Why Can't Rodents Vomit? A Comparative Behavioral, Anatomical, and Physiological Study

The vomiting (emetic) reflex is documented in numerous mammalian species, including primates and carnivores, yet laboratory rats and mice appear to lack this response. It is unclear whether these rodents do not vomit because of anatomical constraints (e.g., a relatively long abdominal esophagus) or lack of key neural circuits. Moreover, it is unknown whether laboratory rodents are representative of Rodentia with regards to this reflex. Here we conducted behavioral testing of members of all three major groups of Rodentia; mouse-related (rat, mouse, vole, beaver), Ctenohystrica (guinea pig, nutria), and squirrel-related (mountain beaver) species. Prototypical emetic agents, apomorphine (sc), veratrine (sc), and copper sulfate (ig), failed to produce either retching or vomiting in these species (although other behavioral effects, e.g., locomotion, were noted). These rodents also had anatomical constraints, which could limit the efficiency of vomiting should it be attempted, including reduced muscularity of the diaphragm and stomach geometry that is not well structured for moving contents towards the esophagus compared to species that can vomit (cat, ferret, and musk shrew). Lastly, an in situ brainstem preparation was used to make sensitive measures of mouth, esophagus, and shoulder muscular movements, and phrenic nerve activity-key features of emetic episodes. Laboratory mice and rats failed to display any of the common coordinated actions of these indices after typical emetic stimulation (resiniferatoxin and vagal afferent stimulation) compared to musk shrews. Overall the results suggest that the inability to vomit is a general property of Rodentia and that an absent brainstem neurological component is the most likely cause. The implications of these findings for the utility of rodents as models in the area of emesis research are discussed. © 2013 Horn et al

Identification of neural networks that contribute to motion sickness through principal components analysis of fos labeling induced by galvanic vestibular stimulation

Motion sickness is a complex condition that includes both overt signs (e.g., vomiting) and more covert symptoms (e.g., anxiety and foreboding). The neural pathways that mediate these signs and symptoms are yet to identified. This study mapped the distribution of c-fos protein (Fos)-like immunoreactivity elicited during a galvanic vestibular stimulation paradigm that is known to induce motion sickness in felines. A principal components analysis was used to identify networks of neurons activated during this stimulus paradigm from functional correlations between Fos labeling in different nuclei. This analysis identified five principal components (neural networks) that accounted for greater than 95% of the variance in Fos labeling. Two of the components were correlated with the severity of motion sickness symptoms, and likely participated in generating the overt signs of the condition. One of these networks included neurons in locus coeruleus, medial, inferior and lateral vestibular nuclei, lateral nucleus tractus solitarius, medial parabrachial nucleus and periaqueductal gray. The second included neurons in the superior vestibular nucleus, precerebellar nuclei, periaqueductal gray, and parabrachial nuclei, with weaker associations of raphe nuclei. Three additional components (networks) were also identified that were not correlated with the severity of motion sickness symptoms. These networks likely mediated the covert aspects of motion sickness, such as affective components. The identification of five statistically independent component networks associated with the development of motion sickness provides an opportunity to consider, in network activation dimensions, the complex progression of signs and symptoms that are precipitated in provocative environments. Similar methodology can be used to parse the neural networks that mediate other complex responses to environmental stimuli. © 2014 Balaban et al

Poster Session II, July 14th 2010 — Abstracts Characterization of grip force during badminton strokes

AbstractBadminton is one of the most popular racket sports for which the grip remains crucial for performance. For ergonomic purposes, the hand–handle interface of tennis racket has been studied quite extensively. However, the literature shows a very limited knowledge on badminton grip force intensity. Particularly, the relationship between grip force and different badminton strokes is still poorly understood. Therefore, the purpose of this study was to measure the differences of grip force intensity between four basic badminton strokes, forehand (FH), backhand (BH), smash (SH) and net roll (NR). Ten asymptomatic adult badminton players took part in this study. Grip force was recorded using an embedded capacitive pressure-sensing mat (TekScan 9811) wrapped around a badminton racket handle, from which total grip force could be determined. The sensor was loaded using a force rating of 0-1000N (R2=0,93) and the sampling rate was 500 Hz. The subjects were instructed to hit 20 shuttlecocks, for each stroke, into a target on the court. Only successful trials were analyzed. A one-way repeated measure ANOVA (stroke) was used to compare the effect of grip force. Tukey post-hoc test was used when significant level (p<.05) was reached. Average peak force magnitude was 117,0N±45, 7N, 166, 1N±58, 3N, 209, 0N±56, 1N and 83, 8N±59, 2N for FH, BH, SH and NR conditions respectively. The statistical analysis revealed that grip force applied on the handle was strongly depending upon the stroke, NR grip force was significantly greater than BH (p<.01) and SH (p<.01) grip force. Moreover, the grip force applied in the SH condition was higher than BH condition (p<.01). Data analysis showed that each player had an individual grip force pattern repeatable, but it was observed a strong intersubject variability. The strokes in badminton are a mix of power, precision and manoeuvrability. These characteristics appear to be contradictory: e.g. the literature shows that an increase grip force (power) led to a decrease in wrist motion (manoeuvrability). The main result of the present study is that the subjects took into account these constraints and the type of the strokes by adapting their grip force. Particularly, the precision (NR) and power stroke (SH) were inversely related: a lower grip force led to a greater precision probably allowed by a greater wrist range of motion

Discharge patterns of phrenic motoneurons during fictive coughing and vomiting in decerebrate cats

In decerebrate, paralyzed, and ventilated cats, we recorded the activity of 100 spontaneously active phrenic motor axons during the increased phrenic discharges characteristic of fictive vomiting (FV) and coughing (FC). During control respiratory cycles, approximately one-half the neurons were recruited in the first decile of inspiration; recruitment continued throughout inspiration. During FV, the duration of phrenic discharge was halved; 20 of 26 motoneurons studied were recruited in the first decile of the burst. During FC, recruitment times did not change compared with control, although the duration of the phrenic burst doubled. Discharge frequencies increased and recruitment order of phrenic motoneurons was virtually unaffected during FC and FV. Limited recruitment of previously inactive neurons in the filaments from which we recorded was found during FV and FC. During FV, 1 previously inactive motoneuron was recruited in 16 filaments containing 25 spontaneously active motor axons. During FC, 3 new motoneurons were recruited in addition to the 64 already active in 35 filaments. Recruitment during FV and FC was absent even when recording from filaments known, on the basis of antidromic activation, to contain inactive motor axons. During FV, 10 of 26 motoneurons began their discharges with doublets (interspike interval &lt; 10 ms); doublets occurred in only 4 of 67 motoneurons during FC. Already active phrenic motoneurons contributed to the intense phrenic activity associated with both respiratory (coughing) and nonrespiratory (vomiting) behavior by increases in discharge frequency, earlier recruitment, and doublets; the contribution of previously quiescent motoneurons remains uncertain. </jats:p

The COX inhibitors indomethacin and meloxicam exhibit anti-emetic activity against cisplatin-induced emesis in piglets

International audienc