scholarly journals Effects of mecamylamine on the Golgi recurrent collateral—Renshaw-cell synapse in the spinal cord

1961 ◽  
Vol 3 (2) ◽  
pp. 141-148 ◽  
Author(s):  
S. Ueki ◽  
K. Koketsu ◽  
E.F. Domino
2008 ◽  
Vol 99 (2) ◽  
pp. 583-594 ◽  
Author(s):  
Tuan V. Bui ◽  
Giovanbattista Grande ◽  
P. Ken Rose

In some motoneurons, L-type Ca2+ channels that partly mediate persistent inward currents (PICs) have been estimated to be arranged in 50- to 200-μm-long discrete regions in the dendrites, centered 100 to 400 μm from the soma. As a consequence of this nonuniform distribution, the interaction between synaptic inputs to motoneurons and these channels may vary according to the distribution of the synapses. For instance, >93% of synapses from Renshaw cells have been observed to be located 65 to 470 μm away from the cell body of motoneurons. Our goal was to assess whether Renshaw cell synapses are distributed in a position to more effectively control the activation of the L-type Ca2+ channels. Using compartmental models of motoneurons with L-type Ca2+ channels distributed in 100-μm-long hot spots centered 100 to 400 μm away from the soma, we compared the inhibition generated by four distributions of inhibitory synapses: proximal, distal, uniform, and one based on the location of Renshaw cell synapses on motoneurons. Regardless of whether the synapses were activated tonically or transiently, in the presence of L-type Ca2+ channels, inhibitory synapses distributed according to the Renshaw cell synapse distribution generate the largest inhibitory currents. The effectiveness of a particular distribution of inhibitory synapses in the presence of PICs depends on their ability to deactivate the channels underlying PICs, which is influenced not only by the superposition between synapses and channels, but also by the distance away from the somatic voltage clamp.


2012 ◽  
Vol 108 (12) ◽  
pp. 3370-3381 ◽  
Author(s):  
Jennifer M. Humphreys ◽  
Patrick J. Whelan

Monoamines can modulate the output of a variety of invertebrate and vertebrate networks, including the spinal cord networks that control walking. Here we examined the multiple changes in the output of locomotor networks induced by dopamine (DA). We found that DA can depress the activation of locomotor networks in the neonatal mouse spinal cord following ventral root stimulation. By examining disinhibited rhythms, where the Renshaw cell pathway was blocked, we found that DA depresses a putative recurrent excitatory pathway that projects onto rhythm-generating circuitry of the spinal cord. This depression was D2 but not D1 receptor dependent and was not due exclusively to depression of excitatory drive to motoneurons. Furthermore, the depression in excitation was not dependent on network activity. We next compared the modulatory effects of DA on network function by focusing on a serotonin and a N-methyl-dl-aspartate-evoked rhythm. In contrast to the depressive effects on a ventral root-evoked rhythm, we found that DA stabilized a drug-evoked rhythm, reduced the frequency of bursting, and increased amplitude. Overall, these data demonstrate that DA can potentiate network activity while at the same time reducing the gain of recurrent excitatory feedback loops from motoneurons onto the network.


2002 ◽  
Vol 87 (6) ◽  
pp. 3117-3125 ◽  
Author(s):  
Michelle Dourado ◽  
Peter B. Sargent

We used anatomical and physiological approaches to characterize nicotinic receptors (AChRs) on Renshaw cells of the neonatal rat spinal cord. Confocal imaging of Renshaw cells, identified by their characteristic pattern of gephyrin immunoreactivity, revealed that these neurons are immuno-positive for the α4 and β2 AChR subunits but not for the α7 subunit. We used whole cell recording in spinal cord slices to characterize synaptic transmission from α-motor neurons to Renshaw cells, which could be identified pharmacologically by the sensitivity of transmission to d-tubocurarine. α-Motor neuron-to-Renshaw cell synapses were blocked by 10 μM dihydro-β-erythroidine (dHβE), but not 50 nM methyllycaconitine (MLA), a selective α7 antagonist. These findings support a role for α4β2-like AChRs, but not α7 AChRs, in rapid excitatory transmission between α-motor neurons and Renshaw cells in rat spinal cord.


2012 ◽  
Vol 32 (24) ◽  
pp. 8413-8423 ◽  
Author(s):  
B. L. d'Incamps ◽  
E. Krejci ◽  
P. Ascher

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Boris Lamotte d’Incamps ◽  
Gardave S. Bhumbra ◽  
Joshua D. Foster ◽  
Marco Beato ◽  
Philippe Ascher

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