Pharmacological experiments indicate that neuropeptides can effectively tune neuronal activity and modulate locomotor output patterns. However, their functions in shaping innate locomotion often remain elusive. For example, somatostatin has been previously shown to induce locomotion when injected in the brain ventricles but to inhibit fictive locomotion when bath-applied in the spinal cord in vitro. Here, we investigated the role of somatostatin in innate locomotion through a genetic approach by knocking out somatostatin 1.1 (sst1.1) in zebrafish. We automated and carefully analyzed the kinematics of locomotion over a hundred of thousand bouts from hundreds of mutant and control sibling larvae. We found that the deletion of sst1.1 did not impact acousto-vestibular escape responses but led to abnormal exploration. sst1.1 mutant larvae swam over larger distance, at higher speed and performed larger tail bends, indicating that Somatostatin 1.1 inhibits spontaneous locomotion. Altogether our study demonstrates that Somatostatin 1.1 innately contributes to slowing down spontaneous locomotion.

药理实验表明，神经肽可以有效调节神经元活动并调节运动输出模式。然而，它们在塑造先天运动方面的功能往往仍然难以捉摸。例如，先前已证明，生长抑素注射到脑室中时会诱导运动，但在体外注射到脊髓中时会抑制虚构的运动。在这里，我们通过基因方法敲除斑马鱼中的生长抑素 1.1 ( sst1.1 )，研究了生长抑素在先天运动中的作用。我们对数百个突变体和对照同级幼虫十万次运动的运动学进行了自动化和仔细分析。我们发现sst1.1的删除不会影响声前庭逃逸反应，但会导致异常探索。sst1.1突变幼虫以更高的速度游动更远的距离并进行更大的尾部弯曲，表明生长抑素 1.1 抑制自发运动。总而言之，我们的研究表明，生长抑素 1.1 天生有助于减慢自发运动。