PSYCHOLOGICAL AND BIOLOGICAL INTERACTIONS IN THE MOOD AND ANXIETY DISORDERS

躁郁症患者的评估、研究和治疗 精神分裂-情感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估 治疗这些疾病的常规药物和新药。 卡马西平等抗惊厥药物已被证明是 急性和预防性治疗慢性阻塞性肺疾病的临床疗效 躁郁症。我们已经确定了可能的临床和 锂与卡马西平等治疗反应的生化标志物比较 探员们。例如，卡马西平的抗躁狂反应者似乎 更严重的疾病，更烦躁不安，更快的骑自行车比 无响应者，即倾向于与锂相关的变量 没有回应。在试图阐明可能的作用机制时，我们 发现α-2去甲肾上腺素和“外周型”苯二氮卓类 受体机制可能对抗惊厥药物很重要，如果不是 卡马西平的精神药物作用。其他神经递质，调节剂， 和多肽类物质可能是卡马西平阳性的原因 对情绪和行为的影响正在研究中。该科还寻求 确定脑电生理和代谢的局部改变 与行为和认知的改变有关的活动 情感性疾病。边缘系统兴奋性的临床探讨 利用一种新型的刺激剂普鲁卡因也在使用中。 普鲁卡因选择性地增加颞叶的快速活动 与各种行为和认知改变以及 分泌皮质醇、促肾上腺皮质激素和催乳素。大鼠的动物模型 电生理和药理学点燃和可卡因诱导 行为敏感化被研究并暗示条件反射和 学习过程中诱发的渐进性行为改变。这些 模型可能有助于提供新的临床和生化见解 行为渐进性和长期性变化的基础机制 在包括可卡因引起的各种临床症状中 精神病理学和情感性疾病。

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.