pituitrin has been researched along with Mood-Disorders* in 3 studies
2 review(s) available for pituitrin and Mood-Disorders
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Vasopressin in health and disease with a focus on affective disorders.
The therapies of mood and anxiety disorders are not solved, because current antidepressants have delayed onset of therapeutic action and a significant number of patients are non-responsive. Research on the field was leaning towards neuropeptides as therapeutic targets. Vasopressin (VP) is a hot candidate, as beyond its peripheral actions VP is implicated in interneuronal communication and modulates the hypothalamo-pituitary-adrenal (HPA), the key stress axis, as well as behavioural functions. Affective disorders are stress related disorders and the most frequently occurring abnormality in depressed subjects is hyperactivity of the HPA. VP with nucleus paraventricularis hypothalami origin is a direct adrenocorticotrophin secretagogue through its V1b receptor. VP seems to have special importance under prolonged stress conditions, which are known to be strong predictive factor of depressive disorder and can induce depressive-like symptoms. Preclinical and clinical data summarized in this review underline the importance of VP in the development of anxiety- and depressive-like symptoms. Orally active nonpeptiderg V1b antagonists were developed and seemed to have effective anxiolytic and antidepressant profile in preclinical studies, which was not fully confirmed by clinical observations. It seems that V1a receptors on special brain areas could have same importance. Taken together current knowledge strongly implies an importance of vasopressinergic regulation in affective disorders and consider VP as endogenous anxiogenic/depressogenic substance. However, wide range of side effects could develop as a result of an intervention on the VP system; therefore there is a need for area-specific targeting of VP receptors (e.g. with modified nanoparticles). Topics: Animals; Anti-Anxiety Agents; Antidepressive Agents; Antidiuretic Hormone Receptor Antagonists; Anxiety; Anxiety Disorders; Depression; Depressive Disorder; Diabetes Insipidus; Disease Models, Animal; Humans; Hypothalamo-Hypophyseal System; Inappropriate ADH Syndrome; Mice; Mice, Inbred BALB C; Mice, Knockout; Molecular Targeted Therapy; Mood Disorders; Pituitary-Adrenal System; Rats; Rats, Brattleboro; Rats, Mutant Strains; Receptors, Vasopressin; Stress, Psychological; Vasopressins | 2012 |
Interaction of prefrontal cortical and hypothalamic systems in the pathogenesis of depression.
Topics: Anorexia; Arousal; Brain Mapping; Circadian Rhythm; Corticotropin-Releasing Hormone; Depression; Glucocorticoids; Humans; Hydrocortisone; Hypothalamic Hormones; Hypothalamo-Hypophyseal System; Hypothalamus; Magnetic Resonance Imaging; Models, Neurological; Models, Psychological; Mood Disorders; Neuropsychological Tests; Neurotransmitter Agents; Oxytocin; Paraventricular Hypothalamic Nucleus; Phototherapy; Pituitary-Adrenal System; Prefrontal Cortex; Receptors, Glucocorticoid; Receptors, Neurotransmitter; Sleep Initiation and Maintenance Disorders; Stress, Physiological; Stroke; Thyroid Gland; Tomography, Emission-Computed; Tomography, Emission-Computed, Single-Photon; Vasopressins | 2000 |
1 other study(ies) available for pituitrin and Mood-Disorders
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Vasopressin mediates the response of the combined dexamethasone/CRH test in hyper-anxious rats: implications for pathogenesis of affective disorders.
To investigate the neuroendocrine alterations linked to inborn emotionality in two Wistar rat lines selectively bred for either high (HAB) or low (LAB) anxiety-related behavior, we administered the combined dexamethasone (DEX)/corticotropin-releasing hormone (CRH) test. DEX (12:00 M. (noon); 30 microg/kg) resulted in a significantly less efficient suppression of the diurnal increase in the circulating corticotropin (ACTH) levels in the male HAB rats than in the male LAB rats. In addition, plasma ACTH and corticosterone responses to subsequent CRH (7:30 P.M.; 50 ng/kg) were significantly higher in male HAB rats. The rise in ACTH after CRH in the DEX-pretreated male HAB rats points toward an enhanced activity and involvement of endogenous vasopressin synthesized in the hypothalamic paraventricular nucleus (PVN) and acting at pituitary corticotrope cells. We tested this hypothesis by in situ hybridization and in vivo microdialysis, and found an increase in both basal synthesis and release of vasopressin within the PVN of the male HAB rats. As expected, pretreatment with a selective vasopressin type 1 receptor antagonist abolished the CRH-stimulated increase in ACTH secretion in the DEX-pretreated male HAB rats. The results indicate that vasopressin-mediated effects are critically involved in the profound disturbance of the hypothalamic-pituitary-adrenocortical system in male HAB rats, thus revealing striking parallels to the neuroendocrine situation in human depression. Topics: Adrenalectomy; Adrenocorticotropic Hormone; Animals; Antidiuretic Hormone Receptor Antagonists; Anxiety; Binding Sites; Corticosterone; Corticotropin-Releasing Hormone; Dexamethasone; Feedback; Glucocorticoids; Immunohistochemistry; In Situ Hybridization; Male; Mood Disorders; Paraventricular Hypothalamic Nucleus; Radioimmunoassay; Rats; Receptors, Glucocorticoid; Receptors, Mineralocorticoid; RNA, Messenger; Sex Characteristics; Vasopressins | 2002 |