Adrenalectomy: Its effects on systemic tryptophan metabolism in normal and protein malnourished rats

Miller, Maravene; Hasson, Rachelle; Morgane, Peter J.; Resnick, Oscar

doi:10.1016/s0361-9230(80)80015-3

Cited by 9 publications

(4 citation statements)

References 45 publications

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“…However, other than being smaller there were no adverse effects associated with this severe malnutrition such as increased mortality. This corresponds to previous reports that show 8% protein diet-fed dams displayed lactational deficiency resulting in reduced postnatal growth and modulated peripheral metabolism, but no other overt symptoms of malnutrition as generated by lower protein levels (Resnick et al, 1982;Miller et al, 1980;Gabr, 1981). Resnick (Resnick et al, 1982) concluded that the 8% protein model is useful for studying "hidden" forms of malnutrition in man (Resnick et al, 1982).…”

Section: Discussionsupporting

confidence: 88%

Developmental programming of appetite and growth in male rats increases hypothalamic serotonin (5-HT)5A receptor expression and sensitivity

et al. 2020

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Background: Though it is well established that neonatal nutrition plays a major role in lifelong offspring health, the mechanisms underpinning this have not been well defined. Early postnatal accelerated growth resulting from maternal nutritional status is associated with increased appetite and body weight. Likewise, slow growth correlates with decreased appetite and body weight. Food consumption and food-seeking behaviour are directly modulated by central serotonergic (5-hydroxytryptamine, 5-HT) pathways. This study examined the effect of a rat maternal postnatal low protein (PLP) diet on 5-HT receptor mediated food intake in offspring. Methods: Microarray analyses, in situ hybridization or laser capture microdissection of the ARC followed by RT-PCR were used to identify genes up-or down-regulated in the arcuate nucleus of the hypothalamus (ARC) of 3-month-old male PLP rats. Third ventricle cannulation was used to identify altered sensitivity to serotonin receptor agonists and antagonists with respect to food intake. Results: Male PLP offspring consumed less food and had lower growth rates up to 3 months of age compared to Control offspring from dams fed a normal diet. 97 genes were upregulated (including the 5-HT5A receptor (5-HT5AR) and 149 downregulated genes in PLP rats compared to Controls. The former obesity medication fenfluramine and the 5-HT receptor agonist 5-Carboxamidotryptamine (5-CT) significantly suppressed food intake in both groups, but the PLP offspring were more sensitive to d-fenfluramine and 5-CT compared to Controls. The effect of 5-CT was antagonized by the 5-HT5AR antagonist SB699551. 5-CT also reduced NPY-induced hyperphagia in both Control and PLP rats but was more effective in PLP offspring. Conclusions: Postnatal low protein programming of growth in rats enhances the central effects of serotonin on appetite by increasing hypothalamic 5-HT5AR expression and sensitivity. These 4 findings provide insight into the possible mechanisms through which a maternal low protein diet during lactation programs reduced growth and appetite in offspring.

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Section: Discussionsupporting

confidence: 88%

Developmental programming of appetite and growth in male rats increases hypothalamic serotonin (5-HT)5A receptor expression and sensitivity

et al. 2020

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“…In the human, TPH was not detected immunohistochemically in the adrenal cortex (Meyer and Brinck 1999). An interesting connection between adrenal gland and brain 5-HT synthesis was made by Miller et al (1980), who demonstrated that brain tryptophan utilization was determined by the presence or absence of the adrenal gland. GTP cyclohydrolase is present in the adrenal gland, and this makes the tetrahydrobiopterin that is a necessary cofactor of the tyrosine, tryptophan, and phenylalanine hydroxylases (Nagatsu et al, 1995).…”

Section: E 5-hydroxytryptamine Presence and Function In The Adrenal mentioning

confidence: 99%

Serotonin and Blood Pressure Regulation

et al. 2012

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“…Indeed it has been suggested, that the HPA axis changes observed in depression may represent a 'natural antidepressant response' (Young, 1994). However, corticosterone has also been shown in previous studies to regulate 5-HT synthesis (Rastogi and Singhal, 1978;Miller et al, 1980;Culman et al, 1984) and may have other effects on 5-HT neurotransmission (see Chaouloff, 2000).…”

Section: Introductionmentioning

confidence: 97%

Altered Glucocorticoid Rhythm Attenuates the Ability of a Chronic SSRI to Elevate Forebrain 5-HT: Implications for the Treatment of Depression

Gartside

Leitch

Young

2003

Neuropsychopharmacol

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Both glucocorticoids and selective serotonin reuptake inhibitors (SSRIs) alter aspects of 5-HT function including somatodendritic 5-HT 1A autoreceptor sensitivity. Many depressed patients prescribed SSRIs have pre-existing flattened diurnal gluococorticoid rhythm. In these patients, interactions between flattened glucocorticoid rhythm and chronic SSRIs, which impact on the SSRI's ability to elevate forebrain 5-HT, may alter clinical efficacy. To address this issue rats underwent implantation of slow-release corticosterone (75 mg pellet s.c.) (to flatten the glucocorticoid rhythm) or sham surgery, and injection of fluoxetine (10 mg/kg/day i.p., 12 days) or vehicle. Using microdialysis in the frontal cortex we found that (21 h after the last injection) extracellular 5-HT was elevated in fluoxetine-or corticosterone-treated animals, but not in those treated with corticosterone plus fluoxetine. In fluoxetine-treated animals, blockade of terminal reuptake by local perfusion of fluoxetine increased 5-HT to the same level as it did in controls, suggesting normal terminal 5-HT release after chronic fluoxetine. However, 5-HT levels following local reuptake blockade in both the corticosterone and corticosterone plus fluoxetine groups were lower than controls, suggesting a corticosterone-induced decrease in terminal release. Finally in fluoxetine, corticosterone, and corticosterone plus fluoxetine groups, there was marked 5-HT 1A receptor desensitization, evidenced by attenuation of the decrease in 5-HT release following systemic fluoxetine injection. The data indicate that, despite desensitization of 5-HT 1A autoreceptors, concurrent flattened glucocorticoid rhythm compromises the ability of SSRIs to elevate forebrain 5-HT. These findings suggest a potential mechanism for the reduced antidepressant efficacy of SSRIs in those patients with pre-existing glucocorticoid abnormalities.

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Adrenalectomy: Its effects on systemic tryptophan metabolism in normal and protein malnourished rats

Cited by 9 publications

References 45 publications

Developmental programming of appetite and growth in male rats increases hypothalamic serotonin (5-HT)5A receptor expression and sensitivity

Developmental programming of appetite and growth in male rats increases hypothalamic serotonin (5-HT)5A receptor expression and sensitivity

Serotonin and Blood Pressure Regulation

Altered Glucocorticoid Rhythm Attenuates the Ability of a Chronic SSRI to Elevate Forebrain 5-HT: Implications for the Treatment of Depression

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