Changes in carotid body and nTS neuronal excitability following neonatal sustained and chronic intermittent hypoxia exposure.

Changes in carotid body and nTS neuronal excitability following neonatal sustained and chronic intermittent hypoxia exposure.
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DOI:
10.1016/j.resp.2014.09.015
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发表时间:
2015-01-01
影响因子:
2.3
通讯作者:
MacFarlane PM
MacFarlane PM
中科院分区:
医学4区
文献类型:
--
作者:
Mayer CA;Wilson CG;MacFarlane PM

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我们观察了在慢性间歇性低氧(SH+CIH)前给予新生持续性低氧(SH)是否会改变体外培养的颈动脉小体(CB)化学感受器的活性和孤束尾核(NTS)神经元的兴奋性。持续低氧和CIH暴露模拟了发生持续性呼吸暂停的极早产儿经历的氧气范例。从出生后1岁(P1)开始给予5天的SH(11%O2),然后进行10天的慢性间歇低氧(CIH,5%O2/5分钟,8小时/天,在P6-15之间)。在SH+CIH暴露结束时(P16),基础放电频率降低,单位CB化学传入的缺氧性感觉反应减弱。此外,NTS神经元的基础放电频率和诱发的兴奋性突触后电流(ESPC‘s)的幅度比年龄匹配的正常氧饲养的大鼠增加。这些效应是SH+CIH暴露所独有的,因为SH或CIH单独对化学传入活动或NTS功能都没有类似的影响。这些数据表明,在接触CIH之前对新生儿SH进行预处理,可以独特地改变外周(CB)和中枢神经(NTS)功能的机制,有望扰乱对急性缺氧的呼吸反应。
We investigated whether pre-treatment with neonatal sustained hypoxia (SH) prior to chronic intermittent hypoxia (SH+CIH) would modify in vitro carotid body (CB) chemoreceptor activity and the excitability of neurons in the caudal nucleus of the solitary tract (nTS). Sustained hypoxia followed by CIH exposure simulates an oxygen paradigm experienced by extremely premature infants who developed persistent apnea. Rat pups were treated with 5 days of SH (11% O2) from postnatal age 1 (P1) followed by 10 days of subsequent chronic intermittent hypoxia (CIH, 5% O2/5mins, 8hrs/day, between P6–15) as described previously. At the end of SH+CIH exposure (P16), basal firing frequency was reduced, and the hypoxic sensory response of single unit CB chemoafferents was attenuated. Further, basal firing frequency and the amplitude of evoked excitatory post-synaptic currents (ESPC’s) of nTS neurons was augmented compared to age-matched rats raised in normoxia. These effects were unique to SH+CIH exposure as neither SH or CIH alone elicited any comparable effect on chemoafferent activity or nTS function. These data indicated that pre-treatment with neonatal SH prior to CIH exposure uniquely modified mechanisms of peripheral (CB) and central (nTS) neural function in a way that would be expected to disturb the ventilatory response to acute hypoxia.
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