SEROTION AT THE PHRENIC MOTOR NUCLEUS AND RESPIRATION
SEROTION AT THE PHRENIC MOTOR NUCLEUS AND RESPIRATION
批准号:
3449185
负责人:
JOSEPH R HOLTMAN
金额:
$4.83万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1985
资助国家:
美国
项目状态:
已结题
起止时间:
1985-08-01 至 1988-07-31
关键词:
decerebration dorsal raphe nucleus electrophysiology experimental brain lesion fluorescent dye /probe high performance liquid chromatography hypercapnia hypoxia innervation microinjections motor neurons neural information processing neuroanatomy neurochemistry neuropharmacology neurotransmitters phrenic nerve pulmonary respiration respiratory airflow measurement serotonin
中文摘要
我们已经证明5-羟色胺存在于膈运动核(PMN)。
在似乎起源于脑干中缝核的神经元中。这个
这项研究提案的总体目标是确认
以中缝核团为主要来源的神经化学技术
中性粒细胞中的5-羟色胺,并通过生理学技术评估
这种神经递质的功能是在这个脊髓呼吸系统
原子核。具体目的是:1)确认中缝核团是
中性粒细胞5-羟色胺的主要来源(S)
5-羟色胺能神经支配在这些核团中各有贡献;2)决定
中性粒细胞5-羟色胺能活动的改变对正常有什么影响
呼吸活动;3)确定5-羟色胺能的变化
中性粒细胞DO活性对呼吸反应的影响
高碳酸血症和低氧的生理刺激决定了什么
中性粒细胞5-羟色胺能活动的改变与刺激
中缝核团和已知的脑干呼吸核团。应使用的方法
包括:1)中缝核团的化学损伤和测量
中性粒细胞中5-羟色胺的高压液相色谱检测
呼吸活动的几个指标(潮气量、呼吸频率、
分钟容量、气管压力、呼气末二氧化碳和血气)in
麻醉和去大脑的猫,安装有气体测定仪;3)
鞘内给药以改变中枢5-羟色胺能活动
PMN和4)电刺激和化学刺激(谷氨酸微量注射)
脑干核团。这些研究很重要,因为它们将提供
关于控制PMN的神经通路和神经递质的信息
活动。这些信息对于理解正常呼吸很重要。
但对于理解中枢神经系统呼吸系统疾病是至关重要的。可能的
涉及PMN及其中枢输入的呼吸系统疾病包括
婴儿猝死综合征与睡眠呼吸暂停。了解该组织的作用
神经递质和神经通路参与中枢控制
呼吸作用将加深我们对这些呼吸系统疾病的理解,
并可能为这些疾病的治疗提供合理的依据。
英文摘要
We have shown that serotonin is present at the phrenic motor nucleus (PMN)
in neurons that appear to originate from the brainstem raphe nuclei. The
overall objectives of this research proposal are to confirm by
neurochemical techniques that the raphe nuclei are the primary source of
serotonin at the PMN and to evaluate by physiological techniques what the
function of this neurotransmitter is at this spinal cord respiratory
nucleus. The specific aims are to: 1) confirm that the raphe nuclei are
the primary source(s) of the serotonin at the PMN and how much of the
serotonergic innervation each of these nuclei contributes; 2) determine
what alterations in serotonergic activity at the PMN do to normal
respiratory activity; 3) determine what alterations in serotonergic
activity at the PMN do to the respiratory responses elicited by the
physiological stimuli of hypercapnia and hypoxia and 4) determine what
alterations in serotonergic activity at the PMN do to stimulation of the
raphe nuclei and known brainstem respiratory nuclei. Methods to be used
include: 1) chemical lesioning of the raphe nuclei and measurement of
serotonin at the PMN by high pressure liquid chromatography; 2) measurement
of several indices of respiratory activity (tidal volume, respiratory rate,
minute volume, trachael pressure, end tidal CO2 and blood gases) in
anesthetized and decerebrated cats fitted with a pneumotachograph; 3)
intrathecal administration of drugs to alter serotonergic activity at the
PMN and 4) electrical and chemical (glutamate microinjection) stimulation
of brain stem nuclei. These studies are important since they will provide
information about the neuropathways and neurotransmitters controlling PMN
activity. This information is important for understanding normal breathing
but is critical for understanding CNS respiratory disorders. Possible
respiratory disorders involving the PMN and its central inputs include
Sudden Infant Death Syndrome and Sleep Apnea. Knowledge of the role of the
neurotransmitters and neuropathways involved in the central control of
respiration will further our understanding of these respiratory disorders,
and may provide a rational basis for the treatment of these disorders.
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海外基金