Anatomical and functional relationships between deep cerebellar nuclei and cerebellar cortical Crus II in vivo in mice

2016 ◽  
Vol 610 ◽  
pp. 73-78 ◽  
Author(s):  
Nan Ding ◽  
Hua Jin ◽  
Bin-Bin Zhang ◽  
Ao Guo ◽  
Jin-Di Shi ◽  
...  
Keyword(s):  
Cerebellar Nuclei ◽  
Deep Cerebellar Nuclei ◽  
Functional Relationships

scholarly journals Corrigendum: Long-Lasting Response Changes in Deep Cerebellar Nuclei in vivo Correlate With Low-Frequency Oscillations

2019 ◽  
Vol 13 ◽  
Author(s):  
Letizia Moscato ◽  
Ileana Montagna ◽  
Licia De Propris ◽  
Simona Tritto ◽  
Lisa Mapelli ◽  
...  
Keyword(s):  
Low Frequency ◽  
Cerebellar Nuclei ◽  
Deep Cerebellar Nuclei ◽  
Low Frequency Oscillations

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.

scholarly journals Unusually slow spike frequency adaptation in deep cerebellar nuclei neurons preserves linear transformations on the sub-second time scale

2021 ◽  
Author(s):  
Mehak M Khan ◽  
Christopher H Chen ◽  
wade G regehr
Keyword(s):  
Brain Slices ◽  
Cerebellar Nuclei ◽  
Spike Frequency ◽  
Initial Increase ◽  
Projection Neurons ◽  
Spike Frequency Adaptation ◽  
Linear Transformations ◽  
Deep Cerebellar Nuclei ◽  
Frequency Adaptation

Purkinje cells (PCs) are spontaneously active neurons of the cerebellar cortex that inhibit glutamatergic projection neurons within the deep cerebellar nuclei (DCN) that in turn provide the primary cerebellar output. Brief reductions in PC firing rapidly increase DCN neuron firing. However, prolonged reductions in PC inhibition, as seen in some disease states, certain types of transgenic mice, and in acute slices of the cerebellum, do not evoke large sustained increases in DCN firing. Here we test whether there is a mechanism of spike-frequency adaptation in DCN neurons that could account for these properties. We find that prolonged optogenetic suppression of PC synapses in vivo transiently elevates PC firing that strongly adapts within ten seconds. We perform current-clamp recordings at near physiological temperature in acute brain slices to examine how DCN neurons respond to prolonged depolarizations. Adaptation in DCN neurons is exceptionally slow and bidirectional. A depolarizing current step evokes large initial increases in firing that decay to less than 20% of the initial increase within approximately ten seconds. Such slow adaptation could allow DCN neurons to adapt to prolonged changes in PC firing while maintaining their linear firing frequency-current relationship on subsecond time scales.

scholarly journals Long-Lasting Response Changes in Deep Cerebellar Nuclei in vivo Correlate With Low-Frequency Oscillations

2019 ◽  
Vol 13 ◽  
Author(s):  
Letizia Moscato ◽  
Ileana Montagna ◽  
Licia De Propris ◽  
Simona Tritto ◽  
Lisa Mapelli ◽  
...  
Keyword(s):  
Low Frequency ◽  
Cerebellar Nuclei ◽  
Deep Cerebellar Nuclei ◽  
Low Frequency Oscillations

scholarly journals Mapping of long-term cognitive and motor deficits in pediatric cerebellar brain tumor survivors into a cerebellar white matter atlas

2021 ◽  
Author(s):  
Frederik Grosse ◽  
Stefan Mark Rueckriegel ◽  
Ulrich-Wilhelm Thomale ◽  
Pablo Hernáiz Driever
Keyword(s):  
Brain Tumor ◽  
Executive Function ◽  
Cognitive Function ◽  
White Matter ◽  
Cerebellar Nuclei ◽  
Motor Deficits ◽  
Deep Cerebellar Nuclei ◽  
Cerebellar White Matter ◽  
Lesion Symptom Mapping

Abstract Purpose Diaschisis of cerebrocerebellar loops contributes to cognitive and motor deficits in pediatric cerebellar brain tumor survivors. We used a cerebellar white matter atlas and hypothesized that lesion symptom mapping may reveal the critical lesions of cerebellar tracts. Methods We examined 31 long-term survivors of pediatric posterior fossa tumors (13 pilocytic astrocytoma, 18 medulloblastoma). Patients underwent neuronal imaging, examination for ataxia, fine motor and cognitive function, planning abilities, and executive function. Individual consolidated cerebellar lesions were drawn manually onto patients’ individual MRI and normalized into Montreal Neurologic Institute (MNI) space for further analysis with voxel-based lesion symptom mapping. Results Lesion symptom mapping linked deficits of motor function to the superior cerebellar peduncle (SCP), deep cerebellar nuclei (interposed nucleus (IN), fastigial nucleus (FN), ventromedial dentate nucleus (DN)), and inferior vermis (VIIIa, VIIIb, IX, X). Statistical maps of deficits of intelligence and executive function mapped with minor variations to the same cerebellar structures. Conclusion We identified lesions to the SCP next to deep cerebellar nuclei as critical for limiting both motor and cognitive function in pediatric cerebellar tumor survivors. Future strategies safeguarding motor and cognitive function will have to identify patients preoperatively at risk for damage to these critical structures and adapt multimodal therapeutic options accordingly.

scholarly journals A model of on/off transitions in neurons of the deep cerebellar nuclei: deciphering the underlying ionic mechanisms

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hugues Berry ◽  
Stéphane Genet
Keyword(s):  
Cerebellar Nuclei ◽  
Biophysical Model ◽  
High Threshold ◽  
Deep Cerebellar Nuclei ◽  
Functional Link ◽  
Electrophysiological Properties ◽  
Voltage Dependent ◽  
Ionic Mechanisms ◽  
The Central Nervous System ◽  
Overall Functioning

AbstractThe neurons of the deep cerebellar nuclei (DCNn) represent the main functional link between the cerebellar cortex and the rest of the central nervous system. Therefore, understanding the electrophysiological properties of DCNn is of fundamental importance to understand the overall functioning of the cerebellum. Experimental data suggest that DCNn can reversibly switch between two states: the firing of spikes (F state) and a stable depolarized state (SD state). We introduce a new biophysical model of the DCNn membrane electro-responsiveness to investigate how the interplay between the documented conductances identified in DCNn give rise to these states. In the model, the F state emerges as an isola of limit cycles, i.e. a closed loop of periodic solutions disconnected from the branch of SD fixed points. This bifurcation structure endows the model with the ability to reproduce the $\text{F}\to \text{SD}$ F → SD transition triggered by hyperpolarizing current pulses. The model also reproduces the $\text{F}\to \text{SD}$ F → SD transition induced by blocking Ca currents and ascribes this transition to the blocking of the high-threshold Ca current. The model suggests that intracellular current injections can trigger fully reversible $\text{F}\leftrightarrow \text{SD}$ F ↔ SD transitions. Investigation of low-dimension reduced models suggests that the voltage-dependent Na current is prominent for these dynamical features. Finally, simulations of the model suggest that physiological synaptic inputs may trigger $\text{F}\leftrightarrow \text{SD}$ F ↔ SD transitions. These transitions could explain the puzzling observation of positively correlated activities of connected Purkinje cells and DCNn despite the former inhibit the latter.

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