title: Reorganization of functional brain maps after exercise training: Importance of cerebellar-thalamic-cortical pathway.
abstract: Exercise training (ET) causes functional and morphologic changes in normal and injured brain. While studies have examined effects of short-term (same day) training on functional brain activation, less work has evaluated effects of long-term training, in particular treadmill running. An improved understanding is relevant as changes in neural reorganization typically require days to weeks, and treadmill training is a component of many neurorehabilitation programs. Adult, male rats (n=10) trained to run for 40 min/day, 5 days/week on a Rotarod treadmill at 11.5 cm/s, while control animals (n=10) walked for 1 min/day at 1.2 cm/s. Six weeks later, [(14)C]-iodoantipyrine was injected intravenously during treadmill walking. Regional cerebral blood flow-related tissue radioactivity was quantified by autoradiography and analyzed in the three-dimensionally reconstructed brain by statistical parametric mapping. Exercised compared to nonexercised rats demonstrated increased influence of the cerebellar-thalamic-cortical (CbTC) circuit, with relative increases in perfusion in deep cerebellar nuclei (medial, interposed, lateral), thalamus (ventrolateral, midline, intralaminar), and paravermis, but with decreases in the vermis. In the basal ganglia-thalamic-cortical circuit, significant decreases were noted in sensorimotor cortex and striatum, with associated increases in the globus pallidus. Additional significant changes were noted in the ventral pallidum, superior colliculus, dentate gyrus (increases), and red nucleus (decreases). Following ET, the new dynamic equilibrium of the brain is characterized by increases in the efficiency of neural processing (sensorimotor cortex, striatum, vermis) and an increased influence of the CbTC circuit. Cerebral regions demonstrating changes in neural activation may point to alternate circuits, which may be mobilized during neurorehabilitation.
authors.affiliation: Department of Psychiatry and the Behavioral Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. holschne@usc.edu
authors.forename: D P
authors.initials: DP
authors.lastname: Holschneider
authors.forename: J
authors.initials: J
authors.lastname: Yang
authors.forename: Y
authors.initials: Y
authors.lastname: Guo
authors.forename: J-M I
authors.initials: JM
authors.lastname: Maarek
mesh_terms: D000818:Animals; D000983:Antipyrine / Q000031:analogs & derivatives / Q000378:metabolism; D001345:Autoradiography; D001522:Behavior, Animal; D001931:Brain Mapping; D002531:Cerebellum / Q000502:physiology*; D002540:Cerebral Cortex / Q000502:physiology*; D002560:Cerebrovascular Circulation; D007091:Image Processing, Computer-Assisted; D008297:Male; D008954:Models, Biological; D009434:Neural Pathways / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D013788:Thalamus / Q000502:physiology*; D014316:Tritium / Q000378:metabolism
chemical_list: D014316:Tritium; D000983:Antipyrine; C008135:iodoantipyrine