Search

Physical exercise can reduce the cognitive decline associated with traumatic brain injury, yet little is known about the optimal administration schedules. Here, different protocols of voluntary wheel running were evaluated for their effects on object recognition memory (ORM), neuroprotection (NeuN + cells), microglial reactivity (Iba1 staining) and neurogenesis (DCX + cells) after controlled cortical impact injury (CCI). CCI-lesioned rats were divided into a sedentary group and three exercise groups: early discontinued exercise (3 weeks of exercise initiated 4 days post-injury, followed by 4 weeks in a sedentary state); delayed exercise (3 weeks of exercise initiated 4 weeks post-injury), and early continuous exercise (7 weeks of exercise starting 4 days post-injury). The deficits induced by CCI in a 24 h ORM test were reversed in the delayed exercise group and reduced in the early discontinued and early continuous groups. The early discontinued protocol also reduced the loss of NeuN + cells in the hilus, while attenuated microglial reactivity was found in the dorsal hippocampus of both the early exercising groups. Running at the end of the experiment increased the number of DCX + cells in the early continuous and delayed groups, and an inverted U-shaped relationship was found between the mean daily exercise time and the amount of neurogenesis. Thus, exercise had benefits on memory both when it was commenced soon and later after injury, although the neural mechanisms implicated differed. Accordingly, the effects of exercise on memory and neurogenesis appear to not only depend on the specific temporal schedule but also, they may be influenced by the amount of daily exercise., (Copyright © 2020 Elsevier Inc. All rights reserved.)

A number of experiments have shown that physical exercise improves acquisition and retention for a variety of learning tasks in rodents. Most of these works have been conducted with tasks associated with a considerable level of stress, physical effort and/or food deprivation that might interact with exercise, thus hindering the interpretation of the results. On the other hand, it is well established that post-training epinephrine is able to facilitate memory consolidation, but only a few works have studied its effect on the process of acquisition. The present work was aimed at studying whether 17 days of voluntary physical exercise (running wheels) and/or post-training epinephrine (0.01 or 0.05 mg/kg) could improve the acquisition of a spatial task in the Barnes maze, and whether the combination of the two treatments have additive effects. Our results showed that exercise improved acquisition, and 0.01 mg/kg of epinephrine tended to enhance it, by reducing the distance needed to find the escape hole. The combination of both treatments failed to further improve the acquisition level. We concluded that both treatments exerted their effect on acquisition by enhancing the process of learning itself, and that exercise is able to improve acquisition even using tasks with a low level of stress and physical effort., (Copyright © 2013 Elsevier B.V. All rights reserved.)

The effect of long-term voluntary exercise (running wheel) on anxiety-like behaviour (plus maze and open field) and learning and memory processes (object recognition and two-way active avoidance) was examined on Wistar rats. Because major individual differences in running wheel behaviour were observed, the data were analysed considering the exercising animals both as a whole and grouped according to the time spent in the running wheel (low, high, and very-high running). Although some variables related to anxiety-like behaviour seem to reflect an anxiogenic compatible effect, the view of the complete set of variables could be interpreted as an enhancement of defensive and risk assessment behaviours in exercised animals, without major differences depending on the exercise level. Effects on learning and memory processes were dependent on task and level of exercise. Two-way avoidance was not affected either in the acquisition or in the retention session, while the retention of object recognition task was affected. In this latter task, an enhancement in low running subjects and impairment in high and very-high running animals were observed.

The present experiments determined the consequences of blocking muscarinic cholinergic receptors of the prelimbic (PL) cortex in the acquisition and retention of an odor-reward associative task. Rats underwent a training test (five trials) and a 24-h retention test (two retention trials and two relearning trials). In the first experiment, rats were bilaterally infused with scopolamine (20 or 5 microg/site) prior to training. Although scopolamine rats showed acquisition equivalent to PBS-injected controls, they exhibited weakened performance in the 24-h retention test measured by number of errors. In the second experiment, rats were injected with scopolamine (20 microg/site) immediately or 1 h after training and tested 24 h later. Scopolamine rats injected immediately showed severe amnesia detected in two performance measures (errors and latencies), demonstrating deficits in retention and relearning, whereas those injected 1 h later showed good 24-h test performance, similar to controls. These results suggest that muscarinic transmission in the PL cortex is essential for early memory formation, but not for acquisition, of a rapidly learned odor discrimination task. Findings corroborate the role of acetylcholine in consolidation processes and the participation of muscarinic receptors in olfactory associative tasks.

