Brief sensory deprivation triggers synaptic plasticity in the glomerular layer of the murine olfactory bulb
Thu-P1-020
Presented by: Li Huang
The ability of neural circuits to adapt to changing stimuli is critical for learning, memory, and adaptation. In sensory systems, homeostatic forms of neuronal plasticity can be triggered by sensory deprivation. In the olfactory bulb, it has recently been demonstrated that while excitatory neurons remain unchanged, only a subtype of interneurons, axon-bearing dopaminergic (DA) neurons, decrease their intrinsic excitability in response to 24h of deprivation—a functional change complemented at the structural level with shortening of the axon initial segment.
However, whether this experience-dependent alteration is mirrored at the synapses remains unclear. Using whole-cell patch-clamp in brain slices of P20-40 mice who underwent 24h naris occlusion, this project investigated the synaptic changes in spontaneous excitatory and inhibitory events occurring in glomerular layer neurons, external tufted cells (ETCs) and the DA neurons of both subtypes (i.e.axon-bearing and anaxonic).
After 24h occlusion, anaxonic DA neurons–which have been previously shown resistant to change their intrinsic firing–display synaptic plasticity through receiving excitatory currents of reduced amplitude (EPSC,control:-26.91pA±2.247pA,occluded: -18.86pA±1.14pA, p<.05). This change was not found in their axon-bearing DA counterparts. Moreover, ETCs, excitatory interneurons also previously found to show no change intrinsically after 24h deprivation, received larger inhibitory currents (IPSC:control:377.9fC±77.51fC,occluded:614.2fC±60.42fC,p<.01).
Taken together with the role of these cells, these results suggest a network mediated up-regulation of activity after deprivation. Moreover, this provides support to the notion that the circuit is able to flexibly recruit different types of plasticity at different cell types depending on the demand it faces.
Funding:Cambridge Trust,Royal Society Research Grant RGS\R1\191481,Isaac Newton Trust/Wellcome Trust ISSF/University of Cambridge Joint Research Grants
However, whether this experience-dependent alteration is mirrored at the synapses remains unclear. Using whole-cell patch-clamp in brain slices of P20-40 mice who underwent 24h naris occlusion, this project investigated the synaptic changes in spontaneous excitatory and inhibitory events occurring in glomerular layer neurons, external tufted cells (ETCs) and the DA neurons of both subtypes (i.e.axon-bearing and anaxonic).
After 24h occlusion, anaxonic DA neurons–which have been previously shown resistant to change their intrinsic firing–display synaptic plasticity through receiving excitatory currents of reduced amplitude (EPSC,control:-26.91pA±2.247pA,occluded: -18.86pA±1.14pA, p<.05). This change was not found in their axon-bearing DA counterparts. Moreover, ETCs, excitatory interneurons also previously found to show no change intrinsically after 24h deprivation, received larger inhibitory currents (IPSC:control:377.9fC±77.51fC,occluded:614.2fC±60.42fC,p<.01).
Taken together with the role of these cells, these results suggest a network mediated up-regulation of activity after deprivation. Moreover, this provides support to the notion that the circuit is able to flexibly recruit different types of plasticity at different cell types depending on the demand it faces.
Funding:Cambridge Trust,Royal Society Research Grant RGS\R1\191481,Isaac Newton Trust/Wellcome Trust ISSF/University of Cambridge Joint Research Grants