Abstract
The architecture of parallel fiber axons contacting cerebellar Purkinje neurons retains spatial information over long distances. Parallel fiber synapses can trigger local dendritic calcium spikes, but whether and how this calcium signal leads to plastic changes that decode the parallel fiber input organization is unknown. By combining voltage and calcium imaging, we show that calcium signals, elicited by parallel fiber stimulation and mediated by voltage-gated calcium channels, increase non-linearly during high-frequency bursts of electrically constant calcium spikes, because they locally and transiently saturate the endogenous buffer. We demonstrate that these non-linear calcium signals, independently of NMDA or metabotropic glutamate receptor activation, can induce parallel fiber long-term potentiation. Two-photon imaging in coronal slices revealed that calcium signals inducing long-term potentiation can be observed by stimulating either the parallel fiber or the ascending fiber pathway. We propose that local dendritic calcium spikes, evoked by synaptic potentials, provide a unique mechanism to spatially decode parallel fiber signals into cerebellar circuitry changes.
Highlights
Neuronal dendrites can fire action potentials mediated by voltage-gated calcium channels (VGCC) that may be sufficient to induce long-term potentiation (LTP) of synaptic potentials [1,2]
We show that local high-frequency dendritic spikes generate D[Ca2+]i signals that summate nonlinearly because they transiently saturate the endogenous calcium buffer (ECB)
We report that dendritic calcium firing leading to LTP can occur by activation of adjacent parallel fiber (PF)-excitatory postsynaptic potential (EPSP), and by activity in the sparser AF tract, implying a less stringent spatial organization of synaptic inputs compared to the one necessary for mGluR1- and endocannabinoid-mediated PF-long-term depression (LTD) [25]
Summary
Neuronal dendrites can fire action potentials mediated by voltage-gated calcium channels (VGCC) that may be sufficient to induce long-term potentiation (LTP) of synaptic potentials [1,2]. Calcium signals mediated by VGCCs differ from those mediated by ionotropic or metabotropic glutamate receptors. Whereas the latter signals co-localize with activated receptors, either by direct calcium influx or by secondary intracellular pathways, the extent of the former signals is determined by the spread of the dendritic spike. In the cerebellar Purkinje neuron (PN), calcium spikes can be elicited by parallel fiber (PF) stimulation and can be localized to small regions [3]. The function of calcium spikes elicited by neighboring presynaptic fibers is unknown. Dendritic excitation has been associated with PF synaptic plasticity in relation to the climbing fibre (CF)-excitatory postsynaptic potential (EPSP) providing the calcium signal underlying coincident PF and CF detection and PF- long-term depression (LTD) [4], but the role of local PF-elicited calcium spikes in long-term synaptic plasticity is unexplored
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