The Pronociceptive Effect of Paradoxical Sleep Deprivation in Rats: Evidence for a Role of Descending Pain Modulation Mechanisms

Tomim, Dabna Hellen; Pontarolla, Felipe Mendes; Bertolini, Jessica F.; Arase, Mauricio; Tobaldini, Gláucia; Lima, Marcelo M.S.; Fischer, Luana

doi:10.1007/s12035-014-9059-0

Cited by 49 publications

(35 citation statements)

References 66 publications

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“…15,45,76 Moreover, there is abundant indirect evidence that ON-cells contribute to hyperalgesia in neuropathy, opioid-induced hyperalgesia, and other persistent pain states. 10,14,21,59,62,70,71,73 A better understanding of the interactions between the PB and RVM in conditions of injury and inflammation should therefore provide critical insights into the plasticity of pain-modulation in persistent pain. 11,15,20,61 …”

Section: Discussionmentioning

confidence: 99%

Parabrachial complex links pain transmission to descending pain modulation

Roeder

Chen

Davis

et al. 2016

PAIN

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The rostral ventromedial medulla (RVM) has a well-documented role in pain modulation, and exerts anti-nociceptive and pro-nociceptive influences mediated by two distinct classes of neurons, OFF-cells and ON-cells. OFF-cells are defined by a sudden pause in firing in response to nociceptive inputs, whereas ON-cells are characterized by a “burst” of activity. Although these reflex-related changes in ON- and OFF-cell firing are critical to their pain-modulating function, the pathways mediating these responses have not been identified. The present experiments were designed to test the hypothesis that nociceptive input to the RVM is relayed through the parabrachial complex (PB). In electrophysiological studies, ON- and OFF-cells were recorded in the RVM of lightly anesthetized male rats before and after an infusion of lidocaine or muscimol into PB. The ON-cell burst and OFF-cell pause evoked by noxious heat or mechanical probing were substantially attenuated by inactivation of the lateral, but not medial, parabrachial area. Retrograde tracing studies showed that neurons projecting to the RVM were scattered throughout PB. Few of these neurons expressed calcitonin gene-related peptide (CGRP), suggesting that the RVM projection from PB is distinct from that to the amygdala. These data show that a substantial component of “bottom-up” nociceptive drive to RVM pain-modulating neurons is relayed through the parabrachial complex. While the parabrachial complex is well-known as an important relay for ascending nociceptive information, its functional connection with the RVM allows the spinoparabrachial pathway to access descending control systems as part of a recurrent circuit.

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Section: Discussionmentioning

confidence: 99%

Parabrachial complex links pain transmission to descending pain modulation

Roeder

Chen

Davis

et al. 2016

PAIN

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“…29 Additionally, sleep deprivation may lead to a disturbance of the descending pain inhibitory control system. 30,31 In addition, deficiency of serotonin descending pain inhibitory was suggested to be associated with migraine pathophysiology. 32 Second, regarding the mechanism of impact of headaches on sleep, chronic pain may lead to alterations of neuron activity in the raphe magnus, which can regulate the sleep cycle.…”

Section: Discussionmentioning

confidence: 99%

Associations Between Sleep Quality and Migraine Frequency

Lin

Lee

et al. 2016

Medicine

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Migraine has been associated with sleep disturbances. Relationship between sleep quality and migraine frequency is yet to be determined. The present study aimed to investigate sleep disturbances among low-frequency, moderate-frequency, high-frequency, and chronic migraineurs, with and without auras, with well-controlled confounding variables.This cross-sectional controlled study included 357 subjects from an outpatient headache clinic in Taiwan. Standardized questionnaires were utilized to collect demographic, migraine, sleep, depression, anxiety, and restless leg syndrome characteristics in all participants. According to frequency of migraine attacks, patients were divided into 4 groups: with 1 to 4 migraine days per month, 5 to 8 migraine days in a month, 9 to 14 migraine days in a month, and >14 migraine days per month. The Pittsburgh Sleep Quality Index (PSQI) and subgroup items were used to evaluate sleep quality. The association between migraine frequency and sleep quality was investigated using multivariable linear regression and logistic regression.The PSQI total score was highest in patients with high frequent migraine (10.0 ± 3.4) and lowest in controls (7.0 ± 3.4) with a significant trend analysis (P for trend = 0.006). Migraine frequency had an independent effect on the items “Cannot get to sleep within 30 minutes” (P < 0.001), “Wake up in the middle of the night or early morning” (P < 0.001), “Bad dreams” (P = 0.001), “Pain” (P = 0.004), and “Quality of sleep” (P < 0.001). The result showed the effect of migraine frequency in both the aura-present (P for trend = 0.008) and the aura-absent subgroups (P for trend = 0.011).High migraine frequency correlates with poor sleep quality and a higher prevalence of poor sleepers. These associations occur in migraine with aura and without aura.

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“…Also neurotransmitters, like dopamine are involved in sleep and pain [25]. Furthermore, sleep deprivation decreases morphine analgesia, possibly by decreasing descending pain inhibitory activity and by increasing descending pain facilitatory activity [97]. Conversely, sleep improves from intrathecal morphine infusion in patients with severe pain [98].…”

Section: Discussionmentioning

confidence: 99%