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The aim of this research is to evaluate whether posttraining systemic epinephrine is able to improve object recognition memory in rats with memory deficits produced by traumatic brain injury. Forty-nine two-month-old naïve male Wistar rats were submitted to surgical procedures to induce traumatic brain injury (TBI) or were sham-operated. Rats were trained in an object recognition task and, immediately after training, received an intraperitoneal injection of distilled water (Sham-Veh and TBI-Veh group) or 0.01 mg/kg epinephrine (TBI-Epi group) or no injection (TBI-0 and Sham-0 groups). Retention was tested 3 h and 24 h after acquisition. The results showed that brain injury produced severe memory deficits and that posttraining administration of epinephrine was able to reverse them. Systemic administration of distilled water also had an enhancing effect, but of a lower magnitude. These data indicate that posttraining epinephrine and, to a lesser extent, vehicle injection reduce memory deficits associated with TBI, probably through induction of a low-to-moderate emotional arousal. [ABSTRACT FROM AUTHOR]

Bilateral damage to the pedunculopontine tegmental nucleus (PPTg) has been found to impair several learning tasks; however, it is not clear whether this effect could be at least partially attributable to changes in the rat emotional reactivity and/or spontaneous locomotion. Therefore, the present work has tested the effects of bilateral electrolytic lesions of the PPTg on the behaviour of rats in the elevated plus-maze and the open field test. Because the behaviour of rats in learning and emotional tasks can be sensitive to routine experimental manipulations, we also have tested the effects of brief pre-surgical handling procedures on anxiety-like behaviours and locomotion in both lesioned and control rats. Lesions of the pedunculopontine tegmental nucleus (1) did not have any effects on spontaneous locomotor activity and (2) did not increase emotional reactivity. In fact, there was a slight bias towards a reduction in anxiety-like behaviours in lesioned rats, as evidenced by a significant increase in the number of open arm entries. Pre-surgical handling induced a slight decrease of emotional reactivity and a slight increase of exploratory activity. We conclude that damage to the pedunculopontine tegmental nucleus is not accompanied by either an enhancement of emotional reactivity or by an altered spontaneous locomotion. [Copyright &y& Elsevier]

(1) Background: Stroke is a major cause of permanent disability in multiple functions, including the cognitive domain. Since both cognitive training and aerobic physical exercise may exert positive effects on cognition after stroke, one may expect synergistic benefits when combining both interventions. (2) Methods: We carried out a systematic search of studies testing, in adult stroke patients, whether structured aerobic exercise combined with cognitive training led to higher cognitive benefits than either of these interventions when applied singly, or than interventions not including aerobic exercise or cognitive training. (3) Results: Five fair-quality randomized controlled trials fulfilled the search criteria. Exercise intensity was moderate-vigorous and cognitive training was mainly computer-based. The studies were heterogeneous regarding the cognitive tests used, and for this reason, a meta-analysis was not performed. Only three studies included follow-up assessment. The combined intervention was associated with pre-post improvement in at least one cognitive test in all the studies, and with higher positive effects compared to other conditions (although statistical significance was not always reached) in four studies. (4) Conclusions: Further trials including a long-term follow-up and comprehensive neuropsychological testing should be undertaken to determine whether combined aerobic exercise and cognitive training leads to additive cognitive benefits after stroke. [ABSTRACT FROM AUTHOR]

The effects of posttraining excitotoxic lesions of the pedunculopontine tegmental nucleus (PPTg) on two-way active avoidance after changing the conditioned stimulus (CS) used during prelesion training were examined. Prelesion training was carried out with either a tone or a light as the CS, and this CS was changed during postlesion training. Replacing the tone with a light reduced the performance of control and lesioned rats, but the degree of reduction was higher in the latter. Replacing the light with a tone had slight detrimental effects in lesioned rats but not in controls. Thus, posttraining PPTg lesions slowed down the reacquisition of shuttle-box avoidance under conditions of CS transfer, an effect that may be attributable to disruption of attention and/or gating of sensory stimuli. [ABSTRACT FROM AUTHOR]

• 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]

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. Unlabelled Image • Early and delayed voluntary wheel running reduce memory deficits after TBI in rats. • Early exercise attenuates hippocampal microglial reactivity and neuron loss. • Restored neurogenesis mediates memory recovery by close-to-training exercise. • Moderate amounts of daily exercise lead to the highest neurogenesis levels. [ABSTRACT FROM AUTHOR]