scholarly journals Microcircuit Rules Governing Impact of Single Interneurons on Purkinje Cell Output In Vivo

Cell Reports ◽  
2020 ◽  
Vol 30 (9) ◽  
pp. 3020-3035.e3 ◽  
Author(s):  
Charlotte Arlt ◽  
Michael Häusser
Keyword(s):  
Purkinje Cell

Spatial distribution of excitatory and inhibitory synapses on a Purkinje cell in a rat cerebellar culture

1993 ◽  
Vol 70 (4) ◽  
pp. 1316-1325 ◽  
Author(s):  
T. Hirano ◽  
K. Kasono
Keyword(s):  
Spatial Distribution ◽  
Purkinje Cell ◽  
Purkinje Cells ◽  
Spatial Organization ◽  
Lucifer Yellow ◽  
Inhibitory Synapses ◽  
Presynaptic Neuron ◽  
Presynaptic Terminals ◽  
Excitatory And Inhibitory Synapses

1. The spatial distribution of excitatory and inhibitory synapses on cultured Purkinje cells was studied with fluorescence, scanning electron microscopy (SEM), and electrophysiological techniques. 2. Presynaptic terminals were identified with immunohistochemical staining of synaptophysin and the results were correlated with SEM micrographs. 3. Excitatory and inhibitory inputs onto the Purkinje cell were identified from the direction and pharmacology of the postsynaptic current. 4. The localization of the presynaptic terminals on the Purkinje cell was observed after electrophysiological identification by filling the presynaptic neuron with Lucifer yellow and the Purkinje cell with Texas red. 5. The axon and presynaptic terminals of excitatory and inhibitory inputs had a different spatial organization. Excitatory inputs from granule cells were exclusively localized on the dendrites of Purkinje cells, whereas inhibitory contacts were found on both the soma and dendrites. This result is similar to that described in vivo.

scholarly journals Loss of the golgin GM130 causes Golgi disruption, Purkinje neuron loss, and ataxia in mice

2016 ◽  
Vol 114 (2) ◽  
pp. 346-351 ◽  
Author(s):  
Chunyi Liu ◽  
Mei Mei ◽  
Qiuling Li ◽  
Peristera Roboti ◽  
Qianqian Pang ◽  
...  
Keyword(s):  
Golgi Apparatus ◽  
Purkinje Cell ◽  
Secretory Pathway ◽  
Neuronal Degeneration ◽  
Cell Loss ◽  
Cell Number ◽  
Causative Role ◽  
Neurodegenerative Process ◽  
And Function

The Golgi apparatus lies at the heart of the secretory pathway where it is required for secretory trafficking and cargo modification. Disruption of Golgi architecture and function has been widely observed in neurodegenerative disease, but whether Golgi dysfunction is causal with regard to the neurodegenerative process, or is simply a manifestation of neuronal death, remains unclear. Here we report that targeted loss of the golgin GM130 leads to a profound neurological phenotype in mice. Global KO of mouse GM130 results in developmental delay, severe ataxia, and postnatal death. We further show that selective deletion of GM130 in neurons causes fragmentation and defective positioning of the Golgi apparatus, impaired secretory trafficking, and dendritic atrophy in Purkinje cells. These cellular defects manifest as reduced cerebellar size and Purkinje cell number, leading to ataxia. Purkinje cell loss and ataxia first appear during postnatal development but progressively worsen with age. Our data therefore indicate that targeted disruption of the mammalian Golgi apparatus and secretory traffic results in neuronal degeneration in vivo, supporting the view that Golgi dysfunction can play a causative role in neurodegeneration.

scholarly journals Maturation of Purkinje cell firing properties relies on neurogenesis of excitatory neurons

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Meike E van der Heijden ◽  
Elizabeth P Lackey ◽  
Ross Perez ◽  
Fatma S Ișleyen ◽  
Amanda M Brown ◽  
...  
Keyword(s):  
Purkinje Cell ◽  
Purkinje Cells ◽  
Time Window ◽  
Mouse Development ◽  
Cerebellar Neurons ◽  
Cell Functions ◽  
Excitatory Neurons ◽  
Cell Firing ◽  
Firing Properties

