Journal
EUROPEAN JOURNAL OF NEUROSCIENCE
Volume 34, Issue 2, Pages 213-220Publisher
WILEY
DOI: 10.1111/j.1460-9568.2011.07763.x
Keywords
brain slice; hippocampus; NR2B receptors; P2X4 receptors; plasticity; whole-cell recording
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Funding
- Wellcome Trust
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P2X4 receptors are calcium-permeable cation channels gated by extracellular ATP. They are found close to subsynaptic sites on hippocampal CA1 neurons. We compared features of synaptic strengthening between wild-type and P2X4 knockout mice (21-26 days old). Potentiation evoked by a tetanic presynaptic stimulus (100 Hz, 1 s) paired with postsynaptic depolarization was less in P2X4(-/-) mice than in wild-type mice (230 vs. 50% potentiation). Paired-pulse ratios and the amplitude and frequency of spontaneous excitatory postsynaptic currents (EPSCs) were not different between wild-type and knockout mice. Prior hyperpolarization (ten 3 s pulses to -120 mV at 0.17 Hz) potentiated the amplitude of spontaneous EPSCs in wild-type mice, but not in P2X4(-/-) mice; this potentiation was not affected by nifedipine, but was abolished by 10 mm 1,2-bis(o-aminophenoxy) ethane-N,N,N',N'-tetra-acetic acid (BAPTA) in the recording pipette. The amplitude of N-methyl-D-aspartate EPSCs (in 6-cyano-7-nitroquinoxaline-2,3-dione, 10 or 30 mu m, at -100 mV) facilitated during 20 min recording in magnesium-free solution. In wild-type mice, this facilitation of the N-methyl-D-aspartate EPSC was reduced by about 50% by intracellular BAPTA (10 mm), ifenprodil (3 mu m) or 4-(4-fluorophenyl)-2-(4-methylsulphinylphenyl)-5-(4-pyridyl) 1H-imidazole (5 mu m). In P2X4(-/-) mice, the facilitation was much less, and was unaffected by intracellular BAPTA, ifenprodil (3 mu m) or mitogen-activated protein (MAP) kinase inhibitor 4-(4-fluorophenyl)-2-(4-methylsulphinylphenyl)-5-(4-pyridyl) 1H-imidazole (5 mu m). This suggests that the absence of P2X4 receptors limits the incorporation of NR2B subunits into synaptic N-methyl-D-aspartate receptors.
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