PSYCHOLOGICAL AND BIOLOGICAL INTERACTIONS IN THE MOOD AND ANXIETY DISORDERS

情绪和焦虑症的心理和生物相互作用

• 批准号: 3921848
• 负责人: R M POST
• 金额: --
• 依托单位: NATIONAL INSTITUTE OF MENTAL HEALTH
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3921848
• 关键词: Macaca mulatta; Rodentias; adrenergic agents; adrenocorticotropic hormone; anticonvulsants; behavior disorders; behavior test; benzodiazepine receptor; bipolar depression; brain metabolism; cognition disorders; cortisol; disease /disorder model; drug metabolism; electroencephalography; hormone regulation /control mechanism; human subject; human therapy evaluation; limbic system; lithium; mental disorder chemotherapy; mental disorder diagnosis; mood disorders; neuroendocrine system; neuropeptides; neuropharmacology; neurophysiology; neurotransmitter metabolism; neurotransmitters; placebos; procainamide; prolactin; psychobiology; psychological stressor; psychopharmacology; psychosomatic disorders; schizoid personality; schizophrenia; stress

Evaluation, study, and treatment of patients with manic-depressive and schizoaffective illness are the primary goals of the Section. double-blind, placebo-controlled clinical trails are employed to evaluate routinely used and novel agents for the treatment of these disorders. Anticonvulsants such as carbamazepine have been demonstrated to be clinically effective in the acute and prophylactic treatment of manic-depressive illness. We have identified possible clinical and biochemical markers of response to lithium versus carbamazepine and other agents. For example, antimanic responders to carbamazepine appear to be more severely ill, more dysphoric, and more rapidly cycling than non-responders, i.e., variables that tend to be associated with lithium nonresponse. In attempting to elucidate possible mechanisms of action, we have found tat alpha-2 noradrenergic and "peripheral- type" benzodiazepine receptor mechanisms may be important to the anticonvulsant if not the psychotropic effects of carbamazepine. Other neurotransmitter, modulator, and peptide substances are being studied which may account for carbamazepine's positive effects on mood and behavior. The Section also seeks to identify regional alterations in brain electrophysiological and metabolic activity that are related to changes in behavior and cognition in affective illness. A clinical probe of limbic system excitability utilizing a novel provocative agent, procaine, is also being employed. Procaine selectively increases fast activity over the temporal lobe in association with a variety of behavioral and cognitive alterations and secretion of cortisol, ACTH, and prolactin. Animal models of electrophysiological and pharmacological kindling and cocaine-induced behavioral sensitization are studied and implicate conditioning and learning processes in the progressive behavioral changes induced. These models may help provide new clinical and biochemical insights into the mechanisms that underlie the progressive and long-term changes in behavior in a variety of clinical syndromes including cocaine-induced psychopathology and affective illness.

躁狂抑郁症患者的评估，研究和治疗 分裂性疾病是本节的主要目标。 双盲，安慰剂控制的临床步道已采用 评估常规使用和新颖的药物以治疗这些药物 疾病。 诸如卡马西平之类的抗惊厥药 证明在急性和 预防性治疗躁狂抑郁症。 我们有 确定了反应的可能的临床和生化标记 锂与卡马西平和其他代理。 例如， 对卡马西平的抗球员反应者似乎更严重 生病，烦躁不安，比无反应者更快地骑自行车， 即，倾向于与锂相关的变量 无响应。 试图阐明可能的机制 行动，我们发现Tat alpha-2甲肾上腺素能和“周围 - 类型“苯二氮卓受体机制可能对 卡马西平的抗惊厥药的精神作用。 其他神经递质，调节剂和肽物质正在 研究了可能解释卡马西平对 情绪和行为。 本节还旨在确定区域 大脑电生理和代谢活性的改变 与情感的行为和认知变化有关的 疾病。 利用边缘系统兴奋性的临床探测 还采用了一种新颖的挑衅代理Procaine。 Procaine选择性地增加了颞叶的快速活动 与各种行为和认知 皮质醇，ACTH和催乳素的改变和分泌。 动物 电生理和药理点燃的模型以及 研究可卡因引起的行为敏化并暗示 渐进行为中的调理和学习过程 引起的变化。 这些模型可能有助于提供新的临床和 生化见解对基于的机制 各种行为的渐进和长期变化 临床综合征，包括可卡因诱导的心理病理学和 情感疾病。