Cholinomimetics, but not morphine, increase antinociceptive behavior from pontine reticular regions regulating rapid-eye-movement sleep

Research output: Contribution to journalArticle

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Abstract

Sleep disruption is a significant problem associated with the subjective experience of pain. Both rapid-eye-movement (REM) sleep and nociception are modulated by cholinergic neurotransmission, and this study tested the hypothesis that antinociceptive behavior can be evoked cholinergically from medial pontine reticular formation (mPRF) regions known to regulate REM sleep. The foregoing hypothesis was investigated by quantifying the effect of mPRF drug administration on tail flick latency (TFL) of cat during polygraphically defined sleep/wake states. The mPRF was microinjected with 0.25 ml saline, carbachol (4.0 μg), neostigmine (6.7 μg), or morphine sulfate (14.7 μg), and TFL measures were obtained in response to radiant heat. During wakefulness TFL (% increase) was not increased by morphine or saline, but was significantly increased by mPRF administration of carbachol (42.4%) and neostigmine (35.2%). Cortical somatosensory potentials (SSEPs) were reliably evoked by tail stimulation before and after mPRF microinjections of carbachol. The results show for the first time that mPRF administration of cholinomimetics significantly increased TFL. During NREM sleep and REM sleep, TFL was significantly increased compared to waking TFL (110% and 321%, respectively). The finding of sleep-dependent alterations in TFL demonstrates that mPRF regions known to regulate REM sleep can modulate supraspinal cholinergic antinociceptive behavior.

Original languageEnglish (US)
Pages (from-to)677-685
Number of pages9
JournalSleep
Volume21
Issue number7
DOIs
StatePublished - Nov 1 1998
Externally publishedYes

Fingerprint

REM Sleep
Morphine
Cholinergic Agents
Tail
Sleep
Carbachol
Neostigmine
Nociception
Wakefulness
Microinjections
Pontine Tegmentum
Synaptic Transmission
Cats
Hot Temperature
Pain
Pharmaceutical Preparations

All Science Journal Classification (ASJC) codes

  • Clinical Neurology
  • Physiology (medical)

Cite this

Cholinomimetics, but not morphine, increase antinociceptive behavior from pontine reticular regions regulating rapid-eye-movement sleep. / Kshatri, A. M.; Baghdoyan, Helen; Lydic, Ralph.

In: Sleep, Vol. 21, No. 7, 01.11.1998, p. 677-685.

Research output: Contribution to journalArticle

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abstract = "Sleep disruption is a significant problem associated with the subjective experience of pain. Both rapid-eye-movement (REM) sleep and nociception are modulated by cholinergic neurotransmission, and this study tested the hypothesis that antinociceptive behavior can be evoked cholinergically from medial pontine reticular formation (mPRF) regions known to regulate REM sleep. The foregoing hypothesis was investigated by quantifying the effect of mPRF drug administration on tail flick latency (TFL) of cat during polygraphically defined sleep/wake states. The mPRF was microinjected with 0.25 ml saline, carbachol (4.0 μg), neostigmine (6.7 μg), or morphine sulfate (14.7 μg), and TFL measures were obtained in response to radiant heat. During wakefulness TFL ({\%} increase) was not increased by morphine or saline, but was significantly increased by mPRF administration of carbachol (42.4{\%}) and neostigmine (35.2{\%}). Cortical somatosensory potentials (SSEPs) were reliably evoked by tail stimulation before and after mPRF microinjections of carbachol. The results show for the first time that mPRF administration of cholinomimetics significantly increased TFL. During NREM sleep and REM sleep, TFL was significantly increased compared to waking TFL (110{\%} and 321{\%}, respectively). The finding of sleep-dependent alterations in TFL demonstrates that mPRF regions known to regulate REM sleep can modulate supraspinal cholinergic antinociceptive behavior.",
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