LTP, which stands for long-term potentiation, is regarded as a neuronal correlate of memory and learning. On dendritic spines, the presence of G protein-activated inwardly rectifying K(+) (GIRK) channels close to excitatory synapses raises the possibility that these channels play a role in synaptic plasticity.
It is uncertain, nevertheless, whether activity-dependent channel modulation impacts excitatory synaptic plasticity. In a related paper, we described the activity-dependent modulation of GIRK channel density in cultured hippocampal neurons, which occurs within 15 minutes and necessitates the activity of receptors (NMDAR) and protein phosphatase-1 (PP1). We discovered that NMDAR activation enhances basal GIRK current and GIRK channel activation mediated by adenosine A(1) receptors, but not GABA(B) receptors, in this study's whole-cell recordings of cultured hippocampus neurons.
We wondered if an NMDAR-induced increase in GIRK channel surface density and current may contribute to the molecular mechanisms underlying this particular depotentiation given the similar involvement of NMDARs, adenosine receptors, and PP1 in depotentiation of long-term potentiation caused by low-frequency stimulation that immediately follows high-frequency stimulation that induces long-term potentiation. Interestingly, depotentiation of long-term potentiation is abolished by GIRK2 null mutation or GIRK channel blocking, proving that GIRK channels are essential for depotentiation, one type of excitatory synaptic plasticity.
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