5 The Role of Biogenic Agents in the Actions of Centrally-Acting Analgesics

Sewell, Robert David Edmund; Spencer, P.S.

doi:10.1016/s0079-6468(08)70150-4

Cited by 16 publications

(4 citation statements)

References 163 publications

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“…This elevated serotonin level could result in a higher pain threshold (Iversen etal. 1977;Sewell and Spencer 1977;Taber 1981). Elevation of the pain threshold associated with diabetes and hyperglycemia can explain previously reported data on the decline of morphine analgesia in diabetic animals .…”

Section: Discussionmentioning

confidence: 67%

The role of opioid receptors in diabetes and hyperglycemia-induced changes in pain threshold in the rat

Akunne

Soliman

1987

Psychopharmacology

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The role of opioid receptors in diabetes and hyperglycemia-induced analgesia was studied in male Sprague-Dawley rats. Animals maintained under controlled environmental conditions were used in all studies. Pain latency was determined by the hot plate test (55 degrees C) and analgesy-meter force method. The results of these studies indicate that streptozotocin-induced diabetic animals have a significantly higher pain threshold (P less than 0.01) than the control groups. The pain threshold was found to be diurnally controlled with a peak at the beginning of the light phase (1000 hours) and a trough at the end of the dark phase (0800 hours). Diabetes-induced analgesia was found to be reversed by both acute or chronic insulin administration. In another study, glucose-induced hyperglycemic rats were found to have a significantly higher pain threshold (P less than 0.01) than control animals, with a peak occurring at the beginning of the dark phase (2000 hours), and a trough at the beginning of the light phase (0800 hours). The administration of the opioid antagonist naloxone (2 mg/kg) reversed the hyperglycemia and diabetic-induced analgesia. The results of these studies might indicate that analgesia found in diabetic or hyperglycemic animals may be related to the endogenous opioid system.

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Section: Discussionmentioning

confidence: 67%

The role of opioid receptors in diabetes and hyperglycemia-induced changes in pain threshold in the rat

Akunne

Soliman

1987

Psychopharmacology

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“…In contrast to morphine, in vitro studies have revealed that methadone is a potent and pethidine a moderate inhibitor of 5-HT uptake into rabbit brain synaptosomes (Ciofalo, 1974) and human platelets (Ahtee & Saarnivaara, 1973) respectively. Sewell & Spencer (1977) have speculated that the inability of 5-HT uptake inhibitors to potentiate the antinociceptive effect of methadone or pethidine may be due to the fact that 5-HT uptake is partially inhibited by the two analgesics. However, in vivo findings argue against this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

“…There is considerable evidence to suggest that the antinociceptive effect of morphine is dependent upon intact central 5-hydroxytryptaminergic pathways (Messing & Lytle, 1977;Sewell & Spencer, 1977). The elevation of brain content of 5-hydroxytryptamine (5-HT) either by the intracerebroventricular (i.c.v.)…”

Section: Introductionmentioning

confidence: 99%

On the Role of 5‐hydroxytryptamine in Drug‐induced Antinociception

Sugrue

1979

British J Pharmacology

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“…Sewell and Spencer [32] reported that cen tral nervous system (CNS) serotonincrgic neurons are involved in pain responsiveness and/or reactivity. Demonstration that fluo xetine, a highly specific inhibitor of 5-HT uptake [14,35], potentiates morphine analge sia [33] in footshock [26], hot plate [23] and tail flick [21] tests for analgesia in rats arc among the pharmacological evidence that en hancement of serotonincrgic function in creases morphine analgesia.…”

Section: Introductionmentioning

confidence: 99%

Role of 5-Hydroxytryptamine in the Regulation of Brain Neuropeptides in Normal and Diabetic Rat

1986

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The effect of 5-hydroxytryptamine (5-HT) alteration on brain dopamine (DA), norepinephrine (NE), β-endorphin (βE) and immunoreactive insulin (IRI) was studied in Sprague-Dawley diabetic and control rats. Diabetes was induced using alloxan (45 mg/kg), 15 days prior to sacrificing. Both control and diabetic animals were treated with either p-chlorophenylalanine (PCPA, 300 mg/kg) 3 days prior to sacrificing or fluoxetine (10 mg/kg) twice daily for 3 days. PCPA treatment significantly decreased brain content of 5-HT and 5-hydroxyindole acetic acid (5-HIAA) while it caused significant increase and decrease in brain βE and insulin levels, respectively, in both normal and diabetic rat. Meanwhile, the administration of fluoxetine resulted in significant increase in brain content of 5-HT, DA, NE and insulin but significant decline of βE in diabetic and saline control rats. The results of this experiment indicate that 5-HT may be regulating both βE and insulin regardless of the availability of pancreatic insulin.

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5 The Role of Biogenic Agents in the Actions of Centrally-Acting Analgesics

Cited by 16 publications

References 163 publications

The role of opioid receptors in diabetes and hyperglycemia-induced changes in pain threshold in the rat

The role of opioid receptors in diabetes and hyperglycemia-induced changes in pain threshold in the rat

On the Role of 5‐hydroxytryptamine in Drug‐induced Antinociception

Role of 5-Hydroxytryptamine in the Regulation of Brain Neuropeptides in Normal and Diabetic Rat

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