Digital Repository

Involvement of neuropeptide Y in the acute, chronic and withdrawal responses of morphine in nociception in neuropathic rats: Behavioral and neuroanatomical correlates

Show simple item record

dc.contributor.author Upadhya, Manoj A. en_US
dc.contributor.author Dandekar, Manoj P. en_US
dc.contributor.author Kokare, Dadasaheb M. en_US
dc.contributor.author Singru, Praful S. en_US
dc.contributor.author SUBHEDAR, NISHIKANT K. en_US
dc.date.accessioned 2018-12-06T09:16:34Z
dc.date.available 2018-12-06T09:16:34Z
dc.date.issued 2009-08 en_US
dc.identifier.citation Neuropeptides, 43(4). en_US
dc.identifier.issn 0143-4179 en_US
dc.identifier.issn 1532-2785 en_US
dc.identifier.uri http://dr.iiserpune.ac.in:8080/xmlui/handle/123456789/1395
dc.identifier.uri https://doi.org/10.1016/j.npep.2009.05.003 en_US
dc.description.abstract Although morphine is a potent antinociceptive agent, its chronic use developed tolerance in neuropathic pain (NP). Furthermore, opioid antagonist naloxone attenuated the antinociceptive effect of neuropeptide Y (NPY). The present study investigated the role of NPY and NPY Y1/Y5 receptors in acute and chronic actions of morphine in neuropathic rats using thermal paw withdrawal test and immunocytochemistry. In acute study, intracerebroventricular (icv) administration of morphine, NPY or NPY Y1/Y5 receptors agonist [Leu31, Pro34]-NPY produced antinociception, whereas selective NPY Y1 receptors antagonist BIBP3226 caused hyperalgesia. While NPY or [Leu31, Pro34]-NPY potentiated, BIBP3226 attenuated morphine induced antinociception. Chronic icv infusion of morphine via osmotic minipumps developed tolerance to its antinociceptive effect, and produced hyperalgesia following withdrawal. However, co-administration of NPY or [Leu31, Pro34]-NPY prevented the development of tolerance and withdrawal hyperalgesia. Sciatic nerve ligation resulted in significant increase in the NPY-immunoreactive (NPY-ir) fibers in ventrolateral periaqueductal gray (VLPAG) and locus coeruleus (LC); fibers in the dorsal part of dorsal raphe nucleus (DRD) did not respond. While chronic morphine treatment significantly reduced NPY-ir fibers in VLPAG and DRD, morphine withdrawal triggered significant augmentation in NPY-immunoreactivity in the VLPAG. NPY-immunoreactivity profile of LC remained unchanged in all the morphine treatment conditions. Furthermore, removal of sciatic nerve ligation reversed the effects of NP, increased pain threshold and restored NPY-ir fiber population in VLPAG. NPY, perhaps acting via Y1/Y5 receptors, might profoundly influence the processing of NP information and interact with the endogenous opioid system primarily within the framework of the VLPAG. en_US
dc.language.iso en en_US
dc.publisher Elsevier B.V. en_US
dc.subject Morphine en_US
dc.subject Neuropeptide Y en_US
dc.subject Antinociception en_US
dc.subject Neuropathic pain en_US
dc.subject Thermal paw en_US
dc.subject 2009 en_US
dc.title Involvement of neuropeptide Y in the acute, chronic and withdrawal responses of morphine in nociception in neuropathic rats: Behavioral and neuroanatomical correlates en_US
dc.type Article en_US
dc.contributor.department Dept. of Biology en_US
dc.identifier.sourcetitle Neuropeptides en_US
dc.publication.originofpublisher Foreign en_US


Files in this item

Files Size Format View

There are no files associated with this item.

This item appears in the following Collection(s)

Show simple item record

Search Repository


Advanced Search

Browse

My Account