龙虾心脏系统的肽能调节对神经元和肌肉有相反的作用。

IF 2.2 4区 生物学 Q2 BIOLOGY
Integrative Organismal Biology Pub Date : 2025-01-24 eCollection Date: 2025-01-01 DOI:10.1093/iob/obaf002
I S Petropoulos, A E Jordan, P S Dickinson, D J Powell
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引用次数: 0

摘要

神经网络的调节,主要是通过神经肽,产生运动模式的变化,使生物体适应环境变化或感觉输入。调节是复杂的,神经调节剂的受体在神经系统的不同位置表达;因此,神经调节剂可以通过神经肌肉接点(NMJ)和肌肉本身改变周围肌肉动力学。美国龙虾(Homarus americanus)的神经源性心脏神经肌肉系统是研究肽能调节的一个很好的特征模型。肌抑制素(pQDLDHVFLRFamide)是一种内源性肽,有趣的是,它通过作用于龙虾心脏中枢模式发生器(CPG;(心脏神经节)和外周(心肌)。肌抑制素通过降低心脏神经节的爆发频率来降低心跳频率。在这里,我们研究了剩下的问题,肌抑制素是直接对心肌、NMJ,还是两者都起外周作用?为了阐明肌抑制素对心肌的作用,将心肌从CPG中分离出来,局部应用内源性神经递质l-谷氨酸,同时在心脏上过度使用肌抑制素,从而引起收缩。肌抑制素在离体肌肉中增加谷氨酸诱发的收缩幅度,提示肌抑制素直接对心肌施加外周效应。为了检查对NMJ的影响,在对照盐水和肌抑制素存在的情况下,通过刺激运动神经和记录单个肌纤维的细胞膜内电压来诱发兴奋性连接电位。肌抑制素没有调节兴奋性连接电位的振幅,这表明肌抑制素直接作用于肌肉,而不是通过NMJ,导致收缩力的增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Peptidergic Modulation of the Lobster Cardiac System Has Opposing Action on Neurons and Muscles.

Modulation of neuronal networks, primarily through neuropeptides, generates variations in motor patterns that allow organisms to adapt to environmental changes or sensory inputs. Modulation is complex, with receptors for neuromodulators expressed at various locations within a nervous system; neuromodulators can thus alter muscle dynamics peripherally via the neuromuscular junction (NMJ) and the muscle itself. The neurogenic cardiac neuromuscular system of the American lobster (Homarus americanus) is a well-characterized model for investigating peptidergic modulation. Myosuppressin (pQDLDHVFLRFamide) is an endogenous peptide that interestingly decreases contraction frequency while also increasing contraction force by acting at both the lobster heart central pattern generator (CPG; the cardiac ganglion) and the periphery (cardiac muscles). Myosuppressin decreases heartbeat frequency by decreasing the burst frequency of the cardiac ganglion. Here, we investigated the remaining question, does myosuppressin exert its peripheral effects directly on the cardiac muscle, the NMJ, or both? To elucidate myosuppressin's effects on the cardiac muscle, the muscle was isolated from the CPG, and contractions were evoked using focal application of the endogenous neurotransmitter, l-glutamate, while superfusing myosuppressin over the heart. Myosuppressin increased glutamate-evoked contraction amplitude in the isolated muscle, suggesting that myosuppressin exerts its peripheral effects directly on the cardiac muscle. To examine effects on the NMJ, excitatory junction potentials were evoked by stimulating the motor nerve and recording the intracellular membrane voltage from a single muscle fiber both in control saline and in the presence of myosuppressin. Myosuppressin did not modulate the amplitude of excitatory junction potentials suggesting that myosuppressin acts directly on the muscle and not via the NMJ, to cause an increase in contraction force.

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来源期刊
CiteScore
3.70
自引率
6.70%
发文量
48
审稿时长
20 weeks
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