scholarly journals Extensor motoneurone properties are altered immediately before and during fictive locomotion in the adult decerebrate rat

2015 ◽  
Vol 593 (10) ◽  
pp. 2327-2342 ◽  
Author(s):  
C. W. MacDonell ◽  
K. E. Power ◽  
J. W. Chopek ◽  
K. R. Gardiner ◽  
P. F. Gardiner
1996 ◽  
Vol 109 (3) ◽  
Author(s):  
J.F. Iles ◽  
S. Nicolopoulos-Stournaras

1992 ◽  
Vol 595 (1) ◽  
pp. 107-115 ◽  
Author(s):  
Osamu Taguchi ◽  
Leszek Kubin ◽  
Allan I. Pack

1982 ◽  
Vol 48 (6) ◽  
pp. 1279-1288 ◽  
Author(s):  
S. R. Soffe ◽  
A. Roberts

1. In curarized, late developmental stage Xenopus embryos, episodes of rhythmic motor root discharge, termed fictive swimming (17), may be evoked by touch or by dimming the lights, as in unparalyzed animals. Motoneurons are tonically depolarized throughout each episode, are phasically excited to fire 1 spike per cycle, and receive a midcycle inhibitory postsynaptic potential (IPSP) in phase with motor root activity on the opposite side. 2. Rostral hemisection of the spinal cord abolishes motor root discharge on the operated side caudal to the cut but leaves activity on the intact side unaffected. In motoneurons, the tonic depolarization is abolished on the hemisected side but is still present on the intact side. This is evidence that the tonic depolarization is a descending drive. 3. Midcycle IPSPs normally seen in motoneurons during fictive swimming are abolished by rostral hemisection of the opposite side of the cord but are still recorded on the cut side. The simplest conclusion is that the inhibitory interneurons responsible lie on the opposite side of the spinal cord to the motoneurons they inhibit, and so represent a reciprocal inhibitory pathway. 4. The phasic excitatory postsynaptic potentials (EPSPs), which drive motoneuron spikes during swimming, are still present on the intact side of a rostrally hemisected cord but are abolished on the operated side. We conclude that the excitatory interneurons responsible lie on the same side of the cord as the motoneurons they excite.


1993 ◽  
Vol 69 (3) ◽  
pp. 647-657 ◽  
Author(s):  
J. Tegner ◽  
T. Matsushima ◽  
A. el Manira ◽  
S. Grillner

1. The effect of spinal GABAergic neurons on the segmental neuronal network generating locomotion has been analyzed in the lamprey spinal cord in vitro. It is shown that gamma-aminobutyric acid (GABA)A- and GABAB-mediated effects influence the burst frequency and the intersegmental coordination and that the GABA system is active during normal locomotor activity. 2. Fictive locomotor activity was induced by superfusing the spinal cord with a Ringer solution containing N-methyl-D-aspartate (NMDA, 150 microM). The efferent locomotor activity was recorded by suction electrodes from the ventral roots or intracellularly from interneurons or motoneurons. If a GABA uptake blocker was added to the perfusate, the burst rate decreased. This effect was counteracted by GABAB receptor blockade by phaclofen or 2-(OH)-saclofen. If instead a GABAB receptor agonist (baclofen) was added during fictive locomotion, a depression of the burst rate occurred. It was concluded that a GABAB receptor activation due to an endogenous release of GABA caused a depression of the burst activity with a maintained well-coordinated locomotor activity. 3. If a GABAA receptor antagonist (bicuculline) is applied during fictive locomotion elicited by NMDA, a certain increase of the burst rate occurred. Conversely, if a selective GABAA agonist (muscimol) was administered, the burst rate decreased. Similarly, if the GABAA receptor activity was potentiated by activation of a benzodiazepine site by diazepam, the burst rate was reduced. If, however the GABAergic effect was first enhanced by an uptake blocker (nipecotic acid), an administration of a GABAA antagonist (bicuculline) increased the burst rate, but in addition, the burst pattern became less regular with recurrent shorter periods without clear reciprocal burst activity. The GABAA receptor activity appears important for the rate control and for permitting a regular burst pattern. 4. The intersegmental coordination in the lamprey is characterized by a rostrocaudal constant phase lag of approximately 1% of the cycle duration between the activation of consecutive segments during forward swimming. This rostrocaudal phase lag can be reversed during backward swimming, which can be induced also experimentally in the isolated spinal cord by providing a higher excitability to the caudal segments. In a split-bath configuration, a GABA uptake blocker or a GABAB agonist was administered to the rostral part of the spinal cord, which caused a reversal of the phase lag as during backward swimming. If GABAA receptors were blocked under similar conditions, the intersegmental coordination became irregular. It is concluded that an increased GABA activity in a spinal cord region can modify the intersegmental coordination.(ABSTRACT TRUNCATED AT 400 WORDS)


1987 ◽  
Vol 409 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Simon Alford ◽  
Thelma L. Williams

2005 ◽  
Vol 93 (2) ◽  
pp. 980-988 ◽  
Author(s):  
Eric J. Schwartz ◽  
Tatyana Gerachshenko ◽  
Simon Alford

Locomotor pattern generation is maintained by integration of the intrinsic properties of spinal central pattern generator (CPG) neurons in conjunction with synaptic activity of the neural network. In the lamprey, the spinal locomotor CPG is modulated by 5-HT. On a cellular level, 5-HT presynaptically inhibits synaptic transmission and postsynaptically inhibits a Ca2+-activated K+ current responsible for the slow afterhyperpolarization (sAHP) that follows action potentials in ventral horn neurons. To understand the contribution of these cellular mechanisms to the modulation of the spinal CPG, we have tested the effect of selective 5-HT analogues against fictive locomotion initiated by bath application of N-methyl-d-aspartate (NMDA). We found that the 5-HT1D agonist, L694-247, dramatically prolongs the frequency of ventral root bursting. Furthermore, we show that L694-247 presynaptically inhibits synaptic transmission without altering postsynaptic Ca2+ -activated K+ currents. We also confirm that 5-HT inhibits synaptic transmission at concentrations that modulate locomotion. To examine the mechanism by which selective presynaptic inhibition modulates the frequency of fictive locomotion, we performed voltage- and current-clamp recordings of CPG neurons during locomotion. Our results show that 5-HT decreases glutamatergic synaptic drive within the locomotor CPG during fictive locomotion. Thus we conclude that presynaptic inhibition of neurotransmitter release contributes to 5-HT–mediated modulation of locomotor activity.


2005 ◽  
Vol 569 (1) ◽  
pp. 291-304 ◽  
Author(s):  
J. B. Nielsen ◽  
B. A. Conway ◽  
D. M. Halliday ◽  
M.-C. Perreault ◽  
H. Hultborn

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