Abstract
Long-term potentiation (LTP) at hippocampal CA1 synapses is classically triggered by the synaptic activation of NMDA receptors (NMDARs). More recently, it has been shown that calcium-permeable (CP) AMPA receptors (AMPARs) can also trigger synaptic plasticity at these synapses. Here, we review this literature with a focus on recent evidence that CP-AMPARs are critical for the induction of the protein kinase A (PKA)- and protein synthesis-dependent component of LTP.
Highlights
Long-term potentiation (LTP) is the most intensively studied type of synaptic plasticity in the vertebrate central nervous system (CNS), driven by the widely-held view that the mechanism is engaged by, and is critical for, learning and memory processes (Bliss and Collingridge, 1993)
We found that the rolipram-enhanced LTP was due to the insertion of CP-AMPA receptors (AMPARs) as probed either with IEM 1460 or using rectification index (RI) measurements (Park et al, 2016)
We propose that if a second theta burst stimulation (TBS) occurs while these CP-AMPARs are on the perisynaptic plasma membrane they are driven into the synapse, from where they can be activated by low frequency stimulation to trigger LTP2
Summary
Long-term potentiation (LTP) is the most intensively studied type of synaptic plasticity in the vertebrate central nervous system (CNS), driven by the widely-held view that the mechanism is engaged by, and is critical for, learning and memory processes (Bliss and Collingridge, 1993). Consistent with the earlier report (Plant et al, 2006) that stimulation is required post induction for the full expression of LTP, we observed that if we stopped stimulation following the sTBS protocol LTP was reduced (Figure 3) We interpreted this result to mean that, for a short time window after the synaptic activation of NMDARs, low frequency stimulation is required to induce LTP2 and, when stimulation is paused only LTP1 is observed. We found no change in the RI following cTBS but a significant increase in rectification following sTBS (Park et al, 2016) These observations are consistent with the synaptic insertion of CP-AMPARs into a background of calcium-impermeable (CI) AMPARs. The PKA-dependent component of LTP (i.e., LTP2) can be induced by a single episode of TBS delivered under conditions where cAMP generation is enhanced, such as in the presence of the phosphodiesterase 4 (PDE4) inhibitor rolipram (Barad et al, 1998). We found that the rolipram-enhanced LTP was due to the insertion of CP-AMPARs as probed either with IEM 1460 or using RI measurements (Park et al, 2016)
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