A rapidly learned odor discrimination task based on spontaneous foraging behavior of the rat was used to evaluate the role of N-methyl-D-aspartate (NMDA) receptors (NMDARs) in ongoing memory consolidation. Rats were trained in a single session to discriminate among three odors, one of which was associated with palatable food reward. Previous experiments showed that the NMDAR antagonist DL-APV induced amnesia for this task when injected immediately after training. In the present study, memory was reactivated 24 h after training by exposure to the rewarded odor within the experimental context after which rats received an intracerebroventricular injection of APV. Combined reactivation-drug treatment induced profound amnesia when tested 48 h later. Animals receiving drug alone, in absence of reactivation, showed perfect retention. It is concluded that NMDARs support a consolidation process taking place after memory reactivation.

A rapidly learned odor discrimination task based on spontaneous foraging behavior of the rat was used to evaluate the role of N-methyl-D-aspartate (NMDA) receptors (NMDARs) in ongoing memory consolidation. Rats were trained in a single session to discriminate among three odors, one of which was associated with palatable food reward. Previous experiments showed that the NMDAR antagonist DL-APV induced amnesia for this task when injected immediately after training. In the present study, memory was reactivated 24 h after training by exposure to the rewarded odor within the experimental context after which rats received an intracerebroventricular injection of APV. Combined reactivation-drug treatment induced profound amnesia when tested 48 h later. Animals receiving drug alone, in absence of reactivation, showed perfect retention. It is concluded that NMDARs support a consolidation process taking place after memory reactivation. (Contains 2 figures.)

Copyright of Laocoonte is the property of Sociedad Espanola de Estetica y Teoria de las Artes and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Abstract: We studied whether posttraining epinephrine accelerates the process of acquisition, and whether this effect leads to an enduring high level of performance on a long-term memory test (20 days). Rats were submitted to daily massed (30 trials) two-way active avoidance conditioning sessions followed by systemic epinephrine (0.01 mg/kg) or vehicle, until achieving a learning criterion (80% avoidances in one single session, maximum 14 sessions). By the sixth session, 78% of the animals with posttraining epinephrine attained the learning criterion compared to only the 23% of the rats in the vehicle group. Considering the whole acquisition phase, all the epinephrine treated animals, but only 66.67% in the vehicle group, reached the criterion. On the retention test, both groups maintained the level of performance reached at the end of the acquisition phase. We conclude that epinephrine accelerates the process of acquisition by enhancing memory consolidation, and that this effect might be especially useful in high demanding learning tasks, or for animals with low learning capacities. [Copyright &y& Elsevier]

Septal lesions impair a variety of tasks, including inhibitory avoidance and one way active avoidance. In contrast, these lesions improve two-way active avoidance, probably by reducing anxiety. The present work aimed to study whether anterodorsal medial septal lesion (a) improves performance of two-way active avoidance task (Experiment I), as it has been observed with wider septal lesion, and (b) affect anxiety and/or locomotor activity (Experiment II).This precise region was chosen because some evidences suggest that its lesion do not lead to a reduction of anxiety. Lesioned rats tended to make a higher, but statistically non-significant (P=0.074), number of avoidances regardless of the session, being this difference statistically significant on the retention session (RT). The same lesion did not appear to have an anxiolytic effect, and did not affected basal locomotor activity. Different possible explanations of our results are discussed. [Copyright &y& Elsevier]

• Traumatic brain injury impaired the "when" (temporal order) and "where" (object location) components of episodic-like memory. • Voluntary physical exercise initiated 11 days after injury reversed "when" and "where" memory deficits after TBI. • Enhanced hippocampal BDNF, related to physical exercise treatment, was involved in memory recovery. Physical exercise has been associated with improved cognition and may even reduce memory deficits after brain injuries. The aims of this work were to: 1) assess whether voluntary physical exercise can reduce the deficits associated with traumatic brain injury (TBI) in two different components of episodic-like memory based on object recognition, temporal order memory ("when"), and object location memory ("where"); and 2) determine whether changes in levels of brain-derived neurotrophic factor (BDNF) in the hippocampus and prefrontal cortex, as well as alterations in hippocampal cytokines, insulin-like growth factor-1 (IGF-1) and vascular endothelial growth factor (VEGF), may influence the effects exercise has on either or both tasks. The rats were distributed into a sham group, a TBI group that remained sedentary (TBI-sed), and a TBI group that had access to a running wheel for a 25-day period from post-injury day 11 (TBI-exe). The rats were sacrificed after the "where" memory task, at post-injury day 37. Physical exercise restored the "when" and "where" memories, which had been impaired by the TBI, and increased the concentration of BDNF in the hippocampus, but not the prefrontal cortex. Neither TBI nor exercise were found to significantly affect hippocampal cytokines, IGF-1 or VEGF at this time post-injury. BDNF levels showed significant positive correlations with exercise, and with "when" (but not "where") memory. These results indicate that post-injury physical exercise restores "when" and "where" object recognition memory tasks after TBI, and that increased BDNF seems to be involved in this effect, particularly with regard to "when" memory. [ABSTRACT FROM AUTHOR]