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: 3900950
• 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/3900950
• 关键词: Macaca mulatta; Rodentias; adrenergic agents; adrenocorticotropic hormone; anticonvulsants; anxiety; behavior disorders; benzodiazepine receptor; bipolar depression manic phase; brain metabolism; carbamazepine; cognition disorders; disease /disorder model; drug metabolism; electroencephalography; hormone regulation /control mechanism; human subject; limbic system; lithium; mental disorder chemotherapy; mental disorder diagnosis; neuroendocrine system; neuropeptides; neuropharmacology; neurophysiology; neurotransmitter metabolism; neurotransmitters; procainamide; prolactin; psychobiology; psychopharmacology; psychosomatic disorders; schizoid personality; temporal lobe /cortex

Evaluation, study, and treatment of patients with manic-depressive and schizo-affective illness are the primary goals of the Section. Double-blind, placebo-controlled clinical trials 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 that 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 that may account for carbamazepine's positive effects on mood and behavior are being studied. 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.

对躁狂抑郁症患者的评估、研究和治疗， 情感性疾病是该科的主要目标。 采用双盲、安慰剂对照的临床试验来评价 用于治疗这些疾病的常规使用的和新的药剂。 抗惊厥药如卡马西平已被证明是 临床上有效的急性和预防性治疗 躁狂抑郁症我们已经确定了可能的临床和 锂盐与卡马西平和其他药物反应的生化标志物 剂.例如，卡马西平的抗躁狂反应似乎是 病情更严重，更烦躁，更快地循环， 无应答者，即，与锂有关的变量 无反应为了阐明可能的作用机制，我们 已经发现α-2去甲肾上腺素能和“外周型”苯二氮卓类药物 受体机制可能是重要的抗惊厥药，如果不是 卡马西平的精神作用其他神经递质、调节剂， 和肽类物质可能是导致卡马西平阳性的原因 对情绪和行为的影响正在研究中。该科还力求 确定脑电生理和代谢的局部改变 与行为和认知变化有关的活动， 情感性疾病边缘系统兴奋性的临床探讨 还使用了一种新的激发剂普鲁卡因。 普罗帕酮选择性地增加颞叶的快速活动， 与各种行为和认知改变相关， 皮质醇、促肾上腺皮质激素和催乳素的分泌。动物模型 电生理学和药理学点燃和可卡因诱导 行为敏感化的研究和牵连条件反射， 学习过程中诱发的渐进性行为变化。这些 模型可能有助于提供新的临床和生化见解， 行为的渐进和长期变化的基础机制 在各种临床综合征中，包括可卡因引起的 精神病理学和情感疾病。