Abnormalities of hypothalamic-pituitary-adrenal and hypothalamic-somatotrophic axes in Fawn-Hooded rats

Gómez, Francisca; Graugés, Pilar; López-Calderón, Asunción; Armario, Antonio

doi:10.1530/eje.0.1410290

Cited by 11 publications

(3 citation statements)

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“…Lowered CSF levels of somatostatin, lowered blood levels of somatostatin-like immunoreactivity, or abnormalities in somatostatin gene expression have been associated with depressive mood in patients (Rubinow et al 1983;Dinan 1998;Markou et al 1998) or in animal models of depression (Gomez et al 1999; Abbreviations: POMS ϭ profile of mood states; HDRS ϭ Hamilton depression rating scale; VAS ϭ visual analog scale. a indicates a study including female subjects in which menstrual cycle phase was controlled for.…”

Section: Are There Non-serotonergic Explanations For the Effects Of Rtd?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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Section: Are There Non-serotonergic Explanations For the Effects Of Rtd?mentioning

confidence: 99%

Clinical and Physiological Consequences of Rapid Tryptophan Depletion

Moore

Landolt

Seifritz

et al. 2000

Neuropsychopharmacology

184

121

View full text Add to dashboard Cite

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“…The elevated levels of plasma cortisol are reduced by chronic treatment with the TCAs imipramine and clomipramine, and with the MAO-A inhibitor, clorgyline [88]. FH rats also exhibit reduced growth rate consistent with an abnormality of the hypothalamic-somatotrophic (HSM) axis [89]. FH rats exhibit increased immobility in the forcedswim test in some studies (but not all; see [90,91]) and increased ethanol intake and preference [92].…”

Section: Fawn-hoodedmentioning

confidence: 99%

Animal Models of Depressive Illness: The Importance of Chronic Drug Treatment

Mitchell

Redfern²

2005

CPD

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A wide diversity of animal models has been used to examine antidepressant activity. These range from relatively simple models sensitive to acute treatment, to highly sophisticated models that reputedly model some aspect of depressive illness and which yield a positive response to prolonged, chronic, drug treatment. In recent years antidepressant drug research has focused on the search for antidepressant therapy that has a more rapid onset of action. To be relevant, therefore, animal models must measure the time course of drug action. This review examines the claims of animal models to be sensitive to chronic drug treatment and considers their relevance. First, the review addresses the criteria necessary to examine the validity of animal models of depressive illness. Second, those animal models sensitive to chronic antidepressant treatment are reviewed with respect to their validity as animal models of either depressive illness and/or antidepressant activity. In particular, the development and utility of two "ethologically-relevant" animal models, the resident-intruder and social hierarchy paradigms, are described in detail. These models of rodent social and agonistic behaviour demonstrate that acute and chronic treatment with antidepressant drugs (regardless of their acute pharmacological activity) induce diametrically opposite changes in rodent agonistic behaviour. It is argued that the common ability of chronic treatment to increase rodent aggression (which in turn results in increased hierarchical status in closed social groups) most likely reflects the increased assertiveness and associated externalization of emotions expressed during recovery from depressive illness. Finally, findings that relate observed behavioural changes to underlying neurochemical changes are briefly reviewed.

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“…The elevated levels of plasma cortisol are reduced by chronic treatment with the TCAs imipramine and clomipramine, and with the MAO-A inhibitor clorgyline (Aulakh et al, 1993). FH rats also exhibit reduced growth rate consistent with an abnormality of the hypothalamic-somatotrophic (HSM) axis (Gomez et al, 1999). FH rats exhibit increased immobility in the forced swim test in some studies (but not all; see Hall et al, 1998a;Lahmame et al, 1996) and increased ethanol intake and preference .…”

Section: The Fawn-hooded Strainmentioning

confidence: 99%