Abstract
The piriform cortex (PCx) is essential for learning of odor information. The current view postulates that odor learning in the PCx is mainly due to plasticity in intracortical (IC) synapses, while odor information from the olfactory bulb carried via the lateral olfactory tract (LOT) is 'hardwired.' Here, we revisit this notion by studying location- and pathway-dependent plasticity rules. We find that in contrast to the prevailing view, synaptic and optogenetically activated LOT synapses undergo strong and robust long-term potentiation (LTP) mediated by only a few local NMDA-spikes delivered at theta frequency, while global spike timing-dependent plasticity (STDP) protocols failed to induce LTP in these distal synapses. In contrast, IC synapses in apical and basal dendrites undergo plasticity with both NMDA-spikes and STDP protocols but to a smaller extent compared with LOT synapses. These results are consistent with a self-potentiating mechanism of odor information via NMDA-spikes that can form branch-specific memory traces of odors that can further associate with contextual IC information via STDP mechanisms to provide cognitive and emotional value to odors.
Highlights
The piriform cortex (PCx) is a main cortical station in olfactory processing, receiving direct odor information from the olfactory bulb via the lateral olfactory tract (LOT) as well as higher brain regions and is thought to be important for odor discrimination and recognition
We recently reported the initiation of local NMDA-spikes in distal apical dendrites of PCx pyramidal neurons by activation of LOT synapses (Kumar et al, 2018)
The piriform cortex was shown to be critical for odor discrimination, recognition and memory and odor memory was attributed to plasticity changes in the PCx (Ghosh et al, 2016; Haberly, 2001; Hasselmo and Barkai, 1995; Saar et al, 2012)
Summary
The piriform cortex (PCx) is a main cortical station in olfactory processing, receiving direct odor information from the olfactory bulb via the lateral olfactory tract (LOT) as well as higher brain regions and is thought to be important for odor discrimination and recognition. STDP protocols failed altogether to induce LTP in LOT synapses because of the severe attenuation of back propagating action potentials (BAPs) to distal apical dendrites of PCx pyramidal neurons, where LOT inputs terminate (Haberly, 2001; Neville and Haberly, 2004). These dendritic NMDA-spikes generate large localized calcium transients, which can serve as post synaptic signals for LTP induction in the activated LOT synapses In support of this hypothesis, it was recently shown that NMDA-spikes were critical for inducing LTP in the dendrites of CA3 pyramidal neurons (Brandalise et al, 2016) and in layer 2-3 pyramidal neurons of somatosensory cortex in-vivo (Gambino et al, 2014; Gordon et al, 2006). For IC apical and basal synapses potentiation was mediated by both NMDA-spikes and STDP protocols but the magnitude of potentiation was smaller compared to that of LOT synapses
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