MONOAMINES EFFECTS ON MOTONEURON DISCHARGE PATTERNS

单胺对运动神经元放电模式的影响

• 批准号: 2735669
• 负责人: Charles Heckman
• 金额: $ 16.6万
• 依托单位: NORTHWESTERN UNIVERSITY AT CHICAGO
• 依托单位国家: 美国
• 财政年份: 1996
• 资助国家: 美国
• 起止时间: 1996-07-01 至 1999-09-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2735669
• 关键词: cats; membrane potentials; motor neurons; neuromuscular transmission; neurotransmitter agonist; neurotransmitter antagonist; neurotransmitter receptor; norepinephrine; serotonin; spinal block; spinal reflex; voltage /patch clamp

DESCRIPTION (Adapted from applicant's abstract) : The goal of this proposal is to test the hypothesis that monoaminergic input acts to preserve the normal threshold hierarchy among spinal motoneurons in a pool. To achieve this goal, investigations of the effects of subtype-specific monoaminergic agents on motoneuron intrinsic properties and synaptic inputs are proposed. The decerebrate cat preparation is utilized because it has both tonic activity in descending monoaminergic tracts and normal motoneuron recruitment. Reversible cold block of the spinal cord is used to eliminate endogenous monoaminergic activity. Intracellular single electrode voltage clamp (SEVC) methods provide measurements of motoneuron intrinsic properties and synaptic inputs. Our aims test the following specific hypotheses: Aim 1: that monoamines act to preserve the normal pattern of synaptic input to motoneurons. Aim 2: that monoamines generate plateau potentials and bistable behaviors in motoneurons without distorting the normal S vs. F threshold differences. Aim 3: that monoamines influence the interaction between synaptic inputs and intrinsic properties of type S and F motoneurons by allowing synaptic inputs to generate plateau potentials in dendrites even when the soma is voltage clamped. These studies have direct relevance to spinal cord injury, where loss of tonic monoaminergic input may contribute to the abnormal motor outflow seen in human patients.

描述（改编自申请人摘要）： 这项提议的目的是检验单胺能输入 在脊髓运动神经元之间保持正常的阈值等级， 游泳池 为了实现这一目标，调查的影响， 亚型特异性单胺能药物对运动神经元内在特性的影响， 提出了突触输入。 去大脑猫制剂， 因为它在下行单胺能束中具有滋补活性， 正常的运动神经元募集 脊髓可逆性冷阻滞 用于消除内源性单胺能活性。 胞内单 电极电压钳（SEVC）方法提供运动神经元的测量 内在属性和突触输入。 我们的目标是测试以下内容 具体假设：目的1：单胺起保护正常 运动神经元的突触输入模式。 目标2：单胺产生 运动神经元无畸变的平台电位和运动行为 正常的S与F阈值差异。 目标3：单胺影响 突触输入与S型神经元内在特性之间的相互作用 和F运动神经元通过允许突触输入产生平台电位 即使索马被电压箝位。 这些研究 与脊髓损伤直接相关，在脊髓损伤中， 输入可能导致在人类患者中观察到的异常运动流出。