Preterm infants that suffer cerebellar insults often develop motor disorders and cognitive difficulty. Excitatory granule cells, the most numerous neuron type in the brain, are especially vulnerable and likely instigate disease by impairing the function of their targets, the Purkinje cells. Here, we use regional genetic manipulations and in vivo electrophysiology to test whether excitatory neurons establish the firing properties of Purkinje cells during postnatal mouse development. We generated mutant mice that lack the majority of excitatory cerebellar neurons and tracked the structural and functional consequences on Purkinje cells. We reveal that Purkinje cells fail to acquire their typical morphology and connectivity, and that the concomitant transformation of Purkinje cell firing activity does not occur either. We also show that our mutant pups have impaired motor behaviors and vocal skills. These data argue that excitatory cerebellar neurons define the maturation time-window for postnatal Purkinje cell functions and refine cerebellar-dependent behaviors.

scholarly journals In Vivo Analysis of the Climbing Fiber-Purkinje Cell Circuit in SCA2-58Q Transgenic Mouse Model

2018 ◽  
Vol 17 (5) ◽  
pp. 590-600 ◽  
Author(s):  
Polina A. Egorova ◽  
Alexandra V. Gavrilova ◽  
Ilya B. Bezprozvanny
Keyword(s):  
Mouse Model ◽  
Purkinje Cell ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model ◽  
Climbing Fiber ◽  
In Vivo Analysis ◽  
Cell Circuit

scholarly journals βIII spectrin controls the planarity of Purkinje cell dendrites by modulating perpendicular axon-dendrite interactions

Development ◽  
2020 ◽  
Vol 147 (24) ◽  
pp. dev194530
Author(s):  
Kazuto Fujishima ◽  
Junko Kurisu ◽  
Midori Yamada ◽  
Mineko Kengaku
Keyword(s):  
Purkinje Cell ◽  
Neural Circuits ◽  
Model System ◽  
Spinocerebellar Ataxia Type ◽  
Crucial Importance ◽  
Electrospun Nanofiber ◽  
Oriented Growth ◽  
Branch Formation ◽  
Purkinje Cell Dendrites

ABSTRACTThe mechanism underlying the geometrical patterning of axon and dendrite wiring remains elusive, despite its crucial importance in the formation of functional neural circuits. The cerebellar Purkinje cell (PC) arborizes a typical planar dendrite, which forms an orthogonal network with granule cell (GC) axons. By using electrospun nanofiber substrates, we reproduce the perpendicular contacts between PC dendrites and GC axons in culture. In the model system, PC dendrites show a preference to grow perpendicularly to aligned GC axons, which presumably contribute to the planar dendrite arborization in vivo. We show that βIII spectrin, a causal protein for spinocerebellar ataxia type 5, is required for the biased growth of dendrites. βIII spectrin deficiency causes actin mislocalization and excessive microtubule invasion in dendritic protrusions, resulting in abnormally oriented branch formation. Furthermore, disease-associated mutations affect the ability of βIII spectrin to control dendrite orientation. These data indicate that βIII spectrin organizes the mouse dendritic cytoskeleton and thereby regulates the oriented growth of dendrites with respect to the afferent axons.

Dynamic Synchronization of Purkinje Cell Simple Spikes

2006 ◽  
Vol 96 (6) ◽  
pp. 3485-3491 ◽  
Author(s):  
Soon-Lim Shin ◽  
Erik De Schutter
Keyword(s):  
Purkinje Cell ◽  
Firing Rate ◽  
Purkinje Cells ◽  
Cerebellar Cortex ◽  
Cerebellar Nuclei ◽  
Temporal Coding ◽  
Sharp Peak ◽  
Deep Cerebellar Nuclei

Purkinje cells (PCs) integrate all computations performed in the cerebellar cortex to inhibit neurons in the deep cerebellar nuclei (DCN). Simple spikes recorded in vivo from pairs of PCs separated by <100 μm are known to be synchronized with a sharp peak riding on a broad peak, but the significance of this finding is unclear. We show that the sharp peak consists exclusively of simple spikes associated with pauses in firing. The broader, less precise peak was caused by firing-rate co-modulation of faster firing spikes. About 13% of all pauses were synchronized, and these pauses had a median duration of 20 ms. As in vitro studies have reported that synchronous pauses can reliably trigger spikes in DCN neurons, we suggest that the subgroup of spikes causing the sharp peak is important for precise temporal coding in the cerebellum.

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