PubMed Health⌕ Search

PubMed · 8072375

Duodenum is not a consistent source of melatonin in rats.

Abstract

Markedly increased melatonin levels in plasma have been observed in response to tryptophan administration. This post-tryptophan melatonin increase has been attributed to the duodenum. Because extra-pineal sources of melatonin may be important in interpreting the meaning of altered melatonin production observed in patient populations, this work was undertaken to confirm whether melatonin is produced in the duodenum and to know whether the duodenum need be considered when investigating the circadian control of melatonin production. We measured melatonin in rat duodenum by HPLC both under basal conditions and following tryptophan load. No melatonin was observed in duodenum under conditions of 2.5 ng/g measurement limits. Neither was there any evidence found for the melatonin precursor N-acetylserotonin. Treatment with N-acetylserotonin resulted in increased melatonin content in the pineal gland, but no evidence for melatonin in the duodenum. In vitro incubation of duodenum tissue with 5-hydroxytryptophan, 5-methoxytryptophan, or N-acetylserotonin revealed no detectable melatonin synthesis, and incubation with melatonin revealed no detectable melatonin degradation. The lack of confirmation of melatonin content and the lack of either synthetic or degradative enzyme activity in duodenum tissue suggest that melatonin production from duodenum need not be considered in human or animal studies of melatonin production.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

G L Brammer. 1994. Duodenum is not a consistent source of melatonin in rats.. https://doi.org/10.1016/0024-3205(94)00561-3

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Dihydropteridine reductase deficiency: levodopa's long-term effectiveness without dyskinesia.

We report an adult patient lacking endogenous synthesis of monoamines (dopamine, serotonin, and catecholamines) due to a severe dihydropteridine reductase (DHPR) deficiency. With levodopa and 5-hydroxytryptophan (5HTP) supplementation, the patient exhibited moderate mental retardation, acute episodes of parkinsonism, and episodes of depression. Despite the use of levodopa from age 3 months, he exhibited no dyskinesia or dopaminergic cell loss as suggested by normal PET imaging of the dopamine transporter.

5-Hydroxytryptophan↗

Anxiolytic effect of serotonin depletion in the novelty-induced hypophagia test.

RATIONALE: Relatively little is known about the neural mechanisms underlying anxiety in the novelty-induced hypophagia test, the only known anxiety test that is responsive to chronic but not acute or subchronic antidepressant treatment. OBJECTIVES: The goal of the present experiment was to characterize the role of serotonin in the ability of novelty to suppress feeding. MATERIALS AND METHODS: Pair-housed male Sprague-Dawley rats were trained to eat graham cracker crumbs individually in their home cage (15 min/day). After stable daily intakes were obtained, the animals were depleted of serotonin using 4-chloro-DL -phenylalanine (150 mg kg(-1) day(-1) x 2 days). Forty-eight hours later, central serotonin was restored by the administration of the peripheral L -aromatic amino acid decarboxylase inhibitor, benserazide (10 mg/kg), followed 15 min later with the immediate precursor of serotonin, 5-hydroxy-L -tryptophan (30 mg/kg). Thirty minutes later, the animals were given access to graham cracker crumbs in a novel environment. RESULTS: The animals demonstrated increased latencies to approach the food and reduced food intake in the novel environment. This effect was attenuated by serotonin depletion. Repletion of central serotonin restored the inhibitory response to novelty. The analysis of serotonin content in different brain regions confirmed that serotonin was depleted by greater than 90%, whereas the repletion treatment resulted in serotonin levels similar to nondepleted animals. CONCLUSIONS: Acute depletion of serotonin acts to reduce anxiety behavior as measured by an inhibitory anxiety response during exposure to novel stimuli. These findings are in agreement with the proposed general role for serotonin in behavioral inhibition and that reductions of serotonin facilitate the adoption of more active coping responses to stress.

5-Hydroxytryptophan↗

Altered levels of serotonin in lymphoblasts derived from migraine patients.

We previously reported that dysfunctions in the autonomic nervous systems of patients with migraines occur not only in the brain, but throughout the whole body. Serotonin and neuropeptides are also known to have important roles in the pathophysiology of migraine. With this background in mind, we analyzed human lymphoblast cell lines from migraine with aura (MwA) patients to investigate the pathophysiology of migraine. The characteristics of these lymphoblasts and the involvement of the lymphoblasts in serotonin metabolism were examined. The lymphoblasts expressed serotonin receptors as well as some enzymes related to serotonin metabolism. The serotonin level in the MwA lymphoblasts was higher than that in the control cells. However, serotonin uptake into the lymphoblasts in MwA patients was similar to that in the control subjects. These findings suggest that lymphoblasts in MwA patients have altered levels of serotonin metabolism. Moreover, we propose that this lymphoblast cell system could serve as a novel modality for migraine research.

5-Hydroxytryptophan↗