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Prostaglandin E2 in the midbrain periaqueductal gray produces hyperalgesia and activates pain-modulating circuitry in the rostral ventromedial medulla.
Pain. 2004 Jul; 110(1-2):419-26.PAIN

Abstract

Recent years have seen significant advances in our understanding of the peripheral and spinal mechanisms through which prostaglandins contribute to nociceptive sensitization. By contrast, the possibility of a supraspinal contribution of these compounds to facilitated pain states has received relatively little attention. One possible mechanism through which prostaglandins could act supraspinally to facilitate nociception would be by recruitment of descending facilitation from brainstem pain-modulating systems. The rostral ventromedial medulla (RVM) is now known to contribute to enhanced responding in a variety of inflammatory and nerve injury models. Its major supraspinal input, the midbrain periaqueductal gray (PAG), expresses prostanoid receptors and synthetic enzymes. The aim of the present study was to determine whether direct application of prostaglandin E(2) (PGE(2)) within the ventrolateral PAG is sufficient to produce hyperalgesia, and whether any hyperalgesia could be mediated by recruiting nociceptive modulating neurons in the RVM. We determined the effects of focal application of PGE(2) in the PAG on paw withdrawal latency and activity of identified nociceptive modulating neurons in the RVM of lightly anesthetized rats. Microinjection of PGE(2) (50 fg in 200 nl) into the PAG produced a significant decrease in paw withdrawal latency. The PGE(2) microinjection activated on-cells, RVM neurons thought to facilitate nociception, and suppressed the firing of off-cells, RVM neurons believed to have an inhibitory effect on nociception. These data demonstrate a prostaglandin-sensitive descending facilitation from the PAG, and suggest that this is mediated by on- and off-cells in the RVM.

Authors+Show Affiliations

Department of Neurological Surgery, L-472, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA. heinricm@ohsu.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15275794

Citation

Heinricher, Mary M., et al. "Prostaglandin E2 in the Midbrain Periaqueductal Gray Produces Hyperalgesia and Activates Pain-modulating Circuitry in the Rostral Ventromedial Medulla." Pain, vol. 110, no. 1-2, 2004, pp. 419-26.
Heinricher MM, Martenson ME, Neubert MJ. Prostaglandin E2 in the midbrain periaqueductal gray produces hyperalgesia and activates pain-modulating circuitry in the rostral ventromedial medulla. Pain. 2004;110(1-2):419-26.
Heinricher, M. M., Martenson, M. E., & Neubert, M. J. (2004). Prostaglandin E2 in the midbrain periaqueductal gray produces hyperalgesia and activates pain-modulating circuitry in the rostral ventromedial medulla. Pain, 110(1-2), 419-26.
Heinricher MM, Martenson ME, Neubert MJ. Prostaglandin E2 in the Midbrain Periaqueductal Gray Produces Hyperalgesia and Activates Pain-modulating Circuitry in the Rostral Ventromedial Medulla. Pain. 2004;110(1-2):419-26. PubMed PMID: 15275794.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prostaglandin E2 in the midbrain periaqueductal gray produces hyperalgesia and activates pain-modulating circuitry in the rostral ventromedial medulla. AU - Heinricher,Mary M, AU - Martenson,Melissa E, AU - Neubert,Miranda J, PY - 2004/02/26/received PY - 2004/04/07/revised PY - 2004/04/19/accepted PY - 2004/7/28/pubmed PY - 2004/10/27/medline PY - 2004/7/28/entrez SP - 419 EP - 26 JF - Pain JO - Pain VL - 110 IS - 1-2 N2 - Recent years have seen significant advances in our understanding of the peripheral and spinal mechanisms through which prostaglandins contribute to nociceptive sensitization. By contrast, the possibility of a supraspinal contribution of these compounds to facilitated pain states has received relatively little attention. One possible mechanism through which prostaglandins could act supraspinally to facilitate nociception would be by recruitment of descending facilitation from brainstem pain-modulating systems. The rostral ventromedial medulla (RVM) is now known to contribute to enhanced responding in a variety of inflammatory and nerve injury models. Its major supraspinal input, the midbrain periaqueductal gray (PAG), expresses prostanoid receptors and synthetic enzymes. The aim of the present study was to determine whether direct application of prostaglandin E(2) (PGE(2)) within the ventrolateral PAG is sufficient to produce hyperalgesia, and whether any hyperalgesia could be mediated by recruiting nociceptive modulating neurons in the RVM. We determined the effects of focal application of PGE(2) in the PAG on paw withdrawal latency and activity of identified nociceptive modulating neurons in the RVM of lightly anesthetized rats. Microinjection of PGE(2) (50 fg in 200 nl) into the PAG produced a significant decrease in paw withdrawal latency. The PGE(2) microinjection activated on-cells, RVM neurons thought to facilitate nociception, and suppressed the firing of off-cells, RVM neurons believed to have an inhibitory effect on nociception. These data demonstrate a prostaglandin-sensitive descending facilitation from the PAG, and suggest that this is mediated by on- and off-cells in the RVM. SN - 0304-3959 UR - https://www.unboundmedicine.com/medline/citation/15275794/Prostaglandin_E2_in_the_midbrain_periaqueductal_gray_produces_hyperalgesia_and_activates_pain_modulating_circuitry_in_the_rostral_ventromedial_medulla_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304395904002180 DB - PRIME DP - Unbound Medicine ER -