Excitation and Inhibition of Spinal Motoneurons

1955 ◽  
Vol 184 (1) ◽  
pp. 223-232 ◽  
Author(s):  
Adele E. U. Edisen

Spinal cord motoneurons of the cat were stimulated by a needle electrode and reflexly via dorsal root impulses. Responses to direct stimulation originated in dendrites, initial axon segment, or myelinated axon, but apparently not in the cell body. The sites were differentiated by latency changes of the response as needle position and stimulus strength are varied, by ability to follow repetitive stimulation, and by responses to asphyxia duration and anesthesia depth. Facilitatory afferent impulses increased the excitability of the motoneurons, whether the direct test stimulus was activating either dendrites or initial axon segment, but inhibitory afferent impulses decreased the direct response only when dendrites were being activated. Facilitation is therefore nonlocalized and can be accounted for by the usual eddy currents. Inhibition is interpreted as a partial depolarization and impedance decrease of the cell body, induced by afferents reaching it directly and resulting in a short circuiting of eddy currents from excited dendrites to initial axon segment. The central delay of the spinal cord monosynaptic response (about 0.8 msec.) is accounted for by conduction time in the afferent fibers (0.5 msec.), determined by antidromic stimulation of these and by the time lag of afferent conditioning effects, and in the motoneurons, 0.2–0.3 msec. It is thus doubtful if any true ‘synaptic delay’ exists. The long intramedullary afferent conduction time also fully accounts for the lag seen in afferent inhibition, in harmony with the existence of a direct inhibitory pathway.

2018 ◽  
Vol 2018 ◽  
pp. 1-5
Author(s):  
Michael G. Hillegass ◽  
Samuel F. Luebbert ◽  
Maureen F. McClenahan

We report a case in which a 34-year-old female with refractory intracranial hypotension headaches due to a spontaneous dural tear was ultimately treated with CT-guided transforaminal epidural placement of a synthetic absorbable sealant (DuraSeal®). The procedure successfully resolved her headaches; however she subsequently developed thoracic neuralgia presumably due to mass effect of the sealant material on the lower thoracic spinal cord and nerve roots. This case report describes the potential for significant spinal cord and nerve root compression as well as the development of chronic neuralgia with the placement of epidural hydrogel and fibrin glue sealants. Careful consideration should be taken into the needle gauge, needle position, injectate volumes, and injection velocity when delivering the sealant to the epidural space. Use of an 18-gauge Tuohy needle with a slow but steady injection pressure, constant patient feedback, and a conservative injectate volume (less than 2 ml per level) may best optimize sealant delivery to minimize the risk of spinal cord compression and neurologic injury.


Author(s):  
Jordan A. Borrell ◽  
Dora Krizsan-Agbas ◽  
Randolph J. Nudo ◽  
Shawn B. Frost

AbstractObjectiveThe purpose of this study was to determine the effects of spinal cord injury (SCI) on spike activity evoked in the hindlimb spinal cord of the rat from cortical electrical stimulation.ApproachAdult, male, Sprague Dawley rats were randomly assigned to a Healthy or SCI group. SCI rats were given a 175 kDyn dorsal midline contusion injury at the level of the T8 vertebrae. At four weeks post-SCI, intracortical microstimulation (ICMS) was delivered at several sites in the hindlimb motor cortex of anesthetized rats, and evoked neural activity was recorded from corresponding sites throughout the dorsoventral depths of the spinal cord and EMG activity from hindlimb muscles.Main resultsIn healthy rats, post-ICMS spike histograms showed reliable, evoked spike activity during a short-latency epoch 10-12 ms after the initiation of the ICMS pulse train (short). Longer latency spikes occurred between ~20-60 ms, generally following a Gaussian distribution, rising above baseline at time LON, followed by a peak response (Lp), and then falling below baseline at time LOFF. EMG responses occurred between LON and Lp (25-27 ms). In SCI rats, short-latency responses were still present, long-latency responses were disrupted or eliminated, and EMG responses were never evoked. The retention of the short-latency responses indicates that spared descending spinal fibers, most likely via the cortico-reticulospinal pathway, can still depolarize spinal cord motor neurons after a dorsal midline contusion injury.SignificanceThis study provides novel insights into the role of alternate pathways for voluntary control of hindlimb movements after SCI that disrupts the corticospinal tract in the rat.


1994 ◽  
Vol 107 (6) ◽  
pp. 1519-1527 ◽  
Author(s):  
Yoshiro Matsui ◽  
Kazutomo Goh ◽  
Norihiko Shiiya ◽  
Toshihumi Murashita ◽  
Masatoshi Miyama ◽  
...  

1993 ◽  
Vol 17 (1-2) ◽  
pp. 101-111 ◽  
Author(s):  
Nozomu Mori ◽  
Yasutaka Tajima ◽  
Hironobu Sakaguchi ◽  
David J. Vandenbergh ◽  
Hiroyuki Nawa ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-10
Author(s):  
Cinzia Mallozzi ◽  
Alida Spalloni ◽  
Patrizia Longone ◽  
Maria Rosaria Domenici

