Titlebook: Signal Transduction in Affective Disorders; Hiroki Ozawa (Instructor),Toshikazu Saito (Profess Conference proceedings 1998 Springer-Verlag

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In Vivo Investigations of Signal-Transduction Systems in Affective Disorders by Magnetic Resonance iving human organs. The nuclei of many species of atoms, such as .H, .Li, and .P, have magnetic properties and can be used for in vivo MRS. Because the principles of MRS are complicated and not easily summarized, only a brief introduction is given here. For details, see other review articles (Nasral

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Stress and BDNF Signal Transduction: Implications for Stress-Related Psychiatric Disorders,sis of depression and PTSD. In support of this hypothesis, basic research studies have demonstrated that chronic stress causes atrophy or, in extreme cases, death of hippocampal neurons in rats and nonhuman primates.

receptors

Participation of Cytoskeletal Elements in Neuronal Signal Transduction: New Insight into the Molecunical efficacy of these drugs (Zemlan and Garver 1990). Furthermore, neuroleptic drugs such as amphetamine and cocaine that block reuptake or catabolism of monoamines do not have an antidepressant effect. Thus, an acute neurochemical effect of antidepressant drugs may not account for the mechanism of action of these drugs.

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Effects of Antidepressants on Transmembrane Signaling,transmission are inconsistent with the delayed onset of their clinical efficacy (Zelman and Garver 1990). Moreover, some monoamine reuptake inhibitors, such as cocaine, do have not an antidepressant effect.

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Immunological Aspects of Mood Disorders: Interaction Between Cytokines and Intracellular Calcium Sih there is not sufficient evidence to support interactions between psychological phenomena and immune function. Here we consider the pathophysiology of mood disorders in regard to immune function and demonstrate the importance of intracellular calcium (Ca.) signaling as a possible factor that associ

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The Role of G Proteins in the Pathophysiology and Treatment of Affective Disorders,Hence, one might assume that there is a close relationship between G protein as the protein molecule in the on-off signal switching and manic-depressive illness (Fig. 1). Since the amine hypothesis of manic-depressive illness was proposed, various hypotheses concerning the pathophysiology of this di