Analgesia, development of tolerance, and 5-hydroxytryptamine turnover in the rat after cerebral and systemic administration of morphine

M. R. Vasko, M. Vogt

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Morphine HCl (10 μ/0.5 μl) was injected into the right striatum, the caudal aqueduct and the region of the nucleus raphe magnus of the rat. Turnover of 5-hyrdroxytryptamine (5-HT) in the brain was assessed by fluorimetric estimation of 5-hydroxyindol-3-ylacetic acid following the administration of probenecid. Injection into the right striatum (a region containing 5-HT terminals) increased 5-HT turnover in the right, but not in the left striatum or in the anterior medulla. The pain threshold was unaltered. Injection into the aqueduct accelerated 5-HT turnover in the anterior medulla, but the striata and spinal cord showed no such change. Analgesia was pronounced. Injection of morphine into the region of the nucleus raphe magnus caused analgesia and increased 5-HT turnover in the posterior medulla and the spinal cord. The action on the cord must have been the result of the stimulation of cells in the raphe. The effects of the local injections of morphine on 5-HT turnover were antagonized by systemic naloxone (1-2mg/kg) in all the regions studied. When morphine was administered subcutaneously three times a day for five days, tolerance developed to the analgesic effect of morphine (7mg/kg). However, tolerance to its acceleration of 5-HT turnover was only seen in the spinal cord, not in striatum or anterior and posterior medulla. When morphine was withdrawn, its effects on analgesia and 5-HT turnover in the spinal cord recovered simultaneously. The results emphasize the likely part played by the descending serotoninergic pathway in the analgesic effect of morphine.

Original languageEnglish (US)
Pages (from-to)1215-1225
Number of pages11
JournalNeuroscience
Volume7
Issue number5
DOIs
StatePublished - May 1982

Fingerprint

Analgesia
Morphine
Serotonin
Spinal Cord
Injections
Analgesics
Probenecid
Pain Threshold
Naloxone
Acids
Brain

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Analgesia, development of tolerance, and 5-hydroxytryptamine turnover in the rat after cerebral and systemic administration of morphine. / Vasko, M. R.; Vogt, M.

In: Neuroscience, Vol. 7, No. 5, 05.1982, p. 1215-1225.

Research output: Contribution to journalArticle

@article{94ed4e465cc24b8384ec4a01866374b1,
title = "Analgesia, development of tolerance, and 5-hydroxytryptamine turnover in the rat after cerebral and systemic administration of morphine",
abstract = "Morphine HCl (10 μ/0.5 μl) was injected into the right striatum, the caudal aqueduct and the region of the nucleus raphe magnus of the rat. Turnover of 5-hyrdroxytryptamine (5-HT) in the brain was assessed by fluorimetric estimation of 5-hydroxyindol-3-ylacetic acid following the administration of probenecid. Injection into the right striatum (a region containing 5-HT terminals) increased 5-HT turnover in the right, but not in the left striatum or in the anterior medulla. The pain threshold was unaltered. Injection into the aqueduct accelerated 5-HT turnover in the anterior medulla, but the striata and spinal cord showed no such change. Analgesia was pronounced. Injection of morphine into the region of the nucleus raphe magnus caused analgesia and increased 5-HT turnover in the posterior medulla and the spinal cord. The action on the cord must have been the result of the stimulation of cells in the raphe. The effects of the local injections of morphine on 5-HT turnover were antagonized by systemic naloxone (1-2mg/kg) in all the regions studied. When morphine was administered subcutaneously three times a day for five days, tolerance developed to the analgesic effect of morphine (7mg/kg). However, tolerance to its acceleration of 5-HT turnover was only seen in the spinal cord, not in striatum or anterior and posterior medulla. When morphine was withdrawn, its effects on analgesia and 5-HT turnover in the spinal cord recovered simultaneously. The results emphasize the likely part played by the descending serotoninergic pathway in the analgesic effect of morphine.",
author = "Vasko, {M. R.} and M. Vogt",
year = "1982",
month = "5",
doi = "10.1016/0306-4522(82)91128-9",
language = "English (US)",
volume = "7",
pages = "1215--1225",
journal = "Neuroscience",
issn = "0306-4522",
publisher = "Elsevier Limited",
number = "5",

}

TY - JOUR

T1 - Analgesia, development of tolerance, and 5-hydroxytryptamine turnover in the rat after cerebral and systemic administration of morphine

AU - Vasko, M. R.

