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Titlebook: Anxiety and Anxiolytic Drugs; Florian Holsboer,Andreas Ströhle Book 2005 Springer-Verlag Berlin Heidelberg 2005 Anxiety.Anxiolytic Drugs.N

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楼主: Opiate
发表于 2025-4-1 04:36:41 | 显示全部楼层
Neuroendocrine Aspects of PTSD,erations in PTSD and highlight alterations relevant to the identification of targets for drug development. Most studies demonstrate alterations consistent with an enhanced negative feedback inhibition of cortisol on the pituitary, an overall hyperreactivity of other target tissues (adrenal gland, hy
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Anxiety Disorders: Clinical Presentation and Epidemiology,owledge is largely related to the classification of anxiety disorders as presented by the Diagnostic and Statistical Manual of Mental Disorders since its third revision (DSM-III). Without going into detail into the history of the classification of anxiety disorders and into the history and developme
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New Pharmacological Treatment Approaches for Anxiety Disorders,s including evolving techniques of genomics and proteomics will generate new drug targets. Drug development design will generate new pharmacological substances with specific action at specific neurotransmitter and neuropeptide receptors or affecting their reuptake and metabolism. New anxiolytic drug
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Pharmacogenomics,uch disorders. For example, pharmacokinetic aspects of antidepressant drug therapy likely also apply to patients with anxiety disorders, and several genetic polymorphisms in the cytochrome P450 (CYP) gene family and drug transporter molecules, such as the multidrug resistance (MDR) gene type 1, have
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Pathophysiology and Pharmacology of GABAA Receptors,ed. A new central nervous system pharmacology is on the horizon. The development of anxiolytic drugs devoid of sedation and of agents that enhance hippocampus-dependent learning and memory has become a novel and highly selective therapeutic opportunity.
发表于 2025-4-2 03:56:19 | 显示全部楼层
Neuroendocrine Aspects of PTSD,pothalamus), or both in PTSD. However, findings of low cortisol and increased reactivity of the pituitary in PTSD are also consistent with reduced adrenal output. The observations in PTSD are part of a growing body of neuroendocrine data providing evidence of insufficient glucocorticoid signaling in stress-related neuropsychiatric disorders.
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