Medullary on-cell activity during tail-flick inhibition produced by heterotopic noxious stimulation

Hernández, Norma Edenia Batista; Dmitrieva, Natalia O.; Vanegas, Horacio

doi:10.1016/0304-3959(94)90134-1

Cited by 21 publications

(12 citation statements)

References 46 publications

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“…Instead, the DNIC pathway includes afferent projections from the dorsal horn to the nucleus reticularis dorsalis (NRD), and descending projections from the NRD to the dorsal horn (Dickenson et al, 1980; Bouhassira et al, 1992; Villanueva and Le Bars, 1995; Le Bars, 2002). Although noxious stimulation activates pain inhibitory neurons from the NRD, it produces the opposite response in the RVM, activating pain facilitating on-cells (Anderson et al, 1977; Hernandez et al, 1994). …”

Section: Discussionmentioning

confidence: 99%

“…Cutaneous receptive field properties and the sensitivity of the dura to mechanical and electrical stimulation were examined. In addition, we tested neurons for the effect of chronic morphine exposure on diffuse noxious inhibitory controls (DNIC) (Bouhassira et al, 1992; Bouhassira et al, 1993; Hernandez et al, 1994; Villanueva and Le Bars, 1995). DNIC, which involves activation of descending inhibitory pathways from the subnucleus reticularis dorsalis (SRD), is impaired in chronic daily headache patients (Pielsticker et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Sustained Morphine-Induced Sensitization and Loss of Diffuse Noxious Inhibitory Controls in Dura-Sensitive Medullary Dorsal Horn Neurons

Okada-Ogawa

Porreca²,

Meng³

2009

J. Neurosci.

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Overuse of medications used to treat migraine headache can produce a chronic daily headache, termed medication overuse headache (MOH). Although “overuse” of opioids, triptans, and over-the-counter analgesics can all produce MOH, the neuronal mechanisms remain unknown. Headache pain is likely to be produced by stimulation of primary afferent neurons that innervate the intracranial vasculature and the resulting activation of medullary dorsal horn (MDH) neurons. The present study compared the receptive field properties of MDH dura sensitive neurons in rats treated with morphine to those given vehicle. Animals were implanted with osmotic mini-pumps or pellets for sustained subcutaneous administration of morphine or vehicle 6–7 days prior to recording from dura-sensitive neurons. Electrical and mechanical activation thresholds from the dura were significantly lower in chronic morphine treated animals when compared to vehicle controls. In addition, sustained morphine increased the cutaneous receptive field sizes. The presence of diffuse noxious inhibitory controls (DNIC) was examined by placing the tail in 55°C water during concomitant noxious thermal stimulation of the cutaneous receptive field, usually located in the ophthalmic region. The DNIC stimulus produced significant inhibition of heat-evoked activity in vehicle, but not chronic morphine treated animals. Inactivation of the rostral ventromedial medulla (RVM) with 4% lidocaine reinstated DNIC in chronic morphine treated animals. These results are consistent with studies demonstrating a loss of DNIC in patients that suffer from chronic daily headache and may partially explain why overuse of medication used to treat migraine can induce headaches.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Sustained Morphine-Induced Sensitization and Loss of Diffuse Noxious Inhibitory Controls in Dura-Sensitive Medullary Dorsal Horn Neurons

Okada-Ogawa

Porreca²,

Meng³

2009

J. Neurosci.

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“…The conditioning stimuli that activate DNIC have been shown to decrease the activity of rostral ventromedial medulla (RVM) ON cells (Herná ndez et al, 1994). Moreover, DNIC reduces the activity of convergent dorsal horn neurons through activation of opioids receptors (Willer et al, 1990;Le Bars et al, 1992a;Bouhassira et al, 1993).…”

Section: A Conditioned Pain Modulationmentioning

confidence: 99%

Human Experimental Pain Models for Assessing the Therapeutic Efficacy of Analgesic Drugs

et al. 2012

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“…Yet, antinociception is more commonly observed. This paradox was previously noted and addressed experimentally, although no compelling cellular mechanism has emerged (Hernandez et al 1994;. Here, we use a specific form of heterotopic antinociception: the suppression of heat-evoked withdrawals by the noxious visceral stimulus colorectal distension (CRD).…”

Section: Introductionmentioning

confidence: 96%

Raphe Magnus Neurons Help Protect Reactions to Visceral Pain From Interruption by Cutaneous Pain

Brink

Hellman²,

Lambert³

et al. 2006

Journal of Neurophysiology

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Brink, Thaddeus S., Kevin M. Hellman, Aaron M. Lambert, and Peggy Mason. Raphe magnus neurons help protect reactions to visceral pain from interruption by cutaneous pain. J Neurophysiol 96: 3423-3432, 2006. First published August 23, 2006 doi:10.1152/jn.00793.2006. Suppression of reactions to one noxious stimulus by a spatially distant noxious stimulus is termed heterotopic antinociception. In lightly anesthetized rats, a noxious visceral stimulus, colorectal distension (CRD), suppressed motor withdrawals but not blood pressure or heart rate changes evoked by noxious hindpaw heat. Microinjection of muscimol, a GABA A receptor agonist, into raphe magnus (RM) reduced CRD-evoked suppression of withdrawals, evidence that RM neurons contribute to this heterotopic antinociception. To understand how brain stem neurons contribute to heterotopic antinociception, RM neurons were recorded during CRDelicited suppression of hindpaw withdrawals. Although subsets of RM neurons that were excited (ON cells) or inhibited (OFF cells) by noxious cutaneous stimulation were either excited or inhibited by CRD, ON cells were inhibited and OFF cells excited by an intracerebroventricularly administered opioid, evidence that the nociception-facilitating and -inhibiting functions of ON and OFF cells, respectively, are predicted by the cellular response to noxious cutaneous stimulation alone and not by the response to CRD. When recorded during CRD-elicited antinociception, RM cell discharge resembled the pattern observed in response to CRD stimulation alone. However, when hindpaw withdrawal suppression was incomplete, RM cell discharge resembled the pattern observed in response to heat alone. We propose that ON cells excited by CRD facilitate responses to CRD itself, which in turn augments excitation of OFF cells that then act to suppress cutaneous nociception. RM cells may thereby contribute to the dominance of quiet recuperative reactions evoked by potentially life-threatening visceral stimuli over transient somatomotor activity elicited by lessinjurious noxious cutaneous stimuli.

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Medullary on-cell activity during tail-flick inhibition produced by heterotopic noxious stimulation

Cited by 21 publications

References 46 publications

Sustained Morphine-Induced Sensitization and Loss of Diffuse Noxious Inhibitory Controls in Dura-Sensitive Medullary Dorsal Horn Neurons

Sustained Morphine-Induced Sensitization and Loss of Diffuse Noxious Inhibitory Controls in Dura-Sensitive Medullary Dorsal Horn Neurons

Human Experimental Pain Models for Assessing the Therapeutic Efficacy of Analgesic Drugs

Raphe Magnus Neurons Help Protect Reactions to Visceral Pain From Interruption by Cutaneous Pain

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