AU - Vogt, M.

PY - 1982/5

Y1 - 1982/5

N2 - Morphine HCl (10 μ/0.5 μl) was injected into the right striatum, the caudal aqueduct and the region of the nucleus raphe magnus of the rat. Turnover of 5-hyrdroxytryptamine (5-HT) in the brain was assessed by fluorimetric estimation of 5-hydroxyindol-3-ylacetic acid following the administration of probenecid. Injection into the right striatum (a region containing 5-HT terminals) increased 5-HT turnover in the right, but not in the left striatum or in the anterior medulla. The pain threshold was unaltered. Injection into the aqueduct accelerated 5-HT turnover in the anterior medulla, but the striata and spinal cord showed no such change. Analgesia was pronounced. Injection of morphine into the region of the nucleus raphe magnus caused analgesia and increased 5-HT turnover in the posterior medulla and the spinal cord. The action on the cord must have been the result of the stimulation of cells in the raphe. The effects of the local injections of morphine on 5-HT turnover were antagonized by systemic naloxone (1-2mg/kg) in all the regions studied. When morphine was administered subcutaneously three times a day for five days, tolerance developed to the analgesic effect of morphine (7mg/kg). However, tolerance to its acceleration of 5-HT turnover was only seen in the spinal cord, not in striatum or anterior and posterior medulla. When morphine was withdrawn, its effects on analgesia and 5-HT turnover in the spinal cord recovered simultaneously. The results emphasize the likely part played by the descending serotoninergic pathway in the analgesic effect of morphine.

AB - Morphine HCl (10 μ/0.5 μl) was injected into the right striatum, the caudal aqueduct and the region of the nucleus raphe magnus of the rat. Turnover of 5-hyrdroxytryptamine (5-HT) in the brain was assessed by fluorimetric estimation of 5-hydroxyindol-3-ylacetic acid following the administration of probenecid. Injection into the right striatum (a region containing 5-HT terminals) increased 5-HT turnover in the right, but not in the left striatum or in the anterior medulla. The pain threshold was unaltered. Injection into the aqueduct accelerated 5-HT turnover in the anterior medulla, but the striata and spinal cord showed no such change. Analgesia was pronounced. Injection of morphine into the region of the nucleus raphe magnus caused analgesia and increased 5-HT turnover in the posterior medulla and the spinal cord. The action on the cord must have been the result of the stimulation of cells in the raphe. The effects of the local injections of morphine on 5-HT turnover were antagonized by systemic naloxone (1-2mg/kg) in all the regions studied. When morphine was administered subcutaneously three times a day for five days, tolerance developed to the analgesic effect of morphine (7mg/kg). However, tolerance to its acceleration of 5-HT turnover was only seen in the spinal cord, not in striatum or anterior and posterior medulla. When morphine was withdrawn, its effects on analgesia and 5-HT turnover in the spinal cord recovered simultaneously. The results emphasize the likely part played by the descending serotoninergic pathway in the analgesic effect of morphine.

UR - http://www.scopus.com/inward/record.url?scp=0019985526&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019985526&partnerID=8YFLogxK

U2 - 10.1016/0306-4522(82)91128-9

DO - 10.1016/0306-4522(82)91128-9

M3 - Article

C2 - 6180353

AN - SCOPUS:0019985526

VL - 7

SP - 1215

EP - 1225

JO - Neuroscience

JF - Neuroscience

SN - 0306-4522

IS - 5

ER -