Degeneration of cortical and spinal motor neurons is the typical feature of amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disease for which a pathogenetic role for the Cu/Zn superoxide dismutase (SOD1) has been demonstrated. Mice overexpressing a mutated form of the SOD1 gene (SOD1G93A) develop a syndrome that closely resembles the human disease. The SOD1 mutations confer to this enzyme a “gain-of-function,” leading to increased production of reactive oxygen species. Several oxidants induce tyrosine phosphorylation through direct stimulation of kinases and/or phosphatases. In this study, we analyzed the activities of src and fyn tyrosine kinases and of protein tyrosine phosphatases in synaptosomal fractions prepared from the motor cortex and spinal cord of transgenic mice expressing SOD1G93A. We found that (i) protein phosphotyrosine level is increased, (ii) src and fyn activities are upregulated, and (iii) the activity of tyrosine phosphatases, including the striatal-enriched tyrosine phosphatase (STEP), is significantly decreased. Moreover, the NMDA receptor (NMDAR) subunit GluN2B tyrosine phosphorylation was upregulated in SOD1G93A. Tyrosine phosphorylation of GluN2B subunits regulates the NMDAR function and the recruitment of downstream signaling molecules. Indeed, we found that proline-rich tyrosine kinase 2 (Pyk2) and ERK1/2 kinase are upregulated in SOD1G93A mice. These results point out an involvement of tyrosine kinases and phosphatases in the pathogenesis of ALS.


1992 ◽  
Vol 67 (6) ◽  
pp. 1683-1690 ◽  
Author(s):  
T. Matsushima ◽  
S. Grillner

1. The intersegmental coordination during undulatory locomotion in lamprey is characterized by a constant phase lag between consecutive segments, that is, the ratio between the intersegmental time lag and the cycle duration remains constant. It is shown that the spinal 5-HT (serotonin) system can, in a graded fashion, control the phase lag value from a rostrocaudal to a caudorostral lag corresponding to a reversed direction of swimming. These effects can be explained by a 5-HT-induced depression of Ca(2+)-dependent K+ channels (KCa channels) in network neurons. 2. The actions of the spinal 5-HT system were analyzed in the lamprey spinal cord preparation in vitro. Fictive swimming was induced by bath application of N-methyl-D-aspartate (NMDA). The intersegmental phase lag between ventral root burst activities was measured along the ipsilateral side of the spinal cord. The chamber with the preparation was partitioned into two pools so that the rostral and caudal halves of the preparation could be perfused independently with solutions containing the same level of NMDA (100-150 microM) with or without additional 5-HT or a 5-HT uptake blocker (citalopram). 3. Addition of 5-HT to one of these partitioned pools changed the intersegmental phase lag in this pool, whereas the cycle duration remained unchanged. It was determined by the activity in the "non-5-HT" pool. Addition of 5-HT to the caudal pool resulted in an increased rostrocaudal phase lag. When 5-HT was added to the rostral pool, on the other hand, the phase lag shifted direction to a backward coordination.(ABSTRACT TRUNCATED AT 250 WORDS)


1958 ◽  
Vol 192 (3) ◽  
pp. 447-452 ◽  
Author(s):  
Sadayuki F. Takagi ◽  
Yutaka Oomura

The effect of nicotine on synaptic transmission in the frog and cat spinal cord was studied. Both a regular wick electrode and a microelectrode of the Ling-Gerard type were used. The reflex activity of the bullfrog spinal cord is facilitated by 0.01% nicotine solution, but is depressed and abolished by 0.1% solution. In the cat, intravenous administration of 150 mg/kg fails to block reflex activity, but topical application does block. The intracellular potential, of both frog and cat motoneurones, shows no change in the synaptic potential after application of the drug, but the spike appears after a shorter synaptic delay and one or more additional spikes appear. When the synaptic delay becomes sufficiently short, however, all spikes suddenly disappear, leaving the still unchanged synaptic potential. Occasionally the synaptic delay is again increased just before the spike potentials disappear. The excitability of a frog motoneurone was measured, by a recording microelectrode, before and after nicotine application. The drug first increased and then decreases excitability. Epinephrine can restore a reflex discharge depressed or abolished by nicotine. It is concluded that high concentrations of nicotine block synaptic transmission in the central nervous system, acting on the cell body but not on the synaptic potential.


2019 ◽  
Vol 122 (4) ◽  
pp. 1675-1684 ◽  
Author(s):  
Hang Jin Jo ◽  
Monica A. Perez

The corticospinal pathway contributes to the control of grasping in intact humans. After spinal cord injury (SCI), there is an extensive reorganization in the corticospinal pathway; however, its contribution to the control of grasping after the injury remains poorly understood. We addressed this question by using transcranial magnetic stimulation (TMS) over the hand representation of the motor cortex to elicit motor-evoked potentials (MEPs) in an intrinsic finger muscle during precision grip and power grip with the TMS coil oriented to induce currents in the brain in the latero-medial (LM) direction to activate corticospinal axons directly and in the posterior-anterior (PA) and anterior-posterior (AP) directions to activate the axon indirectly through synaptic inputs in humans with and without cervical incomplete SCI. We found prolonged MEP latencies in all coil orientations in both tasks in SCI compared with control subjects. The latencies of MEPs elicited by AP relative to LM stimuli were consistently longer during power compared with precision grip in controls and SCI subjects. In contrast, PA relative to LM MEP latencies were similar between tasks across groups. Central conduction time of AP MEPs was prolonged during power compared with precision grip in controls and SCI participants. Our results support evidence indicating that inputs activated by AP and PA currents are engaged to a different extent during fine and gross grasping in humans with and without SCI. NEW & NOTEWORTHY The mechanisms contributing to the control of hand function in humans with spinal cord injury (SCI) remain poorly understood. Here, we demonstrate for the first time that the latency of corticospinal responses elicited by transcranial magnetic stimulation anterior-posterior induced currents, relative to latero-medial currents, was prolonged during power compared with precision grip in humans with and without SCI. Gross grasping might represent a stragegy to engage networks activated by anterior-posterior currents after SCI.


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