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Descending control of nociception: Specificity, recruitment and plasticity
Analysis of the circuitry within the RVM reveals that the neural basis for bidirectional control from the midline system is two populations of neurons, ON-cells and OFF-cells, that are differentially recruited by higher structures important in fear, illness and psychological stress to enhance or inhibit pain. Expand
Neurotransmitters in nociceptive modulatory circuits.
The similarity in response properties among the members of each class, their large, somatic "receptive fields," and the wide distribution of the terminal fields of axons of individual neurons to the trigeminal sensory complex and to multiple spinal segments indicate that these neurons exert a global influence over nociceptive responsiveness. Expand
Anatomy and physiology of a nociceptive modulatory system.
The nociceptive modulatory system is diffusely organized, highly interconnected and appears to act as a unit whether activated by opiates or electrical stimulation, and the idea that the system acts as a simple negative feedback circuit is not consistent with its known properties. Expand
A possible neural basis for stress-induced hyperalgesia
stimulation of the dorsomedial nucleus of the hypothalamus is shown to be a critical component of central mechanisms mediating neuroendocrine, cardiovascular and thermogenic responses to mild or “emotional” stressors, and a possible neural circuit for stress‐induced hyperalgesia is suggested. Expand
Medullary pain facilitating neurons mediate allodynia in headache‐related pain
To develop and validate a model of cutaneous allodynia triggered by dural inflammation for pain associated with headaches. To explore neural mechanisms underlying cephalic and extracephalic allodynia.
Disinhibition of off-cells and antinociception produced by an opioid action within the rostral ventromedial medulla
The role of the on-cell as the focus of direct opioid action within the rostral medulla is confirmed, and the proposal that disinhibition of off-cells is central to the antinociception actions of opioids within this region is strongly supported. Expand
Circuitry underlying antiopioid actions of cholecystokinin within the rostral ventromedial medulla.
CCK acting within the RVM attenuates the analgesic effect of systemically administered morphine by preventing activation of the putative pain inhibiting output neurons of the RVB, the OFF cells, which differs from another antiopioid peptide, orphanin FQ/nociceptin, which interferes with opioid analgesia by potently suppressing all OFF-cell firing. Expand
Direct and indirect actions of morphine on medullary neurons that modulate nociception
The present experiments demonstrate that direct opioid responsiveness in the rostral ventromedial medulla is limited to a single physiologically characterized class of presumed nociceptive modulatory neuron, the on-cell. Expand
Putative nociceptive modulating neurons in the rostral ventromedial medulla of the rat: firing of on- and off-cells is related to nociceptive responsiveness.
The hypothesis that off-cells inhibit and on-cells facilitate spinal nociceptive transmission and reflexes is supported, because the correlation between on- and off-cell firing and changes in TF latency is consistent with a nocICEptive modulatory role for either or both cell classes. Expand