Abstract
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.
Highlights
Arginine vasopressin (AVP) is considered to be an etiologic hormone in motion sickness (MS)
When AVP V1b receptors (V1bRs) antagonist SSR149415 was injected at the same time, the decrease in the intake volume of saccharin sodium solution (SSS) elicited by AVP was significantly inhibited
Microinjection of SSR149415 into the vestibular nucleus (VN) inhibited rotatory stimulus- and AVP intraperitoneal injection-induced conditioned taste aversion (CTA) in rats (Fig. 1c and d). These results suggest that rotatory stimulation-induced motion sickness in rats is likely related to humoral modulation by AVP in the vestibular nuclei through V1bR
Summary
Arginine vasopressin (AVP) is considered to be an etiologic hormone in motion sickness (MS). The results from a study by Abe et al suggest that the medial vestibular nucleus, the nucleus of the solitary tract, the area postrema, and the paraventricular nucleus (PVN) of the hypothalamus may be involved in the induction of motion sickness by hypergravity in musk shrew (Suncus murinus) [14]. Vestibular stimuli will increase the expression of AVP in the PVN [18] and the secretion of AVP into the blood [7,8,9] It is unclear whether vestibular stimulus will strengthen the vasopressinergic efferent activity of PVN. If the vestibular stimuli increase the activity of PVN vasopressinergic efferent neurones, AVP will likely induce vomiting through those efferent pathways because there are efferent innervations from the PVN to the emesis centres [19, 20]. The PVN, through its vasopressinergic efferent influence on neurones in the VN we supposed, might play an important role in the autonomic responses to motion sickness-provoking stimuli, or alternatively, AVP, acting as an etiologic hormone in motion sickness [5, 8] through its humoral modulation on neurones in the VN, might influence the development of motion sickness
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