scholarly journals Propriospinal neurons are sufficient for bulbospinal transmission of the locomotor command signal in the neonatal rat spinal cord

2008 ◽  
Vol 586 (6) ◽  
pp. 1623-1635 ◽  
Author(s):  
Kristine C. Cowley ◽  
Eugene Zaporozhets ◽  
Brian J. Schmidt
Keyword(s):  
Spinal Cord ◽  
Neonatal Rat ◽  
Rat Spinal Cord ◽  
Propriospinal Neurons ◽  
Command Signal

Neurochemical excitation of propriospinal neurons facilitates locomotor command signal transmission in the lesioned spinal cord

2011 ◽  
Vol 105 (6) ◽  
pp. 2818-2829 ◽  
Author(s):  
Eugene Zaporozhets ◽  
Kristine C. Cowley ◽  
Brian J. Schmidt
Keyword(s):  
Spinal Cord ◽  
Brain Stem ◽  
Signal Transmission ◽  
Cholinergic Receptor ◽  
Neonatal Rat ◽  
Receptor Antagonists ◽  
Ion Removal ◽  
Propriospinal Neurons ◽  
Command Signal

Previous studies of the in vitro neonatal rat brain stem-spinal cord showed that propriospinal relays contribute to descending transmission of a supraspinal command signal that is capable of activating locomotion. Using the same preparation, the present series examines whether enhanced excitation of thoracic propriospinal neurons facilitates propagation of the locomotor command signal in the lesioned spinal cord. First, we identified neurotransmitters contributing to normal endogenous propriospinal transmission of the locomotor command signal by testing the effect of receptor antagonists applied to cervicothoracic segments during brain stem-induced locomotor-like activity. Spinal cords were either intact or contained staggered bilateral hemisections located at right T1/T2 and left T10/T11 junctions designed to abolish direct long-projecting bulbospinal axons. Serotonergic, noradrenergic, dopaminergic, and glutamatergic, but not cholinergic, receptor antagonists blocked locomotor-like activity. Approximately 73% of preparations with staggered bilateral hemisections failed to generate locomotor-like activity in response to electrical stimulation of the brain stem alone; such preparations were used to test the effect of neuroactive substances applied to thoracic segments (bath barriers placed at T3 and T9) during brain stem stimulation. The percentage of preparations developing locomotor-like activity was as follows: 5-HT (43%), 5-HT/ N-methyl-d-aspartate (NMDA; 33%), quipazine (42%), 8-hydroxy-2-(di- n-propylamino)tetralin (20%), methoxamine (45%), and elevated bath K+ concentration (29%). Combined norepinephrine and dopamine increased the success rate (67%) compared with the use of either agent alone (4 and 7%, respectively). NMDA, Mg2+ ion removal, clonidine, and acetylcholine were ineffective. The results provide proof of principle that artificial excitation of thoracic propriospinal neurons can improve supraspinal control over hindlimb locomotor networks in the lesioned spinal cord.

The in vitro neonatal rat spinal cord preparation: a new insight into mammalian locomotor mechanisms

2004 ◽  
Vol 190 (5) ◽  
pp. 343-357 ◽  
Author(s):  
F. Clarac ◽  
E. Pearlstein ◽  
J. F. Pflieger ◽  
L. Vinay
Keyword(s):  
Spinal Cord ◽  
Neonatal Rat ◽  
Rat Spinal Cord ◽  
Insight Into

scholarly journals The role of substance P as a neurotransmitter in the reflexes of slow time courses in the neonatal rat spinal cord

1985 ◽  
Vol 84 (3) ◽  
pp. 663-673 ◽  
Author(s):  
Hiroyuki Akagi ◽  
Shiro Konishi ◽  
Masanori Otsuka ◽  
Mitsuhiko Yanagisawa
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Neonatal Rat ◽  
Rat Spinal Cord ◽  
Slow Time ◽  
Time Courses

GABA-Receptor–Independent Dorsal Root Afferents Depolarization in the Neonatal Rat Spinal Cord

1998 ◽  
Vol 79 (5) ◽  
pp. 2581-2592 ◽  
Author(s):  
E. Kremer ◽  
A. Lev-Tov
Keyword(s):  
Spinal Cord ◽  
Dorsal Root ◽  
Gaba Receptor ◽  
Neonatal Rat ◽  
Extracellular Potassium ◽  
Rat Spinal Cord ◽  
Extracellular Potassium Concentration ◽  
Dorsal Roots ◽  
Intact Brain ◽  
Dorsal Root Afferents

Kremer, E. and A. Lev-Tov. GABA-receptor–independent dorsal root afferents depolarization in the neonatal rat spinal cord. J. Neurophysiol. 79: 2581–2592, 1998. Dorsal root afferent depolarization and antidromic firing were studied in isolated spinal cords of neonatal rats. Spontaneous firing accompanied by occasional bursts could be recorded from most dorsal roots in the majority of the cords. The afferent bursts were enhanced after elevation of the extracellular potassium concentration ([K+]e) by 1–2 mM. More substantial afferent bursts were produced when the cords were isolated with intact brain stems. Rhythmic afferent bursts could be recorded from dorsal roots in some of the cords during motor rhythm induced by bath-applied serotonin and N-methyl-d-aspartate (NMDA). Bilaterally synchronous afferent bursts were produced in pairs of dorsal roots after replacing the NaCl in the perfusate with sodium-2-hydroxyethansulfonate or after application of the γ-aminobutyric acid-A (GABAA) receptor antagonist bicuculline with or without serotonin (5-HT) and NMDA. Antidromic afferent bursts also could be elicited under these conditions by stimulation of adjacent dorsal roots, ventrolateral funiculus axons, or ventral white commissural (VWC) fibers. The antidromic bursts were superimposed on prolonged dorsal root potentials (DRPs) and accompanied by a prolonged increase in intraspinal afferent excitability. Surgical manipulations of the cord revealed that afferent firing in the presence of bicuculline persisted in the hemicords after hemisection and still was observed after removal of their ventral horns. Cutting the VWC throughout its length did not perturb the bilateral synchronicity of the discharge. These findings suggest that the activity of dorsal horn neurons is sufficient to produce the discharge and that the bilateral synchronicity can be maintained by cross connectivity that is relayed from side to side dorsal to the VWC. Antagonists of GABAB, 5-HT2/5-HT1C, or glutamate metabotropic group II and III receptors could not abolish afferent depolarization in the presence of bicuculline. Depolarization comparable in amplitude to DRPs, could be produced in tetrodotoxin-treated cords by elevation of [K+]e to the levels reported to develop in the neonatal rat spinal cord in response to dorsal root stimulation. A mechanism involving potassium transients produced by neuronal activity therefore is suggested to be the major cause of the GABA-independent afferent depolarization reported in our study. Possible implications of potassium transients in the developing and the adult mammalian spinal cord are discussed.

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