Glycine induces a novel form of long-term potentiation in the superficial layers of the superior colliculus

被引:9
作者
Platt, B
Bate, JR
Roloff, ZV
Withington, DJ [1 ]
机构
[1] Univ Aberdeen, IMS, Dept Biomed Sci, Aberdeen AB25 2ZD, Scotland
[2] Univ Leeds, Dept Physiol, Leeds LS2 9NQ, W Yorkshire, England
基金
英国惠康基金;
关键词
glycine; superior colliculus; long-term potentiation; plasticity; slice; NMDA; strychnine; voltage-dependent calcium channels;
D O I
10.1038/sj.bjp.0702062
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
1 The mammalian superior colliculus (SC) is a midbrain nucleus containing space maps of different sensory modalities which show various forms of age- and activity-dependent plasticity in vivo and in vitro. In the present study, we aimed to characterize the rob of glycine (Gly) receptors in the SC, and we observed that application of glycine (Gly; 500 mu M and 3 mM) for 7 min to SC slices of adult guinea-pigs caused a novel form of long-term potentiation (termed LTPgly) of evoked excitatory postsynaptic potentials recorded in the superficial layers. 2 The strength of potentiation was found to be concentration-dependent and partially independent from synaptic stimulation. 3 LTPgly did not involve NMDA receptor activation as proven by the lack of inhibition by 100 mu M D,L-2-amino-5-phosphonovaleric acid (APV) and 10 mu M MK-801. 4 LTPgly could only be masked but not prevented by strychnine (100 mu M) and remained undisturbed in the presence of picrotoxin (100 mu M). 5 Inhibition of carbonic anhydrase by acetazolamide (20 mu M) had no effect on LTPgly suggesting that the excitatory action of Gly is not due to a differential breakdown of the Cl-/HCO3- gradients. 6 As indicated by the inhibition of LTPgly of the fEPSP slope by the L-type calcium channel blocker nifedipine (20 mu M), voltage-dependent calcium channels are the source for Ca2+ elevation as the intracellular trigger. 7 Our data provide the first evidence for a role of Gly in SC synaptic transmission. They illustrate a so far unknown action of Gly which can lead to long-lasting changes of synaptic efficacy and which is not mediated via NMDA-related or strychnine-sensitive binding sites.
引用
收藏
页码:293 / 300
页数:8
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