Suckling and sucrose ingestion suppress persistent hyperalgesia and spinal Fos expression after forepaw inflammation in infant rats

Ren, Ke; Blass, Elliott M.; Zhou, QiQi; Dubner, Ronald

doi:10.1073/pnas.94.4.1471

Cited by 93 publications

(56 citation statements)

References 42 publications

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“…1). This eating-induced analgesia is distinct from the analgesia elicited by an acute intraoral infusion of sucrose (27)(28)(29) for two reasons. First, sucrose-induced analgesia is present only in infant rats (28).…”

Section: Discussionmentioning

confidence: 97%

Sensory suppression during feeding

Foo

Mason

2005

Proc. Natl. Acad. Sci. U.S.A.

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Feeding is essential for survival, whereas withdrawal and escape reactions are fundamentally protective. These critical behaviors can compete for an animal's resources when an acutely painful stimulus affects the animal during feeding. One solution to the feeding-withdrawal conflict is to optimize feeding by suppressing pain. We examined whether rats continue to feed when challenged with a painful stimulus. During feeding, motor withdrawal responses to noxious paw heat either did not occur or were greatly delayed. To investigate the neural basis of sensory suppression accompanying feeding, we recorded from brainstem pain-modulatory neurons involved in the descending control of pain transmission. During feeding, pain-facilitatory ON cells were inhibited and pain-inhibitory OFF cells were excited. When a nonpainful somatosensory stimulus preactivated ON cells and preinhibited OFF cells, rats interrupted eating to react to painful stimuli. Inactivation of the brainstem region containing ON and OFF cells also blocked pain suppression during eating, demonstrating that brainstem pain-modulatory neurons suppress motor reactions to external stimulation during homeostatic behaviors.homeostasis ͉ nociceptive modulation ͉ pain ͉ raphe magnus ͉ ON and OFF cells B ehaviors such as eating, drinking, micturition, and defecation are essential for an organism's survival and are affected by exposure to aversive stimuli. Stress-induced eating and defecation occur across species and can be triggered by exposure to a painful stimulus (1-4). Yet, very little is known about the effects of feeding (eating and drinking), micturition, and defecation on pain sensitivity. In food-deprived animals, eating takes precedence over pain-motivated behaviors. During eating, fooddeprived cats were less likely to withdraw from acute noxious cutaneous heat (5), and food-deprived chickens showed fewer pain-motivated behaviors in response to chronic pain induced by sodium urate (6). However, responses to a painful stimulus are affected by the hunger͞satiation state (7), and it remains to be determined whether these analgesic effects can be generalized to animals that have been fed freely. Consequently, the aim of Experiment 1 was to examine whether the drive to satisfy hunger still overrides the need to avoid pain in non-food-deprived animals. We found that feeding suppressed pain in rats that were fed ad libitum.The suppression of pain during feeding indicates the activation of endogenous pain modulatory pathways. The brainstem ventromedial medulla (VMM) is a critical area in the descending control of pain and is the final common pathway from the brain to the spinal cord (8-11). The VMM modulates pain bidirectionally: its activation can produce either pain facilitation or pain inhibition (10-16). The pain-facilitatory and pain-inhibitory effects are thought to be mediated by two populations of neurons with opposing responses to noxious stimulation and morphine (17)(18)(19)(20). Cells activated by noxious stimulation are inhibited by opioids. These cel...

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Section: Discussionmentioning

confidence: 97%

Sensory suppression during feeding

Foo

Mason

2005

Proc. Natl. Acad. Sci. U.S.A.

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“…However, there is compelling evidence that an endogenous opioid-sweet taste relationship exists. [22][23][24][25][26][27][28][29][30][31] Calming and/or analgesic effects of sucrose that occur rapidly, last for several minutes, and can be blocked by systemic opioid receptor antagonists have been demonstrated in rats. 29,32 The mechanism of effects suggest an increase in serum and cerebrospinal fluid b-endorphin levels after orally ingested sucrose but not REVIEW ARTICLE intragastrically administered sucrose.…”

Section: Animal Model Studiesmentioning

confidence: 99%

Sucrose for Procedural Pain Management in Infants

2012

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The use of oral sucrose has been the most extensively studied pain intervention in newborn care to date. More than 150 published studies relating to sweet-taste-induced calming and analgesia in human infants have been identified, of which 100 (65%) include sucrose. With only a few exceptions, sucrose, glucose, or other sweet solutions reduced pain responses during commonly performed painful procedures in diverse populations of infants up to 12 months of age. Sucrose has been widely recommended for routine use during painful procedures in newborn and young infants, yet these recommendations have not been translated into consistent use in clinical practice. One reason may be related to important knowledge and research gaps concerning analgesic effects of sucrose. Notably, the mechanism of sweet-taste-induced analgesia is still not precisely understood, which has implications for using research evidence in practice. The aim of this article is to review what is known about the mechanisms of sucrose-induced analgesia; highlight existing evidence, knowledge gaps, and current controversies; and provide directions for future research and practice. Pediatrics 2012;130:918-925

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“…The analgesic efect of sweet solutions is conined to the intraoral route as sucrose reduces pain sensation when administered orally not when applied via gastric gavage [12]. The antinociceptive actions of these solutions are not due to intraoral infusion alone because they are not produced by water or lactose [54,55].…”

Section: Sweet Solution Analgesia In Animal Studiesmentioning

confidence: 99%