of Group III mGluRs had no statistically significant effect on LTD. The inhibition of LTD by activation of Group II mGluRs was even stronger when the Group II agonist was applied during the low-frequency stimulation. Because activation of Group II mGluRs is also known to inhibit LTP, the net effect of such stimulation is the induction of a metaplasticity that greatly restricts the effective range of stimuli that can evoke synaptic plasticity in the hippocampus.

摘要

在取自成年雄性幼鼠的海马切片CA1区，研究了代谢型谷氨酸受体（mGluRs）的引发激活调节长时程抑制（LTD）的能力。在3Hz低频刺激前30 - 40分钟对I组mGluRs进行药理学激活，未能影响LTD。然而，II组mGluRs的激活显著抑制LTD达50%以上，而III组mGluRs的激活对LTD无统计学显著影响。当在低频刺激期间应用II组激动剂时，II组mGluRs激活对LTD的抑制作用更强。由于已知II组mGluRs的激活也会抑制长时程增强（LTP），这种刺激的净效应是诱导一种元可塑性，极大地限制了可在海马中诱发突触可塑性的刺激的有效范围。