Abstract
In the hippocampus, the contributions of N-methyl-D-aspartate receptors (NMDARs) and L-type calcium channels (LTCCs) to neuronal transmission and synaptic plasticity change with aging, underlying calcium dysregulation and cognitive dysfunction. However, the relative contributions of NMDARs and LTCCs in other learning encoding structures during aging are not known. The piriform cortex (PC) plays a significant role in odor associative memories, and like the hippocampus, exhibits forms of long-term synaptic plasticity. Here, we investigated the expression and contribution of NMDARs and LTCCs in long-term depression (LTD) of the PC associational fiber pathway in three cohorts of Sprague Dawley rats: neonatal (1–2 weeks), young adult (2–3 months) and aged (20–25 months). Using a combination of slice electrophysiology, Western blotting, fluorescent immunohistochemistry and confocal imaging, we observed a shift from an NMDAR to LTCC mediation of LTD in aged rats, despite no difference in the amount of LTD expression. These changes in plasticity are related to age-dependent differential receptor expression in the PC. LTCC Cav1.2 expression relative to postsynaptic density protein 95 is increased in the associational pathway of the aged PC layer Ib. Enhanced LTCC contribution in synaptic depression in the PC may contribute to altered olfactory function and learning with aging.
Highlights
The piriform cortex (PC) is a central component of olfactory information processing, underlying odor discrimination and contextualization [1,2]
In conjunction with its role in olfactory encoding, the PC is a site involved in associative memory formation, exhibiting a high degree of synaptic plasticity during early developmental periods, which moderately persists into adulthood [4,5,6,7]
To assess the effect of aging on the roles of N-methyl-D-aspartate receptors (NMDARs) and L-type calcium channels (LTCCs) in synaptic plasticity of the PC, we investigated field excitatory post synaptic potentials in PC slices from three different age cohorts: neonatal (1–2 weeks), adult (2–3 months) and aged (20–25 months)
Summary
The piriform cortex (PC) is a central component of olfactory information processing, underlying odor discrimination and contextualization [1,2]. The age-related increase in LTCCs is associated with a shift in forms of synaptic plasticity in aged rats, exhibiting a reduced NMDAR-dependent and increased LTCCdependent LTP and LTD at Schaffer-collateral-CA1 synapses when compared to young rats [18,19,20]. This age-related modification of presence and function of LTCCs in hippocampal neurons could contribute to dysregulated calcium homeostasis, resulting in synaptic dysfunction and cognitive decline [21], a protective role of increased LTCC plasticity in aging has been proposed [18,19]. By assessing LTD within the associational layer Ib of neonatal, adult and aging rats, we report that, similar to the hippocampus, the PC exhibits an agedependent shift in relative receptor contribution and downstream signalling cascades to synaptic plasticity
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