Brain research
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Reports of beneficial effects of exercise on psychological health in humans are increasingly supported by basic research studies. Exercise is hypothesized to regulate antidepressant-related mechanisms and we therefore characterized the effects of chronic exercise in mouse behavioral paradigms relevant to antidepressant actions. Mice given free access to running wheels showed antidepressant-like behavior in learned helplessness, forced-swim (FST) and tail suspension paradigms. ⋯ A possible functional contribution of a BDNF signaling pathway to FST performance in exercising mice was investigated using the specific MEK inhibitor PD184161 to block the MAPK signaling pathway. Subchronic administration of PD184161 to exercising mice blocked the antidepressant-like behavioral response seen in vehicle-treated exercising mice in the FST. In summary, chronic wheel-running exercise in mice results in antidepressant-like behavioral changes that may involve a BDNF related mechanism similar to that hypothesized for antidepressant drug treatment.
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Comparative Study
Age-related differences in brain activity during verbal recency memory.
In the current event-related fMRI study young and older adults underwent fMRI scanning while performing recognition, recency and reverse alphabetizing tasks. The reverse alphabetizing task served as a control for executive processes, such as working memory manipulation and monitoring (Henson, R. N., Shallice, T., et al., 1999. ⋯ In young adults, activity in these regions was not strongly related to retrieval performance. These results suggest that older adults exhibited deficits in medial temporal and parietal function during retrieval, which was functionally compensated for by increased recruitment of prefrontal and precuneus regions. This functional compensation was sufficient for maintaining recognition but not recency retrieval in older adults.
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Recent evidence suggest that ATP plays a role as an endogenous pain mediator generating and/or modulating pain signaling from the periphery to the spinal cord. In this study we evaluated the effects of intraperitoneal administration of P2 receptor antagonist, pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), evaluating pain related behaviours and monitoring the expression of Fos, a marker of activated neurons, in an experimental mouse model of neuropathic pain (sciatic nerve tying). The PPADS administration decreased both tactile allodynia and thermal hyperalgesia in a time and dose dependent manner. ⋯ Moreover, non-noxious stimulation induced an increase of Fos positive neurons in the spinal cord of animals with tying of sciatic nerve. PPADS administration partially reversed this increase. These results suggest that PPADS reduces neuronal activation at spinal cord level and that P2 receptors are involved in the retrograde signalling progress exciting sensory spinal neurons.
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Aside from anatomical repairs, the reestablishment of sensory and motor innervations for proper functional recovery is one of the fundamental objectives of reconstructive surgery. The heterotopic transfer of autologous tissues is likely to result in a size discrepancy between the donor and recipient nerves, which will have a negative influence on regeneration. Twenty Wistar albino female rats were used in a study that was divided into two main groups: tibial-peroneal (TP) and peroneal-tibial repair (PT). ⋯ In both TP and PT groups, the increase in the axon number, axon area and myelin thickness were statistically different in favor of the vein graft sides. An appearance of vacuoles and degenerated pertinacious material within the myelin sheath of EtoE sides was seen. A histomorphological examination of the sections proximal to, from, and distal to the repair zone over three months revealed less epineural scarring, a thinner epineurium, more regenerated axons and fewer inflammatory cells in groups where vein grafting was used, because the vein graft provided additional mechanical and chemical support in the size discrepancy of the nerve regeneration.
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Behavioral investigations have shown that general anesthetics at low concentration have enhancing effects on learning and memory in some animal models. In the present experiments, in order to elucidate the cellular mechanisms underlying such memory enhancement, the effects of anesthetics at low doses on synaptic plasticity in the hippocampus were investigated. Tight-seal whole-cell recordings were made from CA1 pyramidal cells in hippocampal slices prepared from adult male mice, and the effects of subanesthetic concentrations of the volatile anesthetic sevoflurane on the glutamatergic excitatory postsynaptic currents (EPSCs) were investigated. ⋯ These observations suggest that sevoflurane at anesthetic concentration presynaptically inhibits excitatory synaptic transmission and at subanesthetic concentration postsynaptically enhances excitatory synaptic transmission in the hippocampal CA1 region. Further, subanesthetic sevoflurane seems to exert facilitatory effects on the EPSP-to-spike coupling process in the postsynaptic neurons. These results might provide clues as to the cellular mechanism of light level of sevoflurane anesthesia.