Markovian Analysis of the Sequential Behavior of the Spontaneous Spinal Cord Dorsum Potentials Induced by Acute Nociceptive Stimulation in the Anesthetized Cat

Xi, Ming-Chu, Rong-Huan Liu, Jack Yamuy, Francisco R. Morales, and Michael H. Chase. Electrophysiological properties of lumbar motoneurons in the α-chloralose-anesthetized cat during carbachol-induced motor inhibition. J. Neurophysiol. 78: 129–136, 1997. The present study was undertaken 1) to examine the neuronal mechanisms responsible for the inhibition of spinal cord motoneurons that occurs in α-chloralose-anesthetized cats following the microinjection of carbachol into the nucleus pontis oralis (NPO), and 2) to determine whether the inhibitory mechanisms are the same as those that are responsible for the postsynaptic inhibition of motoneurons that is present during naturally occurring active sleep. Accordingly, the basic electrophysiological properties of lumbar motoneurons were examined, with the use of intracellular recording techniques, in cats anesthetized with α-chloralose and compared with those present during naturally occurring active sleep. The intrapontine administration of carbachol resulted in a sustained reduction in the amplitude of the spinal cord Ia monosynaptic reflex. Discrete large-amplitude inhibitory postsynaptic potentials (IPSPs), which are only present during the state of active sleep in the chronic cat, were also observed in high-gain recordings from lumbar motoneurons after the injection of carbachol. During carbachol-induced motor inhibition, lumbar motoneurons exhibited a statistically significant decrease in input resistance, membrane time constant and a reduction in the amplitude of the action potential's afterhyperpolarization. In addition, there was a statistically significant increase in rheobase and in the delay between the initial-segment (IS) and somadendritic (SD) portions of the action potential (IS-SD delay). There was a significant increase in the mean motoneuron resting membrane potential (i.e., hyperpolarization). The preceding changes in the electrophysiological properties of motoneurons, as well as the development of discrete IPSPs, indicate that lumbar motoneurons are postsynaptically inhibited after the intrapontine administration of carbachol in cats that are anesthetized with α-chloralose. These changes in the electrophysiological properties of lumbar motoneurons were found to be comparable with those that take place during the atonia of active (rapid-eye-movement) sleep in chronic cats. The present results support the conclusion that the neural system that is responsible for motor inhibition during naturally occurring active sleep can also be activated in α-chloralose-anesthetized cats following the injection of carbachol into the NPO.

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Release of glutamate, nitric oxide and prostaglandin E2 and metabolic activity in the spinal cord of rats following peripheral nociceptive stimulation

Pain ◽

10.1016/s0304-3959(01)00258-5 ◽

2001 ◽

Vol 92 (1) ◽

pp. 213-218 ◽

Cited By ~ 68

Author(s):

Gregor Vetter ◽

Gerd Geisslinger ◽

Irmgard Tegeder

Keyword(s):

Nitric Oxide ◽

Spinal Cord ◽

Prostaglandin E2 ◽

Metabolic Activity ◽

Nociceptive Stimulation

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Tight neurovascular coupling in the spinal cord during nociceptive stimulation in intact and spinal rats

Neuroscience ◽

10.1016/j.neuroscience.2017.04.038 ◽

2017 ◽

Vol 355 ◽

pp. 1-8 ◽

Cited By ~ 4

Author(s):

Mathieu Piché ◽

Thierry Paquette ◽

Hugues Leblond

Keyword(s):

Spinal Cord ◽

Neurovascular Coupling ◽

Nociceptive Stimulation

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Wide dynamic range but not nociceptive-specific neurons encode multidimensional features of prolonged repetitive heat pain

Journal of Neurophysiology ◽

10.1152/jn.1993.69.3.703 ◽

1993 ◽

Vol 69 (3) ◽

pp. 703-716 ◽

Cited By ~ 109

Author(s):

R. C. Coghill ◽

D. J. Mayer ◽

D. D. Price

Keyword(s):

Spinal Cord ◽

Pain Intensity ◽

Dynamic Range ◽

Initial Period ◽

Substantial Reduction ◽

Nociceptive Stimulation ◽

Wide Dynamic Range ◽

Noxious Heat ◽

Wdr Neurons ◽

Pain Unpleasantness

1. To better characterize temporal and spatial mechanisms involved in the coding of prolonged nociceptive stimuli in the spinal cord, the responses of dorsal horn wide dynamic range (WDR) and nociceptive-specific (NS) neurons to prolonged, repetitive noxious heat stimuli (45–49 degrees C) were examined in unanesthetized, spinal cord transected rats. To relate these neuronal responses to conscious dimensions of pain, human subjects were presented with identical types of prolonged, repetitive stimuli, so that psychophysical ratings of pain intensity and pain unpleasantness could be compared with the magnitudes and temporal features of the responses of NS and WDR neurons. 2. WDR neurons exhibited high rates of impulse discharge throughout 45 min of repetitive nociceptive stimulation, with only partial reduction (31% decrease from peak rates) occurring after 2 min of stimulation. In sharp contrast, NS neurons stimulated under the same conditions displayed substantial reduction of firing (73% decrease from peak rates) after a brief, initial period of activity that occurred within 2 min after onset of stimulation. Psychophysical ratings of pain intensity and pain unpleasantness, like the responses of WDR neurons, did not decrease substantially from initial levels during 7 min of painful stimulation. Furthermore, these ratings remained at high levels during time periods where the impulse frequencies of NS neurons were only at 27% of maximal levels. 3. Graded nociceptive stimuli were employed to characterize the ability of WDR neurons to encode nociceptive intensity over long durations of repetitive stimulation and to delineate further the relationship between WDR and psychophysical responses. Both WDR discharge frequencies and psychophysical ratings of pain intensity and unpleasantness increased in a monotonic manner to graded increases in stimulus temperatures. 4. These results indicate that pain does not decrease substantially during the course of prolonged, repetitive nociceptive stimulation. The fact that the responses of NS neurons decline significantly, whereas both WDR and psychophysical responses do not, suggests that WDR neurons alone are sufficient to evoke both sensory intensity and affective responses to prolonged pain. Furthermore, because subjects could localize and qualitatively describe pain at times when responses of NS neurons were minimal, WDR neurons alone can encode some spatial and qualitative aspects of pain.

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