BRAIN MECHANISMS OF VOCAL PRODUCTION IN SQUIRREL MONKEYS

松鼠猴发声的大脑机制

• 批准号: 3965718
• 负责人: J D NEWMAN
• 金额: --
• 依托单位: EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT
• 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/3965718
• 关键词: animal communication behavior; audiotape; clonidine; ethology; frontal lobe /cortex; hippocampus; limbic system; naloxone; neural information processing; neuropharmacology; physostigmine; prazosin; psychobiology; tegmentum; vocalization; yohimbine

This project investigates the effect of neurological and pharmacological interventions on the incidence and structure of squirrel monkey vocalizations emitted during standardized conditions in the laboratory. A collaborative study has focused on the effect of various cerebral lesions on the production of the isolation call (IC). We tested whether ablation of midline frontal neocortex lying peripheral to a previously discovered critical band of limbic cortex would interfere with IC production. We found that in the absence of this neocortical tissue there was full recovery of spontaneously produced ICs. Other current work is directed at the chemical substrates mediating vocal production. The role of the adrenergic system in IC production was studied. We established dose-response relationships for the alpha-adrenergic agonist clonidine and alpha-2 antagonist yohimbine, using rate of IC production as the behavioral response measure. Both drugs exhibit dose-dependent effects on IC production, the agonist decreasing and the antagonist increasing calling rate. Since yohimbine reverses the clonidine-induced reduction of IC calling rate, we tested the specificity of an alpha-2 mechanism in mediating this behavior by substituting the alpha-1 antagonist prazosin for yohimbine. We found that this drug, in a dose of 0.25 mg/kg, was completely ineffective in reversing clonidine-induced vocal suppression. In another experiment, we established that adrenergic and opiatergic mechanisms can interact in mediating IC calling rate. Systemic administration of yohimbine concurrently with naloxone resulted in up to 7-fold increases in calling over rates following treatment with either drug alone. The role of cholinergic mechanisms in mediating alarm call production was investigated. We found that a centrally active cholinomimetic, physostigmine, was ineffective by itself, but it blocked the increased calling produced by the anticholinergic compound benactyzine. Cholinergic or anticholinergic compounds tested were without effect on IC production.

这个项目调查了神经学和药理学的影响。 松鼠猴发病及结构的干预措施 在实验室的标准条件下发出的发声。一个 合作研究的重点是各种脑损伤的影响。 关于隔离呼叫(IC)的产生。我们测试了消融是否 中线额叶新皮质位于先前发现的 边缘皮质的临界带会干扰IC的产生。我们 发现在没有这种新皮质组织的情况下， 自发产生的集成电路的回收。 目前的其他工作是针对介导发声的化学底物 制作。肾上腺素能系统在集成电路生产中的作用是 学习。我们建立了剂量-反应关系 α-肾上腺素能激动剂可乐定和α-2拮抗剂育亨宾，使用 以IC产生率作为行为反应指标。两种药物 对IC的产生表现出剂量依赖效应，激动剂减少和 对手提高了呼叫率。由于育亨宾逆转了 可乐定引起IC呼叫率降低，我们检验了其特异性 在调解这一行为时，通过将 育亨宾的α-1拮抗剂哌唑嗪。我们发现这种药物，在一个 0.25 mg/kg剂量对逆转作用完全无效 可乐定引起的发声抑制。在另一项实验中，我们建立了 肾上腺素能和阿片能机制在介导IC中的相互作用 通话费率。育亨宾同时全身给药 纳洛酮导致以下呼叫费率增加了7倍 单独使用任何一种药物进行治疗。胆碱能机制在心肌梗死中的作用 对中介报警电话的产生进行了调查。我们发现一个 中枢活性类胆碱药毒扁豆碱本身无效， 但它阻止了由抗胆碱能药物产生的增加的叫声 复方苯乙肼。测试的胆碱能或抗胆碱能化合物有 不会对IC生产产生影响。