Proceedings of The Physiological Society

Physiology 2016 (Dublin, Ireland) (2016) Proc Physiol Soc 37, PCA278

Poster Communications

Innate aerobic capacity and adult hippocampal neurogenesis

M. S. Nokia1, S. Lensu2, L. G. Koch3, S. Britton4, J. Wikgren1,5, H. Kainulainen2

1. Department of Psychology, University of Jyvaskyla, Jyvaskyla, Finland. 2. Department of Biology of Physical Activity, University of Jyvaskyla, Jyvaskyla, Finland. 3. Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan, United States. 4. Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, United States. 5. yväskylä Centre for Interdisciplinary Brain Research, Jyväskylä, Finland.

New neurons are generated in select regions of the mammalian brain throughout life. Adult hippocampal neurogenesis (AHN) is known to be enhanced in response to aerobic exercise, especially when it is sustained and voluntary (Nokia et al. 2016). However, the effects of innate low or high aerobic capacity on AHN are less studied. In general, high aerobic capacity associates with a diminished risk for various diseases and longevity (Koch et al. 2012). To study whether innate aerobic capacity is also associated with AHN we examined young and adult male rats selectively bred for either High or Low Capacity for Running (HCR vs. LCR rats) (Koch & Britton, 2001). Currently, there is a ~10-fold difference in running capacity between the ratlines. All the experimental procedures were implemented in accordance with the directive 2010/63/EU of the European Parliament and approved by the National Animal Experiment Board, Finland. At sacrifice, the young rats (generation 36) were 8 weeks and the adult rats (generation 35) 6 months old. The brains were quickly extracted, fixed in paraformaldehyde solution and sectioned into 40-micron thick slices. Every 12th slice including the hippocampus was selected for immunohistochemical staining. One set of slices was stained for Ki67, an endogenous marker of dividing cells, and another for doublecortin, a protein expressed in newly divided cells maturing into neurons (see Nokia et al., 2016 for details of the staining procedure). Independent samples t-test was used for comparisons between rat lines. Results from young rats indicated no difference (p=.488) in hippocampal cell proliferation (Ki67) between the HCR (n=17, mean ± standard deviation: 7.4±4.1 cells/mm3) and the LCR (n=19, 6.6±2.6 cells/mm3) rats. There was also no statistically significant difference (p=.063) between the HCR and the LCR rats in the density of newly born hippocampal neurons (doublecortin, 48.0±13.4 vs. 40.0±11.7 cells/mm3, respectively). A clear difference was evident between adult HCR (n=16/12) and LCR (n=16/13) rats both in the number of proliferating cells (p<.001, 2548±1192 vs. 1382±344, respectively) and in the number of maturing neurons (p<.001, 19118±4713 vs. 10038±2343, respectively). Our results indicate that a genetic predisposition for a high or a low aerobic capacity does not affect hippocampal cell proliferation at an early age. However, there is a tendency for a lower number of immature neurons in the hippocampi of LCR rats compared to that observed in HCR rats. As a function of aging, a clear difference emerges between HCR and LCR rats suggesting that low aerobic capacity eventually results in low levels of AHN. Our results indicate a need for an intervention study, to see if we can prevent the decline in AHN in the LCR rats.

Where applicable, experiments conform with Society ethical requirements