Also: Amyotrophic Lateral Sclerosis & Gait in Mice in JNER.
To see a menu of other published PhysioFeature articles, please click here.
Gait Analysis in Guinea Pigs
Ajit Kale, Roberta Nelson, Adyl Kenouche, Scott Glazier, Scott McCue, Ivo Amende, and Thomas G. Hampton.
Mouse Specifics, Inc., Boston, MA. USA.
Web Published: March 18, 2006
Abstract
Gait analysis in rodent models of human diseases is increasingly becoming important for deciphering the pathophysiology of motor dysfunction. Very little is known, however, regarding gait in guinea pigs, despite their widespread use in experimental models, including osteoarthritis, spinal cord injury, and vestibular disorders. We have previously described gait in mouse and rat models of human diseases, including Parkinson’s, Huntington’s, ALS, and spinal cord injury. Here we applied ventral plane videography to study the gait of guinea pigs through a range of walking speeds. Gait in guinea pig share some characteristics common to mice and rats. However, some aspects of gait appear to be specific to guinea pigs which may increase their utility in the study of models of movement disorders.
Methods
Figure 1.
Figure 2.
Figure 3.
Guinea Pigs (male, 275 ± 5 g) were obtained from Harlan (Indianapolis, IN). Gait dynamics were monitored using the DigiGait Imaging system. A minimum of 10 complete strides at walking speeds of 18 cm/s, 27 cm/s, and 36 cm/s was imaged. More than 24 metrics of posture and locomotion were determined, including gait variability, stride frequency, and stepping sequence.
Results
Figure 1 illustrates the ventral view of a guinea pig walking at speed of 18 cm/s. DigiGait software converted the images to grayscale to generate digital prints of the paws as they advanced and retreated from the treadmill belt throughout each stride (Figure 2). Forelimb and hind limb stride length, stance duration, and swing duration were comparable in the guinea pig. The braking duration was longer and the propulsion duration shorter of forelimbs than of hind limbs at all 3 walking speeds. As walking speed was increased from 18 cm/s, to 27 cm/s and 36 cm/s, the stance duration decreased from 421 ms to 309 ms and 255 ms, respectively. Swing duration, however, did not change appreciably (from 119 ms at 18 cm/s to 107 ms at 27 cm/s, and to 102 ms at 36 cm/s). Stride length increased from 10.3 cm to 11.9 cm and 12.8 cm. Step frequency increased from 1.9 Hz at 18 cm/s to 2.4 Hz at 27 cm/s, and to 2.9 Hz at 36 cm/s. The stance width and angles of paw placement narrowed with increasing speed (Figure 3).
Discussion
This is one of the first quantitative descriptions of gait dynamics in the guinea pig. The marching gait of the guinea pig is distinctively different than the alternate gait observed often in rats and mice (1). Gait variability was lower in the guinea pig than what we have reported in mice (2). The paw placement angle of the hind limbs (~8 deg) is notably less open than rats and mice (~15 deg) walking at comparable speeds (3). The stance width of the hind limbs of the guinea pig was reduced by nearly half when the walking speed was doubled from 18 cm/s to 36 cm/s. The stride length increased by ~25%, whereas the step frequency increased by ~50% when the walking speed was raised from 18 cm/s to 36 cm/s. Qualitative descriptors of gait in guinea pigs have been used to describe the effects of osteoarthritis (4), peripheral neuropathy (5), and sarin exposure (6). We were surprised that gait analysis had not been performed yet in guinea pig models to study spinal cord injuries (7) and vestibular disorders (8). The physique and posture of the guinea pig may preclude gait analysis by inspection or via side view imaging. The method of ventral plane videography, which we invented (9), may provide the opportunity for further explore motor function disorders in guinea pig models and accelerate the testing of the efficacy of therapies.
References
Kale, A. et al. 2004. Alcohol Clin. Exp. Res. 12:1839-1848.
Amende, I. et al. 2005. J. Neuroengineering Rehabil. 2:20.
Hampton, T.G. et al. 2004. Physiol. Behav. 82:381-389.
Arsever, C.L. and G.G. Bole. 1986. Arthritis Rheum. 29:251-261.
Terril-Robb, L.A. et al. 1996. Proc. Soc. Exp. Biol. Med. 213:50-58.
Hulet, S.W. et al. 2002. Pharmacol. Biochem. Behav. 72:835-845.
Borgens, R.B. et al. 2004. J. Neurosci. Res. 2004. 76:141-154.
Yin, S. et al. 2006. Otol. Neurotol. 2006. 27:78-85.
