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首页> 外文期刊>Journal of Neurophysiology >Models of respiratory rhythm generation in the pre-Botzinger complex. III. Experimental tests of model predictions.
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Models of respiratory rhythm generation in the pre-Botzinger complex. III. Experimental tests of model predictions.

机译：Botzinger前期情结中的呼吸节律产生模型。三，模型预测的实验测试。

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We used the testable predictions of mathematical models proposed by Butera et al. to evaluate cellular, synaptic, and population-level components of the hypothesis that respiratory rhythm in mammals is generated in vitro in the pre-Botzinger complex (pre-BotC) by a heterogeneous population of pacemaker neurons coupled by fast excitatory synapses. We prepared thin brain stem slices from neonatal rats that capture the pre-BotC and maintain inspiratory-related motor activity in vitro. We recorded pacemaker neurons extracellularly and found: intrinsic bursting behavior that did not depend on Ca(2+) currents and persisted after blocking synaptic transmission; multistate behavior with transitions from quiescence to bursting and tonic spiking states as cellular excitability was increased via extracellular K(+) concentration ([K(+)](o)); a monotonic increase in burst frequency and decrease in burst duration with increasing [K(+)](o); heterogeneity among different cells sampled; and an increase in inspiratory burst duration and decrease in burst frequency by excitatory synaptic coupling in the respiratory network. These data affirm the basis for the network model, which is composed of heterogeneous pacemaker cells having a voltage-dependent burst-generating mechanism dominated by persistent Na(+) current (I(NaP)) and excitatory synaptic coupling that synchronizes cell activity. We investigated population-level activity in the pre-BotC using local "macropatch" recordings and confirmed these model predictions: pre-BotC activity preceded respiratory-related motor output by 100-400 ms, consistent with a heterogeneous pacemaker-cell population generating inspiratory rhythm in the pre-BotC; pre-BotC population burst amplitude decreased monotonically with increasing [K(+)](o) (while frequency increased), which can be attributed to pacemaker cell properties; and burst amplitude fluctuated from cycle to cycle after decreasing bilateral synaptic coupling surgically as predicted from stability analyses of the model. We conclude that the pacemaker cell and network models explain features of inspiratory rhythm generation in vitro.
机译：我们使用了Butera等人提出的可验证的数学模型预测。评估哺乳动物呼吸节奏是由体外起搏器神经元的异种种群结合快速兴奋性突触在体外的前Botzinger复合体（pre-BotC）中产生的假说，以评估细胞，突触和群体水平的假说。我们从新生大鼠制备了薄的脑干切片，以捕获pre-BotC并在体外维持与吸气相关的运动活动。我们在细胞外记录了起搏器神经元，发现：内在的爆发行为不依赖于Ca（2+）电流，并且在阻止突触传递后仍然存在;随着细胞兴奋性的增加，通过细胞外K（+）浓度（[K（+）]（o）），多态行为具有从静止状态到爆发状态和强音峰值的过渡;随着[K（+）]（o）的增加，猝发频率单调增加，猝发持续时间减少;采样的不同细胞之间的异质性;以及通过呼吸网络中的兴奋性突触耦合增加吸气爆发持续时间并降低爆发频率。这些数据证实了该网络模型的基础，该模型由具有起伏机制的异源起搏器细胞组成，该机制由持续性Na（+）电流（I（NaP））和能同步细胞活动的兴奋性突触耦合所主导。我们使用本地“ macropatch”记录调查了前BotC中的人群水平活动，并确认了以下模型预测：前BotC活动在与呼吸有关的运动输出之前100-400 ms，这与产生呼吸节律的异类起搏器细胞群体一致在BotC之前;随着[K（+）]（o）的增加（频率增加），BotC前群体的爆发幅度单调下降，这可以归因于起搏器的细胞特性;根据模型稳定性分析预测，手术减少双侧突触耦合后，突波振幅会在每个周期之间波动。我们得出的结论是，起搏器细胞和网络模型解释了体外吸气节律产生的特征。

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