 |
||||
|
||||
|
||||
|
||||
Previous Article | Next Article
The Journal of Neuroscience, January 1, 2003, 23(1):332-338
Modulatory Effects of
1-,
-Receptor Agonists on Feline Spinal Interneurons with Monosynaptic Input from Group I Muscle Afferents
Ingela Hammar and Elzbieta Jankowska Department of Physiology, Göteborg University, 405 30 Göteborg, Sweden
Previous studies have shown that monoamines may modulate operation of spinal neuronal networks by depressing or facilitating responses of the involved neurons. Recently, activation of interneurons mediating reciprocal inhibition from muscle spindle (Ia) afferents and nonreciprocal inhibition from muscle spindle and tendon organ (Ia/Ib) afferents in the cat was found to be facilitated by noradrenaline (NA). However, which subclass membrane receptors are involved in mediating this facilitation was not established; the aim of the present experiments was to investigate this. Individual Ia- and Ia/Ib-inhibitory interneurons were identified in the cat lumbar spinal cord, and NA agonists were applied close to these neurons by ionophoresis. The agonists included the
1-receptor agonist phenylephrine, the
-receptor agonist isoproterenol. Effects were measured by comparing changes in the number of extracellularly recorded spike potentials evoked by electrical stimulation of muscle nerves and changes in the latency of these potentials before, during, and after application of the tested compounds. Results show that the facilitatory effect of phenylephrine is as strong as that of NA, whereas the facilitatory effect of isoproterenol is weaker. Clonidine depressed activity of both Ia- and Ia/Ib-inhibitory interneurons, whereas tizanidine had no effect. These findings lead to the conclusion that beneficial antispastic effects of clonidine and tizanidine in humans are unlikely to be associated with an enhancement of the actions of Ia- and Ia/Ib-inhibitory interneurons, and the findings also support previous proposals that these compounds exert their antispastic actions via effects on other neuronal populations.
Key words: spinal cord; spinal reflexes; cat; group I afferents; spasticity; noradrenaline; clonidine; tizanidine; phenylephrine; isoproterenol
Copyright © 2003 Society for Neuroscience 0270-6474/03/231332-07$05.00/0
This article has been cited by other articles:
H. Delivet-Mongrain, H. Leblond, and S. Rossignol
Effects of Localized Intraspinal Injections of a Noradrenergic Blocker on Locomotion of High Decerebrate Cats
J Neurophysiol, August 1, 2008; 100(2): 907 - 921.
[Abstract] [Full Text] [PDF]
I. T. Gordon and P. J. Whelan
Monoaminergic Control of Cauda-Equina-Evoked Locomotion in the Neonatal Mouse Spinal Cord
J Neurophysiol, December 1, 2006; 96(6): 3122 - 3129.
[Abstract] [Full Text] [PDF]
C. Langlet, H. Leblond, and S. Rossignol
Mid-Lumbar Segments Are Needed for the Expression of Locomotion in Chronic Spinal Cats
J Neurophysiol, May 1, 2005; 93(5): 2474 - 2488.
[Abstract] [Full Text] [PDF]
E Maupas, P Marque, C F Roques, and M Simonetta-Moreau
Modulation of the transmission in group II heteronymous pathways by tizanidine in spastic hemiplegic patients
J. Neurol. Neurosurg. Psychiatry, January 1, 2004; 75(1): 130 - 135.
[Abstract] [Full Text] [PDF]
|
|
|
|
 |
|