O'Leary D M, O'Connor J J
Department of Human Anatomy and Physiology, University College, Earlsfort Terrace, Dublin 2, Ireland.
Brain Res. 1998 Oct 26;809(1):91-6. doi: 10.1016/s0006-8993(98)00897-x.
The role of metabotropic glutamate receptors (mGluRs) in long-term potentiation (LTP) has remained controversial. However, it has recently been shown that group I mGluR activation, prior to high frequency stimulation (HFS), can facilitate or 'prime' LTP in the area CA1 of the hippocampus. Here we report that, in the dentate gyrus in vitro, activation of both group I and group II mGluRs primes LTP. Control LTP, 60 min after HFS was 145.4+/-3.6% of control. The group I mGluR agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG, 100 microM), resulted in LTP of 180.1+/-12.1% of control, which was significantly greater than control LTP (n=4; P<0.05). The group I/II mGluR agonist 1S, 3R-1-aminocyclopentate-1,3-dicarboxylic acid (1S,3R-ACPD, 10 microM), and the group II mGluR agonist (2S,3S, 4S)-alpha-(carboxy-cyclopropyl)-glycine (L-CCG-1, 20 microM) also produced LTP that was significantly greater than control LTP (177. 7+/-11.5% and 183.2+/-9.1% of control respectively; n=5; P<0.05). The group III mGluR agonist l-2-amino-4-phosphonobutyric acid (L-AP4, 20 microM), failed to significantly prime LTP (153.8+/-5.9% of control; n=5). It also proved difficult to depotentiate the primed LTP. Following low frequency stimulation (LFS), control LTP was reduced to 101.1+/-3.6% of control, and to 145.0+/-2.1%, 141.2+/-14. 7% and 134.0+/-8.7% of control for CHPG, ACPD and L-CCG-1 primed LTP respectively. We conclude that LTP may be primed by mGluR activation in the dentate gyrus and that this priming is mediated through group I and II mGluRs.
代谢型谷氨酸受体（mGluRs）在长时程增强（LTP）中的作用一直存在争议。然而，最近有研究表明，在高频刺激（HFS）之前激活I组mGluR，可以促进或“启动”海马体CA1区的LTP。在此我们报告，在体外齿状回中，I组和II组mGluR的激活均可启动LTP。HFS后60分钟，对照LTP为对照的145.4±3.6%。I组mGluR激动剂（RS）-2-氯-5-羟基苯甘氨酸（CHPG，100μM），导致LTP为对照的180.1±12.1%，显著高于对照LTP（n = 4；P < 0.05）。I/II组mGluR激动剂1S，3R-1-氨基环戊烷-1,3-二羧酸（1S,3R-ACPD，10μM），以及II组mGluR激动剂（2S,3S,4S）-α-（羧基-环丙基）-甘氨酸（L-CCG-1，20μM）也产生了显著高于对照LTP的LTP（分别为对照的177.7±11.5%和183.2±9.1%；n = 5；P < 0.05）。III组mGluR激动剂L-2-氨基-4-膦酰丁酸（L-AP4，20μM），未能显著启动LTP（为对照的153.8±5.9%；n = 5）。去增强启动后的LTP也很困难。低频刺激（LFS）后，对照LTP降至对照的101.1±3.6%，而CHPG、ACPD和L-CCG-1启动的LTP分别降至对照的145.0±2.1%、141.2±14.7%和134.0±8.7%。我们得出结论，齿状回中的LTP可能通过mGluR激活而启动，并且这种启动是通过I组和II组mGluR介导的。
