Short-Term Plasticity at Olfactory Cortex to Granule Cell Synapses Requires CaV2.1 Activation.

Fu-Wen Zhou,Michael T Shipley,Adam C Puche

doi:10.3389/fncel.2018.00387

Fu-Wen Zhou, Michael T Shipley + Show 1 more

Open Access

https://doi.org/10.3389/fncel.2018.00387

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Abstract

Output projections of the olfactory bulb (OB) to the olfactory cortex (OCX) and reciprocal feedback projections from OCX provide rapid regulation of OB circuit dynamics and odor processing. Short-term synaptic plasticity (STP), a feature of many synaptic connections in the brain, can modulate the strength of feedback based on preceding network activity. We used light-gated cation channel channelrhodopsin-2 (ChR2) to investigate plasticity of excitatory synaptic currents (EPSCs) evoked at the OCX to granule cell (GC) synapse in the OB. Selective activation of OCX glutamatergic axons/terminals in OB generates strong, frequency-dependent STP in GCs. This plasticity was critically dependent on activation of CaV2.1 channels. As acetylcholine (ACh) modulates CaV2.1 channels in other brain regions and as cholinergic projections from the basal forebrain heavily target the GC layer (GCL) in OB, we investigated whether ACh modulates STP at the OCX→GC synapse. ACh decreases OCX→GC evoked EPSCs, it had no effect on STP. Thus, ACh impact on cortical feedback is independent of CaV2.1-mediated STP. Modulation of OCX feedback to the bulb by modulatory transmitters, such as ACh, or by frequency-dependent STP could regulate the precise balance of excitation and inhibition of GCs. As GCs are a major inhibitory source for OB output neurons, plasticity at the cortical feedback synapse can differentially impact OB output to higher-order networks in situations where ACh inputs are activated or by active sniff sampling of odors.

Highlights

Sensory processing depends on environmental context and the past experiences of an individual
yellow fluorescent protein (YFP)-labeled glutamatergic cells were observed in layers II-III of olfactory cortex (OCX) as expected for expression of vGLUT2 (Figure 1A)
Addition of ACh did not significantly increase the excitatory postsynaptic currents (EPSCs) attenuation observed with CaV2.1 blocker alone and did not further change paired pulse ratio (PPR) (n = 6; Figures 5B–D). These findings show that ACh is not additive to CaV2.1 channel block, suggesting that ACh’s suppression of the OCX→granule cell (GC) EPSC is independent and upstream of CaV2.1 channels, we cannot exclude ACh having some post-synaptic action

Summary

Introduction

Sensory processing depends on environmental context and the past experiences of an individual. The neural encoding of these past experiences into ‘‘memory’’ is generally thought to occur via synaptic plasticity. Synaptic plasticity within the olfactory bulb (OB) and olfactory cortex (OCX) is thought to be involved in the sensory processing underlying olfactory memory (Wilson et al, 2004). OB mitral/tufted cells (M/TCs) project to the OCX where they synapse the apical dendrites of principal cells (Carson, 1984; Otazu et al, 2015). In turn send dense excitatory feedback projections to the main OB (Shipley and Ennis, 1996; Ennis et al, 2015).

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