Guest, Bruce B. and John R. Gray. Responses of a looming sensitive neuron to compound and paired object approaches. J Neurophysiol 95: 1428 -1441, 2006. First published November 30, 2005 doi:10.1152/jn.01037.2005. The lobula giant movement detector (LGMD) and its target neuron, the descending contralateral movement detector (DCMD), constitute a motion-sensitive pathway in the locust visual system that responds preferentially to objects approaching on a collision course.LGMD receptive field properties, anisotropic distribution of local retinotopic inputs across the visual field, and localized habituation to repeated stimuli suggest that this pathway should be sensitive to approaches of individual objects within a complex visual scene. We presented locusts with compound looming objects while recording from the DCMD to test the effects of nonuniform edge expansion on looming responses. We also presented paired objects approaching from different regions of the visual field at nonoverlapping, closely timed and simultaneous approach intervals to study DCMD responses to multiple looming stimuli. We found that looming compound objects evoked characteristic responses in the DCMD and that the time of peak firing was consistent with predicted values based on a weighted ratio of the half size of each distinct object edge and the absolute approach velocity. We also found that the azimuthal position and interval of paired approaches affected DCMD firing properties and that DCMDs responded to individual objects approaching within 106 ms of each other. Moreover, comparisons between individual and paired approaches revealed that overlapping approaches are processed in a strongly sublinear manner. These findings are consistent with biophysical mechanisms that produce nonlinear integration of excitatory and feed-forward inhibitory inputs onto the LGMD that have been shown to underlie responses to looming stimuli.
BackgroundDuodenitis‐proximal jejunitis (DPJ) is an acute sporadic gastrointestinal disorder of horses of unknown cause.Hypothesis/ObjectivesWe hypothesize that Clostridium difficile toxins are involved in the pathogenesis of DPJ in horses. The objective of this study was to determine whether experimentally delivered C. difficile toxins cause clinical signs and histologic lesions similar to those of naturally occurring DPJ.AnimalsSix healthy mature mixed breed horses.MethodsExperimental study: animal model of animal disease. Fasted horses were administered crude C. difficile toxins via gastroscopy and monitored for up to 48 hour. Blood was collected for complete blood cell count, biochemistry profile, and plasma fibrinogen assay, and abdominal fluid was collected for cytologic analysis and total solids before and after toxin administration. Physical examination and abdominal ultrasonography were performed throughout the study period. Tissues were collected from the gastrointestinal tract and processed for routine histologic analysis, and lesions were scored.ResultsClinical signs were observed in 2 of 6 horses that are typical although not specific for horses with naturally occurring DPJ. Histopathologic lesions were observed in 6 of 6 horses and were similar to those reported in horses with naturally occurring DPJ. Two horses were severely affected.Conclusions and Clinical ImportanceDuodenitis‐proximal jejunitis is likely a syndrome with multiple causes that result in the same clinical and pathologic findings, and our data suggest that the toxins of C. difficile represent one cause of this syndrome. Toxin dose and variation in individual animal susceptibility might affect the clinical signs and lesions after administration of C. difficile toxins.
Calcification of the tunica media of the axial pulmonary arteries (PA) has been reported in a large proportion of racehorses. In humans, medial calcification is a significant cause of arterial stiffening and is implicated in the pathogenesis of cardiac, cerebral, and renal microvascular diseases. Pulse wave velocity (PWV) provides a measure of arterial stiffness. This study aimed to develop a technique to determine PA-PWV in horses and, secondarily, to investigate a potential association between PA-PWV and arterial fibro-calcification. A dual-pressure sensor catheter (PSC) was placed in the main PA of 10 sedated horses. The pressure waves were used to determine PWV along the PA, using the statistical phase offset method. Histological analysis of the PA was performed to investigate the presence of fibro-calcified lesions. The mean (±SD) PWV was 2.3 ± 0.7 m/s in the proximal PA trunk and 1.1 ± 0.1 m/s further distal (15 cm) in a main PA branch. The mean (±SD) of mean arterial pressures in the proximal PA trunk was 30.1 ± 5.2 mmHg, and 22.0 ± 6.0 mmHg further distal (15 cm) within the main PA branch. The mean (±SD) pulse pressure in the proximal PA trunk was 15.0 ± 4.7 mmHg, and 13.5 ± 3.3 mmHg further distal (15 cm) within the main PA branch. Moderate to severe lesions of the tunica media of the PAs were observed in seven horses, but a correlation with PWV could not be established yet. Pulmonary artery PWV may be determined in standing horses. The technique described may allow further investigation of the effect of calcification of large PAs in the pathogenesis of equine pulmonary circulatory disorders. Pulmonary artery pulse wave velocity was determined safely in standing sedated horses. The technique described may allow further investigation of the effect of calcification of large pulmonary arteries in the pathogenesis of pulmonary circulatory disorders in horses.
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