No / In the present study we evaluated the role of 5-HT1A receptors in mediating the inhibitory action of 8-OH-DPAT, a 5-HT1A receptor agonist, in motion sickness in Suncus murinus. 8-OH-DPAT (0.1 mg/kg, i. p) attenuated motion-induced emesis which was associated with an increase in the latency of the onset to the first emetic episode. Pre-treatment with methysergide (a 5-HT1/2/7 receptor antagonist, 1.0 mg/kg, i. p.), WAY-100635 (a 5-HT1A receptor antagonist, 1.0 mg/kg, i. p.), SB269970A (a 5-HT7 receptor antagonist, 1.0 and 5.0 mg/kg, i. p.), ondansetron (a 5-HT3 receptor antagonist, 1.0 mg/kg, i. p) or GR13808 (a 5-HT4 receptor antagonist, 0.5 mg/kg, i. p) failed to modify the inhibitory action of 8-OH-DPAT on motion sickness. Furthermore, the application of either methysergide, WAY-100635, SB269970A, ondansetron or GR13808 alone had no effect on motion sickness in its own right. These data indicate that neither 5-HT1A nor any 5-HT2 receptor subtypes, 5-HT3, 5-HT4 and 5-HT7 receptors are likely to be involved in the inhibition of motion-induced emesis mediated by 8-OH-DPAT.

The human-abetted introduction of commensal species (i.e. those that opportunistically exploit the anthropogenic environment for food and shelter, e.g. rats, cockroaches etc.) to new areas has occurred throughout history. This has resulted in detrimental ecological changes worldwide but, from a viewpoint of human knowledge, a beneficial corollary of these translocations is that the species in question can be used as proxies to study the movement of the humans who transported them. I reconstruct colonisation histories of three widespread commensal mammalian species in the Western Indian Ocean, the black rat Rattus rattus, house mouse Mus musculus and Asian house shrew Suncus murinus, through phylogeographic studies (the geographic distribution of genetic lineages) of maternally-inherited mitochondrial markers, and zooarchaeological data. The DNA analyses are conducted on samples largely derived from museum specimens collected up to 110 years ago, and from archaeological bones (in the case of rats). I show considerable cryptic diversity in all three species, particularly in mice for which we find a potential major new lineage. Certain lineages within each species predominantly reveal long-distance translocations within the Indian Ocean, but high resolution geographic and genetic clustering is also evident, particularly in Asian house shrews. Phylogeographic structuring of the three species in East Africa and the southern Indian Ocean region (e.g. Madagascar, Reunion, etc.) indicate connections with Arabia, the Middle East, and India in the Islamic period from the first millennium AD, and later European connections during the Age of Exploration. Closer to the origins of the three species (the Indian subcontinent in all cases), range expansions in Eurasia and nearby islands relate to early to mid Holocene human populations, but also with signals of later secondary colonisations. Through ancient DNA studies I found genetic continuity between temporally separated populations of black rats suggesting population persistence, and high levels of diversity in Songo Mnara, a Swahili stonetown in Tanzania. Knowledge of the colonisation history and genetic diversity of an introduced species is essential to understand their resilience in novel landscapes, and to identify pathways of invasion and, by proxy, human trade and exchange networks that facilitated their dispersal. My research contributes significantly to that end for three socially, economically and ecologically important species that are well-established in the Indian Ocean region and beyond.

No / The aim of the present study was to investigate an opioid receptor involvement in the adaptation response to motion sickness in Suncus murinus. Different groups of animals were treated intraperitoneally with either saline, morphine (0.1 and 1.0 mg/kg), naloxone (1.0, 10.0 and 5.0 mg/kg) or a combination of naloxone plus morphine in the absence or 30 min prior to a horizontal motion stimulus of I Hz and 40 mm amplitude. For the study of adaptation, different groups received saline on the first trial, and in subsequent trials (every 2 days) they received either saline, naloxone (1.0 and 10.0 mg/kg, ip) or morphine (0.1 mg/kg, ip) 30 min prior to the motion stimulus. Pretreatment with morphine caused a dose-related reduction in emesis induced by a single challenge to a motion stimulus. Pretreatment with naloxone alone did not induce emesis in its own right nor did it modify emesis induced by a single challenge to a motion stimulus. However, pretreatment with naloxone (5.0 mg/kg, ip) revealed an emetic response to morphine (P<.001) (1.0 mg/kg, ip) and antagonised the reduction of motion sickness induced by morphine. In animals that received saline or naloxone (1.0 mg/kg), a motion stimulus inducing emesis decreased the responsiveness of animals to a second and subsequent motion stimulus challenge when applied every 2 days for 11 trials. However, the animals receiving naloxone 10.0 mg/kg prior to the second and subsequent challenges showed no significant reduction in the intensity of emesis compared to the first trial. The data are revealing of an emetic potential of morphine when administered in the presence of a naloxone pretreatment. The administration of naloxone is also revealing of an additional inhibitory opioid system whose activation by endogenous opioid(s) may play a role in the adaptation to motion sickness on repeated challenge in S. murinus.

No / In the present study, we investigated the effect of 5-hydroxytryptamine (5-HT) and 5-HT receptor agonists and antagonists on motion sickness in Suncus murinus, and the possibility that the emetic stimulus of 5-HT can alter the sensitivity of the animals to the different emetic stimulus of motion sickness. 5-HT (1.0, 2.0, 4.0 and 8.0 mg/kg ip) induced emesis and that was antagonised by methysergide (1.0 mg/kg ip), the 5-HT4receptor antagonist sulphamate[1-[2-[(methylsulphonyl)amino]ethyl]-4-piperidinyl]methyl-5-fluoro-2-methoxy-1H-indole-3-carboxylate (GR125487D; 1.0 mg/kg ip) and granisetron (0.5 mg/kg ip). Pretreatment with 5-HT caused a dose-related attenuation of the emetic response induced by a subsequent motion stimulus, which was not significantly modified by methysergide, granisetron or GR125487D pretreatment. (+)-1-(2,5-Dimethoxy-4-iodophenyl)-2-amino-propane (DOI; 0.5 and 1.0 mg/kg ip), 8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT; 0.1 mg/kg ip) but not methysergide, GR125487D or granisetron, attenuated motion-induced emesis, and that was not affected by pretreatment with ketanserin (2.0 mg/kg, ip) or N-{2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl}-N-(2-pyridinyl)cyclohexanecarboxamide trihydrocholoride (WAY-100635; 1.0 mg/kg ip), respectively. Indeed, ketanserin alone (0.1, 0.3, 1.0 and 2.0 mg/kg ip) attenuated motion sickness. These data indicate that 5-HT1/2, 5-HT3 and 5-HT4 receptors are involved in the induction of 5-HT-induced emesis. However, agonist action at the 5-HT1A/7 and 5-HT2 receptors, and antagonist action at the 5-HT2A receptors can attenuate motion sickness in S. murinus.