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<titleInfo><title>Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus</title></titleInfo>

  
  
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  <namePart type="given">Rajiv Kumar</namePart>
  <namePart type="family">Mishra</namePart>
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  <namePart type="given">Peter M</namePart>
  
  
  <namePart type="family">Jonas</namePart>
  
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<abstract lang="eng">CA3 pyramidal neurons are thought to pay a key role in memory storage and pattern completion by activity-dependent synaptic plasticity between CA3-CA3 recurrent excitatory synapses. To examine the induction rules of synaptic plasticity at CA3-CA3 synapses, we performed whole-cell patch-clamp recordings in acute hippocampal slices from rats (postnatal 21-24 days) at room temperature. Compound excitatory postsynaptic potentials (ESPSs) were recorded by tract stimulation in stratum oriens in the presence of 10 µM gabazine. High-frequency stimulation (HFS) induced N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP). Although LTP by HFS did not requier postsynaptic spikes, it was blocked by Na+-channel blockers suggesting that local active processes (e.g.) dendritic spikes) may contribute to LTP induction without requirement of a somatic action potential (AP). We next examined the properties of spike timing-dependent plasticity (STDP) at CA3-CA3 synapses. Unexpectedly, low-frequency pairing of EPSPs and backpropagated action potentialy (bAPs) induced LTP, independent of temporal order. The STDP curve was symmetric and broad, with a half-width of ~150 ms. Consistent with these specific STDP induction properties, post-presynaptic sequences led to a supralinear summation of spine [Ca2+] transients. Furthermore, in autoassociative network models, storage and recall was substantially more robust with symmetric than with asymmetric STDP rules. In conclusion, we found associative forms of LTP at CA3-CA3 recurrent collateral synapses with distinct induction rules. LTP induced by HFS may be associated with dendritic spikes. In contrast, low frequency pairing of pre- and postsynaptic activity induced LTP only if EPSP-AP were temporally very close. Together, these induction mechanisms of synaptiic plasticity may contribute to memory storage in the CA3-CA3 microcircuit at different ranges of activity.</abstract>

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<originInfo><publisher>Institute of Science and Technology Austria</publisher><dateIssued encoding="w3cdtf">2016</dateIssued>
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<language><languageTerm authority="iso639-2b" type="code">eng</languageTerm>
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  <identifier type="issn">2663-337X</identifier>
<part><extent unit="pages">83</extent>
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<ista>Mishra RK. 2016. Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus. Institute of Science and Technology Austria.</ista>
<apa>Mishra, R. K. (2016). &lt;i&gt;Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus&lt;/i&gt;. Institute of Science and Technology Austria.</apa>
<ieee>R. K. Mishra, “Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus,” Institute of Science and Technology Austria, 2016.</ieee>
<chicago>Mishra, Rajiv Kumar. “Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus.” Institute of Science and Technology Austria, 2016.</chicago>
<mla>Mishra, Rajiv Kumar. &lt;i&gt;Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus&lt;/i&gt;. Institute of Science and Technology Austria, 2016.</mla>
<short>R.K. Mishra, Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus, Institute of Science and Technology Austria, 2016.</short>
<ama>Mishra RK. Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus. 2016.</ama>
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