Voltage-Gated Sodium Channels in Cerebellar Purkinje Cells of Mormyrid Fish

Ruiter, Martijin M. De; Zeeuw, Chris I. De; Hansel, Christian

doi:10.1152/jn.00906.2005

Cited by 19 publications

(21 citation statements)

References 48 publications

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“…Its PCs fire a Na + axonal spike (Han and Bell, 2003;de Ruiter et al, 2006) and a Ca 2+ dendritic spike (Han and Bell, 2003;Zhang and Han, 2007), which contribute to GABA release at the axon terminals (present study) and to Ca 2+ influx at the soma and dendrites , respectively. In mammalian PCs, dendritic Ca 2+ spikes trigger Ca 2+ influx via voltage-gated calcium channels and a consequent membrane polarization due to the opening of Ca 2+ -gated K + channels, which in turn dampens PC output (Rancz and Ha¨usser, 2010).…”

Section: Discussionmentioning

confidence: 69%

Synaptic dynamics and long-term plasticity at synapses of Purkinje cells onto neighboring Purkinje cells of a mormyrid fish: A dual cell recording study

Zhang¹,

Magnus²,

Han³

2012

Neuroscience

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Section: Discussionmentioning

confidence: 69%

Synaptic dynamics and long-term plasticity at synapses of Purkinje cells onto neighboring Purkinje cells of a mormyrid fish: A dual cell recording study

Zhang¹,

Magnus²,

Han³

2012

Neuroscience

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“…The mormyrid cerebellum differs in some morphological features from its mammalian counterpart, which has motivated studies attempting to characterize the morphology and physiology of mormyrid Purkinje cells (Han and Bell, 2003;De Ruiter et al, 2006;Han et al, 2006). The present paper extends a previous physiological study of the mormyrid cerebellum (Han et al, 2006) in two ways: by establishing various forms of plasticity at the parallel fiber (PF) to Purkinje cell synapse, and by examining calcium transients associated with synaptic activation and intracellularly evoked calcium spikes.…”

Section: Introductionmentioning

confidence: 81%

“…11 A, B) or when it was followed by small spikes (Fig. 11C,D) (Han and Bell, 2003;De Ruiter et al, 2006). When monitoring calcium signals from ROIs located at the horizontal and vertical dendrites from the same cell, the transients recorded at the horizontal dendrite (the primary CF synaptic contact site) appeared largest (Fig.…”

Section: Calcium Transients Associated With Climbing Fiber Activationmentioning

confidence: 92%

Synaptic Plasticity and Calcium Signaling in Purkinje Cells of the Central Cerebellar Lobes of Mormyrid Fish

Han

Zhang²,

Bell³

et al. 2007

J. Neurosci.

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Climbing fiber (CF)-evoked calcium transients play a key role in plasticity at parallel fiber (PF) to Purkinje cell synapses in the mammalian cerebellum. Whereas PF activation alone causes long-term potentiation (LTP), coactivation of the heterosynaptic CF input, which evokes large dendritic calcium transients, induces long-term depression (LTD). This unique type of heterosynaptic interaction is a hallmark feature of synaptic plasticity in mammalian Purkinje cells. Purkinje cells in the cerebellum of mormyrid electric fish are characterized by a different architecture of their dendritic trees and by a more pronounced separation of CF and PF synaptic contact sites. We therefore examined the conditions for bidirectional plasticity at PF synapses onto Purkinje cells in the mormyrid cerebellum in vitro. PF stimulation at elevated frequencies induces LTP, whereas LTD results from PF stimulation at enhanced intensities and depends on dendritic calcium influx and metabotropic glutamate receptor type 1 activation. LTD can also be observed after pairing of low intensity PF stimulation with CF stimulation. Using a combination of whole-cell patch-clamp recordings and fluorometric calcium imaging, we characterized calcium transients in Purkinje cell dendrites. CF activation elicits calcium transients not only within the CF input territory (smooth proximal dendrites) but also within the PF input territory (spiny palisade dendrites). Paired PF and CF activation elicits larger calcium transients than stimulation of either input alone. A major source for dendritic calcium signaling is provided by P/Q-type calcium channels. Our data show that despite the spatial separation between the two inputs CF activity facilitates LTD induction at PF synapses.

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“…CF activation does not result in complex spikes, but in all-or-none EPSPs. Moreover, Na + action potentials recorded from the somata of mormyrid Purkinje cells have unusually small amplitudes, typically not exceeding 30 mV (de Ruiter et al, 2006). It seems unlikely that these reduced Na + spikes backpropagate, although mormyrid Purkinje cells express the Na + channel α subunits Na v 1.1, Na v 1.2, and Na v 1.6 in their dendrites (de Ruiter et al, 2006).…”

Section: Non-hebbian Stdp In the Cerebellummentioning

confidence: 99%

Non-Hebbian spike-timing-dependent plasticity in cerebellar circuits

Piochon¹,

Kruskal²,

MacLean³

et al. 2013

Front. Neural Circuits

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Spike-timing-dependent plasticity (STDP) provides a cellular implementation of the Hebb postulate, which states that synapses, whose activity repeatedly drives action potential firing in target cells, are potentiated. At glutamatergic synapses onto hippocampal and neocortical pyramidal cells, synaptic activation followed by spike firing in the target cell causes long-term potentiation (LTP)—as predicted by Hebb—whereas excitatory postsynaptic potentials (EPSPs) evoked after a spike elicit long-term depression (LTD)—a phenomenon that was not specifically addressed by Hebb. In both instances the action potential in the postsynaptic target neuron is an instructive signal that is capable of supporting synaptic plasticity. STDP generally relies on the propagation of Na+ action potentials that are initiated in the axon hillhock back into the dendrite, where they cause depolarization and boost local calcium influx. However, recent studies in CA1 hippocampal pyramidal neurons have suggested that local calcium spikes might provide a more efficient trigger for LTP induction than backpropagating action potentials. Dendritic calcium spikes also play a role in an entirely different type of STDP that can be observed in cerebellar Purkinje cells. These neurons lack backpropagating Na+ spikes. Instead, plasticity at parallel fiber (PF) to Purkinje cell synapses depends on the relative timing of PF-EPSPs and activation of the glutamatergic climbing fiber (CF) input that causes dendritic calcium spikes. Thus, the instructive signal in this system is externalized. Importantly when EPSPs are elicited before CF activity, PF-LTD is induced rather than LTP. Thus, STDP in the cerebellum follows a timing rule that is opposite to its hippocampal/neocortical counterparts. Regardless, a common motif in plasticity is that LTD/LTP induction depends on the relative timing of synaptic activity and regenerative dendritic spikes which are driven by the instructive signal.

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Voltage-Gated Sodium Channels in Cerebellar Purkinje Cells of Mormyrid Fish

Abstract: de Ruiter, Martijn M., Chris I. De Zeeuw, and Christian Hansel. Voltage-gated sodium channels in cerebellar Purkinje cells of mormyrid fish.

Cited by 19 publications

References 48 publications

Synaptic dynamics and long-term plasticity at synapses of Purkinje cells onto neighboring Purkinje cells of a mormyrid fish: A dual cell recording study

Synaptic dynamics and long-term plasticity at synapses of Purkinje cells onto neighboring Purkinje cells of a mormyrid fish: A dual cell recording study

Synaptic Plasticity and Calcium Signaling in Purkinje Cells of the Central Cerebellar Lobes of Mormyrid Fish

Non-Hebbian spike-timing-dependent plasticity in cerebellar circuits

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