Decreased expression of the mRNA for somatostatin in the periventricular nucleus of depression-model rats

Zhang, Kai; Hamanaka, Kenji; Kitayama, Isao; Soya, Hideaki; Yoshizato, Hideo; Nakase, Shinji; Uesugi, Yuichi; Inui, Koji; Nomura, Junichi; Okazaki, Yuji

doi:10.1016/s0024-3205(99)00326-4

Cited by 9 publications

(7 citation statements)

References 17 publications

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“…Somatostatin is a hormonal peptide that inhibits immune cell function [8,9]. Interestingly, clinical and experimental data point to decreased concentrations of the CSFsomatostatin-like immunoreactivity in induced stress models [10,11] as well as depression [3,4]. Since the biological half life of somatostatin extends only over a few minutes [12]; accordingly, it became the objective of the current investigation to explore the potential utility of the synthetic somatostatin analogue, octreotide, in alleviating depressive symptoms associated with exposure to different chronic stressful conditions.…”

Section: Abbreviationsmentioning

confidence: 99%

Effects of Octreotide in Chronically Mild Stressed Rats: Possible Role of Immune and Oxidative Stress Pathways

Schaalan

Nassar

2011

Neurochem Res

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Impairment of neuroendocrine, immune and antioxidant defenses contribute to pathophysiology of stress-induced depression. Somatostatin executes diverse regulatory effects on endocrine, exocrine and neural functions; however, the possibility that octreotide, a synthetic somatostatin analogue might mitigate stress-induced depression remains elusive. Hence, the current study aimed to explore the immunomodulatory and antioxidant effects of octreotide in a model of chronic mild stress (CMS). This paradigm was performed by exposing rats to a combination of mild unpredictable stressors for 21 days. Fifty male Wistar rats were divided into five groups; (1) control receiving saline, (2) octreotide given to normal unstressed animals. The remaining three groups were subjected to (3) CMS alone or in combination with octreotide (4) 50 μg/kg or (5) 90 μg/kg. Octreotide increased sucrose preference index and attenuated CMS-induced increases in plasma adrenocorticotrophic hormone and corticosterone levels. In addition, octreotide decreased plasma tumor necrosis factor-alpha concentration. Moreover, it prevented CMS-induced oxidative damage by enhancing the antioxidant defenses superoxide dismutase, glutathione reductase and glutathione in the hippocampus. Furthermore, octreotide normalized the elevated malondialdehyde and lactate dehydrogenase levels in the hippocampus. These results demonstrate a possible antidepressant-like activity of octreotide in CMS due to its antioxidant/antiinflammatory aptitude.

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Section: Abbreviationsmentioning

confidence: 99%

Effects of Octreotide in Chronically Mild Stressed Rats: Possible Role of Immune and Oxidative Stress Pathways

Schaalan

Nassar

2011

Neurochem Res

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“…Mathe 1999;Zhang et al 1999;Holmes et al 1998;Heuser et al 1998). Therefore, somatostatin may be a peptide whose synthesis mediates the depressioninducing effects of RTD.…”

Section: %mentioning

confidence: 99%

Clinical and Physiological Consequences of Rapid Tryptophan Depletion

Moore

Landolt

Seifritz

et al. 2000

Neuropsychopharmacology

184

121

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We review here the rapid tryptophan depletion (RTD) methodology and its controversial association with depressive relapse. RTD has been used over the past decade to deplete serotonin (5-hydroxy-tryptamine, or 5-HT) in humans and to probe the role of the central serotonin system in a variety of psychiatric conditions. Its current popularity was stimulated by reports that RTD reversed the antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors (MAOIs) KEY WORDS : 5-HT; Serotonin; Tryptophan-free drink; Major depressionSerotonin (5-hydroxy-tryptamine, or 5-HT) is involved in many physiologic and behavioral systems and clinical disease states. Much of the information available on the function of serotonin comes from pharmacological agents which mimic or amplify endogenous serotonergic neurotransmission, such as serotonin agonists or SSRIs. Historically, methods to functionally deplete serotonin have been problematic. Even previous approaches that have been moderately successful in experimental animals -such as the 5-HT synthesis inhibitor, parachloro-phenylalanine (PCPA); the neurotoxin 5-6-dihydroxy-tryptamine; or various lesions to the serotonergic raphe nuclei of the brainstem -have been non-specific, rife with secondary effects, or clearly inapplicable to humans (e.g., Engelman et al. 1967;Koella et al. 1968;Jouvet et al. 1967). The advent of rapid tryptophan depletion (RTD) as a method to deplete central serotonin has been met with enthusiasm because of its reversibil- NO . 6 ity, its relative lack of side effects, and its merit in elucidating the pathophysiology of various psychiatric conditions. This paper reviews the RTD methodology and its reported ability to induce a depressive relapse in euthymic patients, and other physiological and clinical effects. RAPID TRYPTOPHAN DEPLETION Availability of Tryptophan and Serotonin SynthesisRTD is based on the current understanding of the 5-HT biosynthetic pathway, in which the first step is generally considered to be the rate-limiting one. The first step entails the hydroxylation of the amino acid TRP (by the enzyme TRP hydroxylase, or TRP-H) into the intermediate product 5-hydroxy-tryptophan, or 5-HTP. 5-HTP is then decarboxylated into 5-HT. Under normal conditions, TRP-H is about 50% saturated with TRP. Increasing or decreasing the availability of TRP correlates highly with the amount of 5-HT produced (e.g., Lin et al. 1969;Schaechter and Wurtman 1990). Because the body cannot synthesize TRP, reducing dietary intake of TRP reduces TRP levels in plasma and diminishes its transport from plasma into the brain.In humans, TRP depletion is accomplished by consuming a TRP-free amino acid drink (e.g., Delgado et al. 1990;Biggio et al. 1974). This drink contains 15 amino acids in the same proportion as in human milk, except that TRP, aspartic acid, and glutamic acid are omitted (see Table 1). Within a matter of hours (4 to 12), plasma TRP declines to 10-50% of baseline levels (Delgado et al. 1990(Delgado et al. , 199...

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“…There is also indirect evidence that somatostatin may be involved in emotional processes such as anxiety and depression (e.g., Viollet et al 2000;Fendt et al 1996;Gheorvassaki et al 1992;Pallis et al 2006Pallis et al , 2007Pallis et al , 2009Zhang et al 1999), although none of these studies has directly stimulated somatostatin function in the brain and documented the outcome in pharmacologically validated animal models of anxiety or depression (see general "Discussion"). Recently, we showed intracerebroventricular (i.c.v.)…”

Section: Introductionmentioning

confidence: 99%

Anxiolytic and antidepressant actions of somatostatin: the role of sst2 and sst3 receptors

Engin

Treit

2009

Psychopharmacology

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Decreased expression of the mRNA for somatostatin in the periventricular nucleus of depression-model rats

Cited by 9 publications

References 17 publications

Effects of Octreotide in Chronically Mild Stressed Rats: Possible Role of Immune and Oxidative Stress Pathways

Effects of Octreotide in Chronically Mild Stressed Rats: Possible Role of Immune and Oxidative Stress Pathways

Clinical and Physiological Consequences of Rapid Tryptophan Depletion

Anxiolytic and antidepressant actions of somatostatin: the role of sst2 and sst3 receptors

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