AVP modulation of the vestibular nucleus via V1b receptors potentially contributes to the development of motion sickness in rat.
AVP modulation of the vestibular nucleus via V1b receptors potentially contributes to the development of motion sickness in rat.
复制标题
AVP 通过 V1b 受体调节前庭核可能导致大鼠晕动病的发生
DOI：
10.1186/s13041-015-0175-1
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发表时间：
2015-12-12
期刊：
影响因子：
3.6
通讯作者：
Jiang ZL
中科院分区：
文献类型：
--
作者：
Xu LH;Tang GR;Yang JJ;Liu HX;Li JC;Jiang ZL
背景精氨酸加压素（AVP）被认为是运动病（MS）的一种致病激素。为探讨AVP在室旁核（PVN）表达的个体差异及其对前庭核（VN）的调节作用是否与MS有关，采用大鼠VN内注射或全身注射AVP和旋转刺激诱导条件性味觉厌恶（CTA）的方法，建立了MS模型。VN使用V1 b受体（V1 bRs）拮抗剂SSR 149415，使CTA变钝。AVP可抑制VN神经元L型钙通道和NMDA受体通道的钙内流，但可被SSR 149415拮抗。旋转刺激后，室旁核和VN内AVP和V1 bRs表达增加，MS易感大鼠更明显。VN内AVP含量较低，AVP mRNA表达较少，AVP阳性纤维稀疏分布，AVP/突触素阳性终末较少。从VN逆行追踪，几乎未发现室旁核内AVP阳性神经元。SNP分析表明，AVP基因rs 105235842位点的等位基因频率和基因型在MS易感组和非易感组之间存在显著差异。结论AVP可能通过V1 bR介导对室旁核神经元的体液调节作用参与大鼠运动病的发生，AVP基因多态性可能是导致室旁核AVP反应性表达个体差异的原因之一; PVN AVP和VN V1 bRs的高表达可能与前庭刺激后大鼠运动病的发生有关。
BackgroundArginine vasopressin (AVP) is considered to be an etiologic hormone in motion sickness (MS). The present study was designed to investigate whether individual differences in AVP expression in the paraventricular nucleus (PVN) and in modulation on the vestibular nucleus (VN) are involved in MS. Systemic application or microinjection of AVP into rat VN and rotatory stimulus were used to induce conditioned taste aversion (CTA) to 0.15 % saccharin sodium solution as a model of MS.ResultsIntra-VN use of SSR149415, an antagonist of V1b receptors (V1bRs), blunted CTA. AVP inhibited Ca2+influxes through L-type Ca2+channels and NMDA receptor channels in cultured VN neurones, but antagonised by SSR149415. More AVP and V1bRs were expressed respectively in the PVN and VN after rotatory stimulus, especially in rats susceptible to MS. In the VN, AVP content was low, the AVP mRNA was less expressed, a few AVP-positive fibres were sparsely distributed, and fewer AVP/synaptophysin-positive terminals were identified. Almost no fluoro-ruby-labelled AVP-positive neurones in the PVN were found with retrograde tracing from the VN. SNP analysis of the reported 9 sites of the AVP gene showed significant difference between the groups susceptible and insusceptible to MS at the site rs105235842 in the allele frequencies and genotypes. However, there was not any difference between these two groups in the SNP of the reported 38 sites of V1bR gene.ConclusionsAVP, through its modulatory, possibly humoral action on the VN neurones via the mediation of V1bR, may contribute to the development of motion sickness in rats; AVP gene polymorphisms may contribute to the individual difference in the responsive expression of AVP in the PVN; and higher expressions of AVP in the PVN and V1bRs in the VN may contribute to the development of motion sickness in rats after vestibular stimulation.