Neuroscience
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It is well established that physical exercise can exert neuroprotection both in clinical settings and animal experiments. A series of studies have demonstrated that physical exercise may be a promising preconditioning method to induce brain ischemic tolerance through the promotion of angiogenesis, mediation of the inflammatory response, inhibition of glutamate over-activation, protection of the blood brain barrier (BBB) and inhibition of apoptosis. Through these mechanisms, exercise preconditioning may reduce the neural deficits associated with ischemia and the development of brain infarction and thus provide brain ischemic tolerance. An awareness of the benefits of exercise preconditioning may lead more patients to accept exercise therapy in cases of ischemic stroke.
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Comparative Study
Morphological and electrophysiological properties of pyramidal-like neurons in the stratum oriens of Cornu ammonis 1 and Cornu ammonis 2 area of Proechimys.
Proechimys (Rodentia: Echimyidae) is a neotropical rodent of the Amazon region that has been successfully colonized in the laboratory and used for experimental medicine. Preliminary studies indicated that Proechimys (casiragua) rodents express an atypical resistance to developing a chronic epileptic condition in common models of temporal lobe epilepsy. Moreover, previous investigation of our laboratory described a remarkably different Proechimy's cytoarchitecture organization of the hippocampal CA2 subfield. ⋯ In addition, the apical dendrites of these neurons were oriented in parallel to apical dendrites of regular pyramidal neurons in stratum pyramidale. Moreover, these neurons were immunoreactive to SM311 as the majority of the neurons of the pyramidal layer. The functional role of these hippocampal neurons of the rodent Proechimys deserves further investigation.
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Non-motor symptoms, such as fear of falling and anxiety, are frequently reported in Parkinson's disease (PD). Recent evidence of anxiety and fear directly influencing balance control in healthy young and older adults, raises the question whether fear of falling and anxiety also directly contribute to the balance deficits observed in PD. The goal of the current study was to examine whether PD patients and controls responded similarly or differently to experimentally induced increases in anxiety. ⋯ These results indicate that during the ON state, static balance in PD patients and controls is equally susceptible to the influence of anxiety. Significant correlations observed between COP changes and measures of fear and anxiety provide evidence to support the proposed neural links between structures controlling emotion and postural control. Future studies should further address this issue by including more severely affected patients, by testing the influence of dopaminergic medication, by including more anxious patients, and by using dynamic measures of balance.
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The involvement of substance P (SP) in neuronal sensitization through the activation of the neurokinin-1-receptor (NK1r) in postsynaptic dorsal horn neurons has been well established. In contrast, the role of SP and NK1r in primary sensory dorsal root ganglion (DRG) neurons, in particular in the soma, is not well understood. In this study, we evaluated whether SP modulated the NMDA-evoked transient increase in cytoplasmic Ca2+ ([Ca2+]cyt) in the soma of dissociated adult DRG neurons. ⋯ In none of the conditions we detected phosphorylation of the NR2B subunit at Ser-1303. Phosphorylation of the NR2B subunit at Tyr1472 was enhanced to a similar extent in cells exposed to NMDA, SP or NMDA+SP, and that enhancement was blocked by BIM. Our findings suggest that NGF and PGE2 may contribute to the injury-evoked sensitization of DRG neurons in part by enhancing their NMDA-evoked [Ca2+]cyt transient in all sized DRG neurons; and that SP may further contribute to the DRG sensitization by enhancing and prolonging the NMDA-evoked increase in [Ca2+]cyt in small- and medium-sized DRG neurons.
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The non-competitive N-methyl-D-aspartate NMDA receptor antagonist ketamine, a dissociative anesthetic capable of inducing analgesia, is known to have psychotomimetic actions, but the detailed mechanisms remain unclear because of its complex properties. The present study elucidated neural mechanisms of the effect of ketamine, at doses that exert psychotomimetic effects without anesthetic and analgesic effects, by evaluating cortical synaptic responses in vivo. Systemic administration (i.p.) of low (1 and 5 mg/kg), subanesthetic (25 mg/kg) and anesthetic (100 mg/kg) doses of ketamine dose-dependently decreased hippocampal stimulation-evoked potential in the medial prefrontal cortex (mPFC) in freely moving rats. ⋯ Ketamine (5 mg/kg, i.p.)-induced synaptic depression was blocked by pretreatment with dopamine D1 receptor antagonist SCH 23390 (10 μg/rat, i.c.v.) but not dopamine D2 receptor antagonist haloperidol (1.5 mg/kg, i.p.), suggesting that dopaminergic modulation mediated via D1 receptors are involved in the synaptic effects of ketamine. Furthermore, ketamine (5 mg/kg, i.p.)-induced synaptic depression was prevented also by GABAA receptor antagonist bicuculline (0.2 or 2 μg/rat, i.c.v.). These findings suggest that ketamine at the dose that exerts psychotomimetic symptoms depresses hippocampus-mPFC synaptic transmission through mechanisms involving dopaminergic modulation mediated via D1 receptors, which may lead to a net augmentation of synaptic inhibition mediated via GABAA receptors.