Abstract
Perfusion of 100 μM melatonin had no effect on low frequency synaptic transmission, but prevented the induction of tetanically induced long-term potentiation (LTP) when recorded in the dendritic region of the CA1 in rat hippocampal slices. Perfusion of 100 μM melatonin in this preparation had no effect on the multiple population spikes recorded in Mg 2+-free medium, and, in grease-gap recordings from the CA1-subiculum slice, 100 μM melatonin had no effect on depolarisations evoked by N-methyl- d-aspartate (NMDA) or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). This suggests that melatonin has the ability to prevent the formation of LTP, and that this effect is not mediated by blockade of NMDA receptors.
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