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

Kolta, Malak G.; Soliman, Karam F.A.; Williams, Byron B.

doi:10.1159/000180298

Cited by 22 publications

(14 citation statements)

References 29 publications

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“…Furthermore, in streptozotocin-treated rats, a decrease in fl-endorphin content in the hypothalamus and neurointermediate lobe of the pituitary has been reported (Forman et al 1985(Forman et al , 1986. A similar decrease in brain content of fl-endorphin has also been reported in alloxan-induced diabetes (Kolta et al 1986). Therefore, attentuation of the naloxone response observed in our study in streptozot0cin-treated animals can be explained on the basis of a decrease in the level of endogenous opioid peptides.…”

Section: Discussionmentioning

confidence: 59%

The hyperalgesic effect of naloxone is attenuated in streptozotocin-diabetic mice

et al. 1989

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In mice with streptozotocin-induced hyperglycemia, nociception was tested after naloxone administration in hot plate and tail immersion tests. The choice of these two tests was to include a supra-spinal nociceptive reflex indicative of higher cognitive process (hot-plate test) as well as a reflex which predominantly represents lower spinal motor mechanisms (tail immersion test). Naloxone-induced hyperalgesia was attenuated in both tests in mice with streptozotocin-induced diabetes. In mice with hyperglycemia induced by intraperitoneal dextrose administration, naloxone hyperalgesia was significantly enhanced in the hot plate test. The basal nociceptive threshold in streptozotocin-treated animals was decreased in the immersion but not in the hot plate test. These results indicate that hyperglycemia per se does not adequately explain the changes in naloxone hyperalgesia in experimental models of diabetes. They also suggest that acute hyperglycemia may modify the interaction of endogenous opioid peptides with their receptors only at supra-spinal sites. However, chronic hyperglycemia appears to affect endogenous opioid peptides both at spinal and supra-spinal levels and their interaction with the opiate receptors.

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Section: Discussionmentioning

confidence: 59%

The hyperalgesic effect of naloxone is attenuated in streptozotocin-diabetic mice

et al. 1989

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“…Moreover, it is well known that feeding of a carbohydrate-rich diet is associated with an increase in the brain level of 5HT (Crandall and Fernstrom 1980;Chiel and Wurtman 1981). Previously, we have found that induction of diabetes in the rat was associated with an elevated brain 5HT level (Kolta et al 1986). The potentiating effect of sympathomimetic amines such as d-amphetamine on opioid antinociceptive activity has been observed in mice (Dewey et al 1970) and humans (Forrest et al 1977).…”

Section: Discussionmentioning

confidence: 85%

“…More recently, the alpha adrenergic agonist clonidine and morphine were shown to potentiate each other in the mouse tail flick test (Spaulding et al 1979). There is also evidence that an elevated level of 5HT is associated with the release offl-endorphin (Kolta et al 1986;Soliman et al 1986). Accumulation and release of antagonistic peptides in the brain, such as ACTH and MStt, might play an important role in the mechanism of opiate tolerance and withdrawal syndrome (Gessa et al 1983).…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemic suppression of morphine withdrawal signs in the rat

Akunne

Soliman

1988

Psychopharmacology

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Male Sprague-Dawley rats maintained under controlled lighting and temperature conditions were used in this experiment. Morphine dependency was induced by giving increasing doses of morphine by intraperitoneal injection (IP group) or by the ingestion of morphine through drinking water (PO group). Animals were injected with 10, 20, 30 and 50 mg/kg morphine sulfate at days 1, 2, 3 and 4, respectively. Another group of animals received increasing concentrations of morphine through drinking water from 0.1, 0.2, 0.3 to 0.4 mg/ml at 48 h intervals. Morphine dependent animals were given naloxone by the intraperitoneal route to precipitate withdrawal. Glucose (3 g/kg or 10 g/kg) was given 10 min prior to the administration of naloxone to the respective groups. Another two groups of animals were made diabetic by the administration of streptozotocin. In one group, animals received increasing concentrations of 10, 20, 30 and 50 mg/kg morphine sulfate by the IP route at days 1, 2, 3 and 4, while the other group was not treated with morphine but was assessed for withdrawal signs to serve as the control. Withdrawal signs were assessed by observing the presence of diarrhea, tremor, piloerection, hunchbacked posture, teeth chattering, salivation, erection, restless activity, territorial exploring, irritability to handling, vocalization and jumping. Results obtained indicate that glucose administration at 10 g/kg abolished most of the withdrawal signs, and we were unable to induce the same degree of morphine dependency in diabetic animals as compared to the non-diabetic groups. It was concluded from this study that hyperglycemia could suppress morphine withdrawal signs.

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“…Diabetes mellitus is accompanied by several psychicontent of their metabolites, and alterations in monoamine receptor density have been reported (Crandall et al, 1981;Lozovsky et aI., 1981;Trulson and Himmel, 1985;Kolta et al, 1986;Trulson et al, 1986;Bitar and Desouza, 1990;Salkovié and Lackovié, 1992). Changes are restricted to a few brain regions, often seen in the striatum and the hypothalamus, with different time courses of appearance (Bitar et al, 1985;Chu et al, 1986;Oliver et al, 1989;Salkovié and Lackovié, 1992;Ramakrishnan and Namasivayam, 1995).…”

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confidence: 96%

Monoamine Transporter Gene Expression in the Central Nervous System in Diabetes Mellitus

Petrišić

Augood²,

Bicknell

1997

Journal of Neurochemistry

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Diabetic animals exhibit altered neurotransmission in brain monoaminergic systems. By means of in situ hybridization, we have investigated the expression of dopamine, noradrenaline, and serotonin transporter (DA-T, NA-T, and 5-HT-T, respectively) mRNAs in the brains of alloxan-and streptozotocin-diabetic rats. The expression of DA-T mANA is decreased in 1-(-11%) and 4-(-17%) week alloxan-diabetic and 4-(-9%) and 8-20%) week streptozotocin-diabetic rats in the ventral medial bundle. The expression of NA-T mRNA is decreased in the locus coeruleus of 8-(-26%) week streptozotocin-diabetic rats, in the noradrenergic Al cell group of 4-(-27%) week alloxan-and 8-(-25%) week streptozotocin-diabetic rats, and in the noradrenergic A2 cell group of 1-(-21%) and 4-(-28%) week alloxan-diabetic and 4-(-27%) and 8-(-25%) week streptozotocin-diabetic animals. The expression of 5-HT-T mRNA in the dorsal raphe nucleus is increased in 1-(+14%) and 4-(+44%) week alloxan-and 4-(+28%) and 8-(-i-44%) week streptozotocin-diabetic rats. The expression of each of the three monoamine transporter genes may be differentially regulated in diabetes and dependent on the duration of diabetes. Altered monoamine transporter gene expression may possibly contribute to the observed dysfunctions in brain monoamine transmission in chronic diabetes.

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

Cited by 22 publications

References 29 publications

The hyperalgesic effect of naloxone is attenuated in streptozotocin-diabetic mice

The hyperalgesic effect of naloxone is attenuated in streptozotocin-diabetic mice

Hyperglycemic suppression of morphine withdrawal signs in the rat

Monoamine Transporter Gene Expression in the Central Nervous System in Diabetes Mellitus

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