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   	<dc:title>Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus</dc:title>
   	<dc:title>ISTA Thesis</dc:title>
   	<dc:creator>Mishra, Rajiv Kumar</dc:creator>
   	<dc:subject>ddc:570</dc:subject>
   	<dc:description>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.</dc:description>
   	<dc:publisher>Institute of Science and Technology Austria</dc:publisher>
   	<dc:date>2016</dc:date>
   	<dc:type>info:eu-repo/semantics/doctoralThesis</dc:type>
   	<dc:type>doc-type:DoctoralThesis</dc:type>
   	<dc:type>DoctoralThesis</dc:type>
   	<dc:type>http://purl.org/coar/resource_type/c_db06</dc:type>
   	<dc:identifier>https://research-explorer.ista.ac.at/record/1396</dc:identifier>
   	<dc:identifier>https://research-explorer.ista.ac.at/download/1396/9183</dc:identifier>
   	<dc:source>Mishra RK. Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus. 2016.</dc:source>
   	<dc:language>eng</dc:language>
   	<dc:relation>info:eu-repo/semantics/altIdentifier/issn/2663-337X</dc:relation>
   	<dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
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