Differentiation of Synaptic Bulbs in Clarke's Column

Nature ◽  
1967 ◽  
Vol 214 (5086) ◽  
pp. 391-392 ◽  
Author(s):  
ALBERT W. SEDAR ◽  
NORMAN MOSKOWITZ
Keyword(s):  
Clarke's Column

Terminals of group la primary afferent fibres in Clarke's column are enriched with l-glutamate-like immunoreactivity

1990 ◽  
Vol 510 (2) ◽  
pp. 346-350 ◽  
Author(s):  
D.J. Maxwell ◽  
W.M. Christie ◽  
O.P. Ottersen ◽  
J. Storm-Mathisen
Keyword(s):  
Primary Afferent ◽  
Clarke's Column

Synaptic processes in the neurons of Clarke's column evoked by an antidromic volley from the dorsolateral column

1971 ◽  
Vol 2 (3) ◽  
pp. 203-209 ◽  
Author(s):  
P. G. Kostyuk ◽  
B. Ya. Pyatigorskii ◽  
�. Lang
Keyword(s):  
Clarke's Column ◽  
Antidromic Volley

Retrograde changes in Clarke's column following neonatal hemicerebellectomy in the rat

1979 ◽  
Vol 156 (4) ◽  
pp. 533-542 ◽  
Author(s):  
Diane E. Smith ◽  
Anthony J. Castro
Keyword(s):  
Clarke's Column

Intracellular Recording from Cells in Clarke's Column.

1958 ◽  
Vol 43 (3-4) ◽  
pp. 303-314 ◽  
Author(s):  
D. R. CURTIS ◽  
J. C. ECCLES ◽  
A. LUNDBERG
Keyword(s):  
Intracellular Recording ◽  
Clarke's Column

scholarly journals Evidence for genetically distinct direct and indirect spinocerebellar pathways mediating proprioception

2020 ◽  
Author(s):  
Iliodora V. Pop ◽  
Felipe Espinosa ◽  
Megan Goyal ◽  
Bishakha Mona ◽  
Mark A. Landy ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Granule Cells ◽  
Mossy Fiber ◽  
Cerebellar Nuclei ◽  
Reticular Nucleus ◽  
Proprioceptive Information ◽  
Lateral Reticular Nucleus ◽  
Axon Collaterals ◽  
Progenitor Domain ◽  
Clarke's Column

AbstractProprioception, the sense of limb and body position, generates a map of the body that is essential for proper motor control, yet we know little about precisely how neurons in proprioceptive pathways develop and are wired. Proprioceptive and cutaneous information from the periphery is sent to secondary neurons in the spinal cord that integrate and relay this information to the cerebellum either directly or indirectly through the medulla. Defining the anatomy of these direct and indirect pathways is fundamental to understanding how proprioceptive circuits function. Here, we use genetic tools in mice to define the developmental origins and unique anatomical trajectories of these pathways. Developmentally, we find that Clarke’s column (CC) neurons, a major contributor to the direct spinocerebellar pathway, derive from the Neurog1 progenitor domain. By contrast, we find that two of the indirect pathways, the spino-lateral reticular nucleus (spino-LRt) and spino-olivary pathways, are derived from the Atoh1 progenitor domain, despite previous evidence that Atoh1-lineage neurons form the direct pathway. Anatomically, we also find that the mossy fiber terminals of CC neurons diversify extensively with some axons terminating bilaterally in the cerebellar cortex. Intriguingly, we find that CC axons do not send axon collaterals to the medulla or cerebellar nuclei like other mossy fiber sources. Altogether, we conclude that the direct and indirect spinocerebellar pathways derive from distinct progenitor domains in the developing spinal cord and that the proprioceptive information from CC neurons is processed only at the level of granule cells in the cerebellum.Significance StatementWe find that a majority of direct spinocerebellar neurons in mice originate from Clarke’s column (CC), which derives from the Neurog1-lineage, while few originate from Atoh1-lineage neurons as previously thought. Instead, we find that spinal cord Atoh1-lineage neurons form mainly the indirect spino-lateral reticular nucleus and spino-olivary tracts. Moreover, we observe that mossy fiber axon terminals of CC neurons diversify proprioceptive information across granule cells in multiple lobules on both ipsilateral and contralateral sides without sending axon collaterals to the medulla or cerebellar nuclei. Altogether, we define the development and the anatomical projections of direct and indirect pathways to the cerebellum from the spinal cord.

Dorsal Spinocerebellar Tract Neurons Are Not Subjected to Postsynaptic Inhibition During Carbachol-Induced Motor Inhibition

1997 ◽  
Vol 78 (1) ◽  
pp. 137-144 ◽  
Author(s):  
Ming-Chu Xi ◽  
Jack Yamuy ◽  
Rong-Huan Liu ◽  
Francisco R. Morales ◽  
Michael H. Chase
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Synaptic Activity ◽  
Motor Inhibition ◽  
Postsynaptic Inhibition ◽  
Postsynaptic Potentials ◽  
Group I ◽  
The Mean ◽  
Spinocerebellar Tract ◽  
Clarke's Column

Xi, Ming-Chu, Jack Yamuy, Rong-Huan Liu, Francisco R. Morales, and Michael H. Chase. Dorsal spinocerebellar tract neurons are not subjected to postsynaptic inhibition during carbachol-induced motor inhibition. J. Neurophysiol. 78: 137–144, 1997. Dorsal spinocerebellar tract (DSCT) neurons in Clarke's column in the lumbar spinal cord of cats anesthetized with α-chloralose were recorded intracellularly. The membrane potential activity and electrophysiological properties of these neurons were examined before and during the state of active-sleep-like motor inhibition induced by the injection of carbachol into the nucleus pontis oralis. The synaptic activity of DSCT neurons during carbachol-induced motor inhibition did not change compared with that during control conditions. In particular, there was an absence of inhibitory postsynaptic potentials (IPSPs) in high-gain recordings from DSCT neurons and the resting membrane potential of DSCT neurons was not significantly hyperpolarized during carbachol-induced motor inhibition. The mean amplitude of both monosynaptic excitatory postsynaptic potentials and disynaptic IPSPs evoked in DSCT neurons following stimulation of group I muscle afferents after the injection of carbachol was similar to that evoked before the injection of carbachol. There were no significant changes in the mean input resistance and membrane time constant of DSCT neurons during carbachol-induced motor inhibition. We conclude that, in contrast to lumbar motoneurons, DSCT neurons in Clarke's column are not postsynaptically inhibited during carbachol-induced motor inhibition. Therefore the population of spinal cord Ib interneurons that inhibit both DSCT neurons and lumbar motoneurons is not likely to be the interneurons that are responsible for the postsynaptic inhibition of motoneurons that occurs during carbachol-induced motor inhibition. The present findings also indicate that transmission through the DSCT is not modulated by postsynaptic inhibition at the level of DSCT neurons during carbachol-induced motor inhibition.

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