Despite respiratory motor neuron death, ventilation is preserved in SOD1^G93A rats. Compensatory respiratory plasticity may counterbalance the loss of these neurons. Phrenic long-term facilitation (pLTF; a form of respiratory plasticity) in naïve rats is 5-HT2 and NADPH oxidase-dependent. Furthermore, 5-HT2A, not 5-HT2B, receptor-induced phrenic motor facilitation is NADPH oxidase-independent in naïve rats. pLTF is NADPH oxidase-dependent in pre-symptomatic, but not end-stage, SOD1^G93A rats. Here, we hypothesized that in the putative phrenic motor nucleus (PMN) of SOD1^G93A rats vs. wild-type littermates: 1) pre-symptomatic rats would have greater 5-HT2B receptor expression that decreases at end-stage; and 2) 5-HT2A receptor expression would increase from pre-symptomatic to end-stage. Putative PMN 5-HT2A receptor expression was reduced when comparing across (but not within) pre-symptomatic vs. end-stage groups (p < 0.05). In contrast, putative PMN 5-HT2B receptor expression was increased when comparing across pre-symptomatic vs. end-stage groups, and within end-stage groups (p < 0.05). These data suggest a potential role for 5-HT2 receptors in pLTF and breathing in SOD1^G93A rats.

尽管呼吸运动神经元死亡，但 SOD1 ^G93A大鼠仍保持通气。补偿性呼吸可塑性可以抵消这些神经元的损失。幼稚大鼠的膈长期促进（pLTF；一种呼吸可塑性）依赖于 5-HT2 和 NADPH 氧化酶。此外，5-HT2A，而不是 5-HT2B，受体诱导的膈运动促进在幼稚大鼠中不依赖 NADPH 氧化酶。pLTF 在症状前但不是末期的 SOD1 ^G93A大鼠中是 NADPH 氧化酶依赖性的。在这里，我们假设在 SOD1 ^G93A大鼠与. 野生型同窝仔鼠：1) 出现症状前的大鼠会有更多的 5-HT2B 受体表达，但在末期会降低；2) 5-HT2A 受体表达会从症状前增加到末期。比较跨（但不在）症状前与. 末期组（p < 0.05）。与此相反，跨过症状前进行比较时提高推定的PMN 5-HT 2B受体表达VS。末期组和末期组内 (p < 0.05)。这些数据表明 5-HT2 受体在 SOD1 ^G93A大鼠pLTF 和呼吸中的潜在作用。