Abstract
This study used in vivo magnetic resonance imaging (MRI) to identify age dependent brain structural characteristics in Dunkin Hartley guinea pigs. Anatomical T2-weighted images, diffusion kurtosis (DKI) imaging, and T2 relaxometry measures were acquired from a cohort of male guinea pigs from postnatal day (PND) 18–25 (juvenile) to PND 46–51 (adolescent) and PND 118–123 (young adult). Whole-brain diffusion measures revealed the distinct effects of maturation on the microstructural complexity of the male guinea pig brain. Specifically, fractional anisotropy (FA), as well as mean, axial, and radial kurtosis in the corpus callosum, amygdala, dorsal-ventral striatum, and thalamus significantly increased from PND 18–25 to PND 118–123. Age-related alterations in DKI measures within these brain regions paralleled the overall alterations observed in the whole brain. Age-related changes in FA and kurtosis in the gray matter-dominant parietal cerebral cortex and dorsal hippocampus were less pronounced than in the other brain regions. The regional data analysis revealed that between-age changes of diffusion kurtosis metrics were more pronounced than those observed in diffusion tensor metrics. The age-related anatomical differences reported here may be important determinants of the age-dependent neurobehavior of guinea pigs in different tasks.
Highlights
The guinea pig is a translationally relevant animal model for preclinical studies of disorders that afflict the developing and the aging brain [1,2,3]
As measured from the anterior olfactory bulb to posterior cerebellum, increased by 15% (F(2,10) = 47.5, p < 0.001), and brain width between the temporal poles increased by 8% (F(2,10) = 262.04, p < 0.001), from juvenile to young adult ages (Table 1)
The same pattern of growth is evident regarding the brain parenchymal tissue volume, which increased by about 28% from juvenile age to adulthood (F(2,10) = 611.79, p < 0.001)
Summary
The guinea pig is a translationally relevant animal model for preclinical studies of disorders that afflict the developing and the aging brain [1,2,3]. In developmental neurobiology and neurotoxicology, the guinea pig is a valuable model, because the temporal development of its brain closely resembles that of the human brain [4,5]. Placentation and hormonal control of pregnancy in humans and guinea pigs are remarkably similar [2]. Levels of metabolic enzymes that inactivate a number of developmental neurotoxicants, organophosphorus compounds, are more comparable between humans and guinea pigs than rats or mice [6]. In the neurobiology of aging, guinea pigs have emerged as a unique model for sporadic Alzheimer’s disease (AD), in part because of their genetic profile. The sequence of numerous proteins known to be involved in
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