Continuous and not continuous 2-week treadmill training enhances the performance in the passive avoidance test in ischemic gerbils.

This study aims to investigate the frequency and total duration effects of the 2-week treadmill training after experimental ischemic stroke in the passive avoidance test. We performed bilateral occlusion of common external carotid arteries, for five minutes, in Mongolian gerbils. The training groups were: continuous training for twelve consecutive days or not continuous training for six non-consecutive days. The groups remained in the treadmill for 15min, with the speed set at 10m/min, and the training started 24h after the stroke. In the Shuttle Box, each animal had ten trials during the Learning Session (LS), which occurred 24h before the stroke. The Retention Test (RT) occurred 24h after the stroke and started on the second, third, seventh and twelfth day after LS. After the experiments, the brains were perfused, and coronal sections of the CA1 area of the hippocampus were cut and stained with hematoxylin and eosin. ANOVA on Ranks was used for Behavioral data analysis and morphological data by percentage. Ischemic training groups showed preservation in neuron density in the CA1 area of the hippocampus, when compared to the control groups. Animals subjected to continuous training, showed a higher latency in the RT when compared to ischemic animals in both weeks [(2nd, H=39.81; P<0.05), (3rd, H=38.08; P<0.05), (7th, H=44.17; P<0.05), and (12th, H=39.55; P<0.05). Animals in the not continuous training showed higher latency in the RT, in the second week only [(2nd, H=39.81; P<0.05), (3rd, H=38.08; P<0.05), (7th, H=44.17; P<0.05), and (12th, H=39.55; P<0.05). These findings suggest that improvement of memory after stroke after treadmill training is dependent on the frequency and total duration of training.

Inverse Phosphatidylcholine/Phosphatidylinositol Levels as Peripheral Biomarkers and Phosphatidylcholine/Lysophosphatidylethanolamine-Phosphatidylserine as Hippocampal Indicator of Postischemic Cognitive Impairment in Rats.

Vascular dementia is a transversal phenomenon in different kinds of neurodegenerative diseases involving acute and chronic brain alterations. Specifically, the role of phospholipids in the pathogenesis of dementia remains unknown. In the present study, we explored phospholipid profiles a month postischemia in cognitively impaired rats. The two-vessel occlusion (2-VO) model was used to generate brain parenchyma ischemia in adult male rats confirmed by alterations in myelin, endothelium, astrocytes and inflammation mediator. A lipidomic analysis was performed via mass spectrometry in the hippocampus and serum a month postischemia. We found decreases in phospholipids (PLs) associated with neurotransmission, such as phosphatidylcholine (PC 32:0, PC 34:2, PC 36:3, PC 36:4, and PC 42:1), and increases in PLs implied in membrane structure and signaling, such as lysophosphatidylethanolamine (LPE 18:1, 20:3, and 22:6) and phosphatidylserine (PS 38:4, 36:2, and 40:4), in the hippocampus. Complementarily, PC (PC 34:2, PC 34:3, PC 38:5, and PC 36:5) and ether-PC (ePC 34:1, 34:2, 36:2, 38:2, and 38:3) decreased, while Lyso-PC (LPC 18:0, 18:1, 20:4, 20:5, and LPC 22:6) and phosphatidylinositol (PI 36:2, 38:4, 38:5, and 40:5), as neurovascular state sensors, increased in the serum. Taken together, these data suggest inverse PC/LPC-PI levels as peripheral biomarkers and inverse PC/LPE-PS as a central indicator of postischemic cognitive impairment in rats.

Behavioral effects and neural changes induced by continuous and not continuous treadmill training, post bilateral cerebral ischemia in gerbils.

This study aims to investigate the effects of treadmill training and the possible influences of the start, regularity, and duration after experimental ischemic stroke. We performed bilateral occlusion of both the carotid arteries for 5 min in Mongolian gerbils. The training groups were: continuous training for 5 consecutive days or not continuous training for 3 non-consecutive days. The groups remained in the treadmill for 15 min, and the training started 12 or 24h after the stroke. In the activity cage (AC), behaviors of crossing and distance traveled were registered. The forced motor behavior was analyzed by a Rota Rod test. After the experiments, the brains were perfused, and coronal sections of the striatum, motor cortex M1, and CA1 area of the hippocampus were cut and stained with hematoxylin and eosin. Behavioral and morphological data analysis was performed by an ANOVA and MANCOVA. Results showed an increased density of neurons in the CA1 area of the hippocampus, motor cortex M1, and the striatum in ischemic training groups compared to the not training ischemic groups. Animals subjected to continuous training that started 24h after ischemia showed a satisfactory behavior in the AC and a higher number of striatal neurons when compared to ischemic animals. The animals in the not continuous training started 12h after the stroke showed an unsatisfactory performance in the AC and Rota Rod. These findings suggest that early training and not continuous training are inadequate for motor behavior improvement after stroke.