Peptide neuromodulation has been implicated to shield neuronal activity from acute temperature changes that can otherwise lead to loss of motor control or failure of vital behaviors. However, the cellular actions neuropeptides elicit to support temperature-robust activity remain unknown. Here, we find that peptide neuromodulation restores rhythmic bursting in temperature-compromised central pattern generator (CPG) neurons by counteracting membrane shunt and increasing dendritic electrical spread. We show that acutely rising temperatures reduced spike generation and interrupted ongoing rhythmic motor activity in the crustacean gastric mill CPG. Neuronal release and extrinsic application of Cancer borealis tachykinin-related peptide Ia (CabTRP Ia), a substance-P-related peptide, restored rhythmic activity. Warming led to a significant decrease in membrane resistance and a shunting of the dendritic signals in the main gastric mill CPG neuron. Using a combination of fluorescent calcium imaging and electrophysiology, we observed that postsynaptic potentials and antidromic action potentials propagated less far within the dendritic neuropil as the system warmed. In the presence of CabTRP Ia, membrane shunt decreased and both postsynaptic potentials and antidromic action potentials propagated farther. At elevated temperatures, CabTRP Ia restored dendritic electrical spread or extended it beyond that at cold temperatures. Selective introduction of the CabTRP Ia conductance using a dynamic clamp demonstrated that the CabTRP Ia voltage-dependent conductance was sufficient to restore rhythmic bursting. Our findings demonstrate that a substance-P-related neuropeptide can boost dendritic electrical spread to maintain neuronal activity when perturbed and reveals key neurophysiological components of neuropeptide actions that support pattern generation in temperature-compromised conditions.

SIGNIFICANCE STATEMENT Changes in body temperature can have detrimental consequences for the well-being of an organism. Temperature-dependent changes in neuronal activity can be especially dangerous if they affect vital behaviors. Understanding how temperature changes disrupt neuronal activity and identifying how to ameliorate such effects is critically important. Our study of a crustacean circuit shows that warming disrupts rhythmic neuronal activity by increasing membrane shunt and reducing dendritic electrical spread in a key circuit neuron. Through the ionic conductance activated by it, substance-P-related peptide modulation restored electrical spread and counteracted the detrimental temperature effects on rhythmic activity. Because neuropeptides are commonly implicated in sustaining neuronal activity during perturbation, our results provide a promising mechanism to support temperature-robust activity.

肽神经调节涉及保护神经元活动免受急性温度变化的影响，否则会导致运动控制丧失或重要行为失败。然而，神经肽引发支持温度稳定活动的细胞作用仍然未知。在这里，我们发现肽神经调节通过抵消膜分流和增加树突电扩散来恢复温度受损的中央模式发生器 (CPG) 神经元的节律性爆发。我们表明急剧上升的温度减少了尖峰的产生并中断了甲壳类胃磨 CPG 中正在进行的有节奏的运动活动。北癌的神经元释放和外在应用速激肽相关肽 Ia (CabTRP Ia)，一种物质 P 相关肽，恢复节律性活动。变暖导致膜电阻的显着降低和主胃磨 CPG 神经元中树突信号的分流。使用荧光钙成像和电生理学的组合，我们观察到随着系统变暖，突触后电位和逆向动作电位在树突状神经细胞内传播的距离变小。在存在 CabTRP Ia 的情况下，膜分流减少，突触后电位和逆向动作电位传播得更远。在升高的温度下，CabTRP Ia 恢复了树枝状电扩散或将其扩展到低温下。使用动态钳对 CabTRP Ia 电导的选择性引入表明，CabTRP Ia 电压依赖性电导足以恢复节律性爆发。我们的研究结果表明，与 P 物质相关的神经肽可以促进树突电扩散，以在受到干扰时维持神经元活动，并揭示神经肽作用的关键神经生理学成分，这些成分支持在温度受损条件下生成模式。

意义声明体温的变化会对生物体的健康产生不利影响。如果神经元活动的温度依赖性变化影响重要行为，则它们可能特别危险。了解温度变化如何破坏神经元活动并确定如何改善这种影响至关重要。我们对甲壳类动物回路的研究表明，变暖通过增加膜分流和减少关键回路神经元中的树突电传播来破坏节律性神经元活动。通过它激活的离子电导，与 P 物质相关的肽调制恢复了电传播并抵消了温度对节律活动的不利影响。因为神经肽通常与在扰动期间维持神经元活动有关，