Article

Cholinergic Coordination of Presynaptic and Postsynaptic Activity Induces Timing-Dependent Hippocampal Synaptic Plasticity

Laboratory of Neurobiology, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27709.
The Journal of Neuroscience : The Official Journal of the Society for Neuroscience (Impact Factor: 6.34). 09/2012; 32(36):12337-48. DOI: 10.1523/JNEUROSCI.2129-12.2012
Source: PubMed

ABSTRACT

Correlated presynaptic and postsynaptic activity is the key factor in inducing Hebbian plasticity and memory. However, little is known about the physiological events that could mediate such coordination. Correlated cholinergic input induces spike timing-dependent plasticity-like hippocampal synaptic plasticity. Cholinergic receptors are localized to both presynaptic and postsynaptic glutamatergic sites and thus have the potential to coordinate presynaptic and postsynaptic activity to induce plasticity. By directly monitoring presynaptic and postsynaptic activities with genetically encoded calcium indicators in mouse septohippocampal cocultures, we found interactive but independent presynaptic and postsynaptic modulations in the cholinergic-dependent synaptic plasticity. Neither presynaptic nor postsynaptic modulation alone is sufficient, but instead a coordinated modulation at both sites is required to induce the plasticity. Therefore, we propose that correlated cholinergic input can coordinate presynaptic and postsynaptic activities to induce timing-dependent synaptic plasticity, providing a novel mechanism by which neuromodulators precisely modulate network activity and plasticity with high efficiency and temporal precision.

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    • "Among the most abundant nAChRs are homopentameric α7-containing receptors (α7-nAChRs), which can be located both pre-and postsynaptically at many kinds of central synapses. The receptors can mediate synaptic plasticity; even brief activation of α7-nAChRs can induce long-term potentiation (LTP; Fuiji et al., 1999; Gu et al., 2012; Ji et al., 2001; Kenney and Gould, 2008; Placzek et al., 2009; Yakel, 2012). A common mechanism driving long-term synaptic plasticity is a change in the number or functionality of postsynaptic glutamate receptors at a glutamatergic synapse (Bear and Abraham, 1996; Bliss and Collingridge, 1993; Derkach et al., 2007; Lau and Zukin, 2007). "
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