Andresen Michael C, Peters James H
Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, Oregon 97239-3098, USA.
Am J Physiol Heart Circ Physiol. 2008 Nov;295(5):H2032-42. doi: 10.1152/ajpheart.00568.2008. Epub 2008 Sep 12.
Cranial nerve visceral afferents enter the brain stem to synapse on neurons within the solitary tract nucleus (NTS). The broad heterogeneity of both visceral afferents and NTS neurons makes understanding afferent synaptic transmission particularly challenging. To study a specific subgroup of second-order neurons in medial NTS, we anterogradely labeled arterial baroreceptor afferents of the aortic depressor nerve (ADN) with lipophilic fluorescent tracer (i.e., ADN+) and measured synaptic responses to solitary tract (ST) activation recorded from dye-identified neurons in medial NTS in horizontal brain stem slices. Every ADN+ NTS neuron received constant-latency ST-evoked excitatory postsynaptic currents (EPSCs) (jitter < 192 micros, SD of latency). Stimulus-recruitment profiles showed single thresholds and no suprathreshold recruitment, findings consistent with EPSCs arising from a single, branched afferent axon. Frequency-dependent depression of ADN+ EPSCs averaged approximately 70% for five shocks at 50 Hz, but single-shock failure rates did not exceed 4%. Whether adjacent ADN- or those from unlabeled animals, other second-order NTS neurons (jitters < 200 micros) had ST transmission properties indistinguishable from ADN+. Capsaicin (CAP; 100 nM) blocked ST transmission in some neurons. CAP-sensitive ST-EPSCs were smaller and failed over five times more frequently than CAP-resistant responses, whether ADN+ or from unlabeled animals. Variance-mean analysis of ST-EPSCs suggested uniformly high probabilities for quantal glutamate release across second-order neurons. While amplitude differences may reflect different numbers of contacts, higher frequency-dependent failure rates in CAP-sensitive ST-EPSCs may arise from subtype-specific differences in afferent axon properties. Thus afferent transmission within medial NTS differed by axon class (e.g., CAP sensitive) but was indistinguishable by source of axon (e.g., baroreceptor vs. nonbaroreceptor).
脑神经内脏传入纤维进入脑干,在孤束核(NTS)内与神经元形成突触。内脏传入纤维和NTS神经元的广泛异质性使得理解传入突触传递极具挑战性。为了研究内侧NTS中一个特定的二阶神经元亚群,我们用亲脂性荧光示踪剂对主动脉减压神经(ADN)的动脉压力感受器传入纤维进行顺行标记(即ADN+),并在水平脑干切片中测量了从内侧NTS中经染料识别的神经元记录到的对孤束(ST)激活的突触反应。每个ADN+ NTS神经元都接收到潜伏期恒定的ST诱发兴奋性突触后电流(EPSC)(抖动<192微秒,潜伏期标准差)。刺激募集曲线显示单一阈值且无阈上募集,这一结果与EPSC由单个分支传入轴突产生一致。在50Hz下给予5次电击时,ADN+ EPSC的频率依赖性抑制平均约为70%,但单次电击失败率不超过4%。无论是相邻的ADN-神经元还是来自未标记动物的其他二阶NTS神经元(抖动<200微秒),其ST传递特性与ADN+神经元并无区别。辣椒素(CAP;100 nM)在一些神经元中阻断了ST传递。无论是ADN+神经元还是来自未标记动物的神经元,对CAP敏感的ST-EPSC都较小,且失败频率比抗CAP反应高出五倍以上。对ST-EPSC的方差-均值分析表明,二阶神经元中量子谷氨酸释放的概率普遍较高。虽然幅度差异可能反映了不同的接触数量,但对CAP敏感的ST-EPSC中较高的频率依赖性失败率可能源于传入轴突特性的亚型特异性差异。因此,内侧NTS内的传入传递因轴突类别(如对CAP敏感)而异,但在轴突来源(如压力感受器与非压力感受器)方面并无区别。