Abstract
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 role of glycine (Gly) receptors in the SC, and we observed that application of glycine (Gly; 500 μM 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.
The strength of potentiation was found to be concentration-dependent and partially independent from synaptic stimulation.
LTPgly did not involve NMDA receptor activation as proven by the lack of inhibition by 100 μM D,L-2-amino-5-phosphonovaleric acid (APV) and 10 μM MK-801.
LTPgly could only be masked but not prevented by strychnine (100 μM) and remained undisturbed in the presence of picrotoxin (100 μM).
Inhibition of carbonic anhydrase by acetazolamide (20 μM) had no effect on LTPgly suggesting that the excitatory action of Gly is not due to a differential breakdown of the Cl−/HCO3− gradients.
As indicated by the inhibition of LTPgly of the fEPSP slope by the L-type calcium channel blocker nifedipine (20 μM), voltage-dependent calcium channels are the source for Ca2+ elevation as the intracellular trigger.
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.
Keywords: Glycine, superior colliculus, long-term potentiation, plasticity, slice, NMDA, strychnine, voltage-dependent calcium channels
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