Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9429413 | Neuroscience Letters | 2005 | 5 Pages |
Abstract
ATP is an important extracellular messenger in the CNS. In the hippocampus, a brain structure relevant for learning and memory processes, it acts both as a modulator and as a mediator of synaptic transmission, with implications for synaptic plasticity phenomena. Recent evidence suggests that ATP modulates activity-dependent long-term potentiation (LTP) of Schaffer collateral-CA1 synapses. However, it remains unclear if ATP also modulates LTP counterpart's phenomenon, long-term depression (LTD), in the rat hippocampus. This study investigated the effect of ATP analogues on homosynaptic LTD, induced by low-frequency stimulation of the Schaffer collaterals (1 Hz; 900 pulses) in the CA1 region of young rat hippocampal slices. The metabolically stable ATP analogues β,γ-ImATP (20 μM), a P2 receptor agonist, and α,β-MeATP (20 μM), a preferential P2X1,3 receptor agonist, did not modify LTD (LTD values of 14.7 ± 0.5% and 14.1 ± 3% for aCSF controls and of 15.1 ± 4% and 19.0 ± 5.2% for β,γ-ImATP and α,β-MeATP, respectively). The ATP analogue β,γ-ImATP (20 μM) did not modify LTD also in the presence of the adenosine A1 receptor antagonist DPCPX (50 nM) (21.5 ± 4.2% for DPCPX only and of 23.8 ± 8.9% for DPCPX plus β,γ-ImATP). Finally, the preferential P2X1,3 receptor antagonist NF023 (10 μM) had also no effect on LTD (18.6 ± 5.2% for aCSF and of 18.7 ± 5.2% for NF023). The present results suggest that ATP does not modulate activity-dependent homosynaptic LTD in the rat CA1 hippocampal region by activating P2 receptors.
Related Topics
Life Sciences
Neuroscience
Neuroscience (General)
Authors
Bruno M. da Silva, Alexandre de Mendonça, Joaquim A. Ribeiro,