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.

躁狂抑郁症患者的评估，研究和治疗 精神分裂性疾病是本节的主要目标。 使用双盲，安慰剂控制的临床试验来评估 常规使用和新颖的药物来治疗这些疾病。 抗惊厥药（例如卡马西平）已被证明是 临床上有效的急性和预防治疗 躁狂抑郁症。我们已经确定了可能的临床和 对锂与卡马西平的反应的生化标志物和其他 代理商。例如，对卡马西平的抗球员反应者似乎是 比病更严重，烦躁不安，骑自行车比 非反应器，即倾向于与锂相关的变量 无响应。为了阐明可能的行动机制，我们 发现α-2甲肾上腺素能和“外围型”苯二氮卓类 如果不是 卡马西平的精神作用。其他神经递质，调制器， 和可能解释卡马西平阳性的肽物质 正在研究对情绪和行为的影响。本节也试图 确定脑电生理和代谢的区域改变 与行为和认知变化有关的活动 情感疾病。边缘系统兴奋性的临床探针 还使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 与各种行为和认知改变以及 皮质醇，ACTH和催乳素的分泌。动物模型 电生理和药理点燃以及可卡因诱导的 研究行为敏化并暗示条件和 逐步行为变化中的学习过程。这些 模型可能有助于提供新的临床和生化见解 行为渐进和长期变化的基础的机制 在各种临床综合征中，包括可卡因诱导的 心理病理学和情感疾病。