School of Clinical Medicine, Faculty of Medicine, University of New South Wales, Australia.
School of Clinical Medicine, Faculty of Medicine, University of New South Wales, Australia; Institute of Neurological Sciences, Prince of Wales Hospital, Randwick, NSW 2031, Australia.
Neuropeptides. 2024 Feb;103:102399. doi: 10.1016/j.npep.2023.102399. Epub 2023 Dec 12.
To determine whether somatostatin (SST) could be a cortico-brainstem neurotransmitter involved in producing the headache of migraine.
There is evidence to support the idea that a cortico-brainstem-trigeminal nucleus neuraxis might be responsible for producing migraine headache; we have suggested that SST may be one of the neurotransmitters involved.
Rats were anesthetised and prepared for recording neurons in either the periaqueductal gray matter (PAG) or nucleus raphe magnus (NRM), as well as the trigeminal nucleus caudalis (TNC). The dura mater and facial skin were stimulated electrically or mechanically. SST, the SST agonist L054264 and the SST antagonist CYN54806 were injected intravenously, by microinjection, or by iontophoresis into the PAG or NRM. Cortical neuronal activity was provoked by cortical spreading depression (CSD) or light flash (LF) and was monitored by recording cortical blood flow (CBF).
Intravenous injection of SST: (a) selectively decreased the responses of TNC neurons to stimulation of the dura, but not skin, for up to 5 h; (b) decreased the ongoing discharge rate of TNC neurons while simultaneously increasing the discharge rate of neurons in either brainstem nucleus and; (c) prevented, or reversed, the effect of CSD and LF on brainstem and trigeminal neuron discharge rates. CSD and LF decreased the discharge rate of neurons in both brainstem nuclei and increased the discharge rate of TNC neurons. These effects were reversed by L054264 and mimicked by CYN54806. Injections of L054264 into the PAG or NRM reduced the response of TNC neurons to dural stimulation and skin stimulation differentially, depending on the nucleus injected. Injections of CYN54806 into either brainstem nucleus potentiated the responses of TNC neurons to dural and skin stimulation, but without a marked differential effect.
These results imply that SST could be a neurotransmitter in a pathway responsible for migraine pain.
确定生长抑素（SST）是否可以作为一种皮质-脑干神经递质参与偏头痛头痛的产生。
有证据支持这样一种观点，即皮质-脑干-三叉神经核轴可能负责产生偏头痛头痛；我们已经提出，SST 可能是涉及的神经递质之一。
麻醉大鼠，准备记录periaqueductal 灰色物质（PAG）或 raphe magnus 核（NRM）以及三叉神经尾核（TNC）中的神经元。电或机械刺激硬脑膜和面部皮肤。通过静脉内注射、微注射或离子电泳将 SST、SST 激动剂 L054264 和 SST 拮抗剂 CYN54806 注入 PAG 或 NRM。通过记录皮质血流（CBF）来引发皮质扩散性抑制（CSD）或光闪烁（LF）引起的皮质神经元活动。
静脉内注射 SST：（a）选择性地降低了 TNC 神经元对硬脑膜刺激的反应，但对皮肤刺激的反应不超过 5 小时；（b）降低了 TNC 神经元的持续放电率，同时增加了脑干核内神经元的放电率；（c）防止或逆转了 CSD 和 LF 对脑干和三叉神经神经元放电率的影响。CSD 和 LF 降低了两个脑干核内神经元的放电率，并增加了 TNC 神经元的放电率。这些作用被 L054264 逆转，并被 CYN54806 模拟。将 L054264 注入 PAG 或 NRM 可根据注入的核不同，降低 TNC 神经元对硬脑膜刺激和皮肤刺激的反应。将 CYN54806 注入任何一个脑干核都可以增强 TNC 神经元对硬脑膜和皮肤刺激的反应，但没有明显的差异作用。
这些结果表明，SST 可能是参与偏头痛疼痛的途径中的一种神经递质。
