Neuroscience
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The purpose of this study was to examine whether mechanisms, involved during the maintenance of familiar movement information in memory, were influenced by the degree of familiarity of the display in which the movements were embedded. Twelve gymnasts who possessed high visual and motor familiarity with the movements employed in this study, were recruited. They were invited to retain for a short period of time familiar movements viewed previously and presented under different displays with the aim of recognizing them at a later stage. ⋯ The results in the 13-20 Hz frequency band showed that functional connectivity was greater within the frontal and right temporal areas during the unfamiliar display (i.e., point-light maintenance condition) compared to the familiar display (i.e., video maintenance condition). Differences in functional connectivity between the two maintenance conditions in the beta frequency band are mainly discussed in the light of the process of anticipation. Subjects' perception of the expected difficulty of the upcoming recognition task is discussed.
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Elucidation of the 'fear circuit' has opened exciting avenues for understanding and treating human anxiety disorders. However, the translation of rodent to human studies, and vice versa, depends on understanding the homology in relevant circuits across species. Although abundant evidence indicates that the hippocampal-amygdala circuit mediates contextual fear learning, previous studies indicate that this pathway is more restricted in primates than in rodents. ⋯ Immature neurons are prominent in the PL and CTA, and are overlapped by anterogradely labeled fibers from CA1', particularly in the medial PL and CTA. Hippocampal inputs to the amygdala are more focused in higher primates compared to rodents, supporting previous anatomic studies and recent data from human functional imaging studies of contextual fear. At the cellular level, a hippocampal interaction with immature neurons in the amygdala suggests a novel substrate for cellular plasticity, with implications for mechanisms underlying contextual learning and emotional memory processes.
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Understanding the cellular events evoked at the peripheral boundary of cerebral ischemia is critical for therapeutic outcome against the insult of cerebral ischemia. The present study reports a repeated longitudinal imaging for cellular-scale changes of neuro-glia-vascular unit at the boundary of cerebral ischemia in mouse cerebral cortex in vivo. Two-photon microscopy was used to trace the longitudinal changes of cortical microvasculature and astroglia following permanent middle cerebral artery occlusion (MCAO). ⋯ At the regions of the distorted microvasculature, an increase in the number of cells labeled with SR101 was detected, which was found as due to labeled neurons. Immunohistochemical results further showed that ischemia provokes neuronal uptake of SR101, which delineate a boundary between dying and surviving cells at the peripheral zone of ischemia in vivo. Finally, reproducibility of the MCAO model was evaluated with magnetic resonance imaging (MRI) in a different animal group, which showed the consistent infarct volume at the MCA territory over the subjects.
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In this study, we investigated effects of intra-central amygdala (intra-CeA) administrations of a cannabinoid agonist, WIN55,212-2 by itself and its interaction with β1-adrenoceptor agents on memory consolidation. We used a step-through inhibitory avoidance (IA) task to assess memory in male Wistar rats. The results showed that post-training intra-CeA administrations of different doses of WIN55,212-2 at doses of 0.1 and 0.25 μg/rat impaired memory consolidation (or induced amnesia) as revealed by a decrease in step-through latency on the test day. ⋯ Although, post-training intra-CeA administrations of β1-adrenoceptor antagonist, atenolol alone at different doses (0.01, 0.025, 0.05 and 0.1 μg/rat) had no significant effect, but its co-administrations at doses of 0.05 and 0.1 μg/rat along with an ineffective dose of WIN55,212-2 (0.05 μg/rat) induced amnesia, and at dose of 0.1 μg/rat along with an effective dose of WIN55,212-2 (0.25 μg/rat) increased amnesia that induced by the later drug. Moreover, the improving effect of isoprenaline (0.025 μg/rat) on amnesia induced by WIN55,212-2 (0.25 μg/rat) was prevented by intra-CeA co-injections of atenolol at doses of 0.01 and 0.025 μg/rat. The present results suggest that a β1-adrenoeceptor mechanism in the central amygdala (CeA) is involved in amnesia induced by post-training intra-CeA injections of WIN55,212-2.
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MMP-9 deficiency protected against photochemical thrombosis-induced brain hemorrhagic transformation (HT), but it did not protect against tissue plasminogen activator-induced brain hemorrhage. The roles of MMP-2 and/or MMP-9 knockout (KO) in mechanical reperfusion induced HT after ischemia have not been investigated. Here we assessed the effects of MMP-2 KO, MMP-9 KO and MMP-2/9 double KO (dKO) in protecting against mechanical reperfusion induced HT and other brain injuries after the early stages of cerebral ischemia in mice of the same genetic background. ⋯ WT). The results suggested that MMP-2 deficiency and MMP-2 and MMP-9 double deficiency were more protective than MMP-9 deficiency against HT after the early stages of ischemia and reperfusion. These studies increase our understanding of MMP-2 and MMP-9 in HT development and will help to selectively target MMPs to protect the post-ischemic brain from injury and HT.