Highlights
  • Review Article | April 30, 2021

    The inflammatory response, by disrupting immunohomeostasis and aggravating brain damage, constitutes a major contributory factor to the pathobiology of stroke. Because the immune system is involved in all stages of stroke, immunosuppressive mechanisms may provide neuroprotection in this setting. The TAM/Gas6 pathway, for instance, has been shown to be involved in modulating post-stroke inflammation, and in the reduction of post-stroke brain injury. In addition to this pathway, those mediated by established immunosuppressive molecules (such as IL-10 and TGF-β), by CD25+CD4+ FoxP3+Tregs, and by the cholinergic anti-inflammatory pathway, also appear to play protective roles in the context of stroke. Taken together, evidence accumulated regarding the function of these mechanisms suggest than an immunoregulatory strategy may prove promising, both as an approach to the study of stroke pathophysiology, and to the discovery of treatments that limit the destructive effects of cerebrovascular disease.

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    The inflammatory response, by disrupting immunohomeostasis and aggravating brain damage, constitutes a major contributory factor to the pathobiology of stroke. Because the immune system is involved in all stages of stroke, immunosuppressive mechanisms may provide neuroprotection in this setting. The TAM/Gas6 pathway, for instance, has been shown to be involved in modulating post-stroke inflammation, and in the reduction of post-stroke brain injury. In addition to this pathway, those mediated by established immunosuppressive molecules (such as IL-10 and TGF-β), by CD25+CD4+ FoxP3+Tregs, and by the cholinergic anti-inflammatory pathway, also appear to play protective roles in the context of stroke. Taken together, evidence accumulated regarding the function of these mechanisms suggest than an immunoregulatory strategy may prove promising, both as an approach to the study of stroke pathophysiology, and to the discovery of treatments that limit the destructive effects of cerebrovascular disease.
    Qian Jiang, Christopher R. Stone, Kenneth Elkin et al.
  • Short Communication | April 30, 2021

    An et al. demonstrate the critical role of astrocytic MAOB in both tonic GABA inhibition of SNpc dopaminergic neurons and parkinsonian motor symptoms in the MPTP PD model.

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    An et al. demonstrate the critical role of astrocytic MAOB in both tonic GABA inhibition of SNpc dopaminergic neurons and parkinsonian motor symptoms in the MPTP PD model.
    Heeyoung An, Jun Young Heo, C. Justin Lee and Min-Ho Nam
  • Original Article | April 30, 2021

    This study shows that Central neurocytoma-derived tumor stem cells have transit-amplifying cell characteristics, and EGFR signaling has a critical role in tumorigenesis of CN.

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    This study shows that Central neurocytoma-derived tumor stem cells have transit-amplifying cell characteristics, and EGFR signaling has a critical role in tumorigenesis of CN.
    Hye Young Shin, Kyung-Seok Han, Hyung Woo Park et al.
  • Original Article | April 30, 2021

    During Morris water maze, the spatial learning and memory (L&M) was impaired, the extracellular concentrations of norepinephrine and field excitatory postsynaptic potential (fEPSP) amplitudes in the hippocampal dentate gyrus (DG) were significantly suppressed in sleep-deprived (SD) rats. Moreover, local activation of β-adrenoceptors by isoproterenol in DG could significantly rescued deficits of spatial L&M, alleviated the fEPSP impairment and increased glutamatergic receptor expression in the DG.

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    During Morris water maze, the spatial learning and memory (L&M) was impaired, the extracellular concentrations of norepinephrine and field excitatory postsynaptic potential (fEPSP) amplitudes in the hippocampal dentate gyrus (DG) were significantly suppressed in sleep-deprived (SD) rats. Moreover, local activation of β-adrenoceptors by isoproterenol in DG could significantly rescued deficits of spatial L&M, alleviated the fEPSP impairment and increased glutamatergic receptor expression in the DG.
    Huan-Jun Lu and Jing lv
Vol.30 No.2 | April 30, 2021

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  • Published online June 16, 2021

    Sleep deprivation (SD) leads to cognitive impairment, especially hippocampus-dependent learning and memory (L&M). The hippocampal dentate gyrus (DG) is the key structure involved in spatial L&M while long-term potentiation (LTP) is an important cellular mechanism responsible for L&M. Physiological and behavioral evidences support the hypothesis that norepinephrine (NE) and β-adrenoceptors (β-AR) may play an important role in regulating L&M, including LTP. However, it is enigmatic how β-AR influences the LTP disruption or memory impairment under SD circumstances. In the present study, the rats were subjected to SD for 18 h per day for 21 consecutive days and cognitive capacity was assessed by the Morris water maze (MWM) test. We examined the extracellular concentration of NE in the DG using in vivo brain microdialysis and HPLC analysis. The amplitudes of field excitatory postsynaptic potential (fEPSP) were subsequently measured in the DG during MWM test in freely moving conscious rats. The extracellular concentrations of NE and fEPSP amplitudes in the DG were significantly increased during MWM test, while these responses were suppressed in SD rats. When fEPSP amplitudes in the DG were measured after local injection of isoproterenol (an agonist of β-AR), SD rats significantly alleviated the fEPSP impairment and rescued deficits of spatial L&M. In addition, the reduced expression of N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors in SD rats significantly increased by activation of β-AR by isoproterenol in the DG. In conclusion, we propose that β-adrenergic signaling can improve memory impairment in sleep-deficient rats by regulating synaptic efficiency and glutamatergic receptor expression.

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    Heeyoung An, Wuhyun Koh, SeungHee Kang et al.
  • Published online May 28, 2021

    Sleep deprivation (SD) leads to cognitive impairment, especially hippocampus-dependent learning and memory (L&M). The hippocampal dentate gyrus (DG) is the key structure involved in spatial L&M while long-term potentiation (LTP) is an important cellular mechanism responsible for L&M. Physiological and behavioral evidences support the hypothesis that norepinephrine (NE) and β-adrenoceptors (β-AR) may play an important role in regulating L&M, including LTP. However, it is enigmatic how β-AR influences the LTP disruption or memory impairment under SD circumstances. In the present study, the rats were subjected to SD for 18 h per day for 21 consecutive days and cognitive capacity was assessed by the Morris water maze (MWM) test. We examined the extracellular concentration of NE in the DG using in vivo brain microdialysis and HPLC analysis. The amplitudes of field excitatory postsynaptic potential (fEPSP) were subsequently measured in the DG during MWM test in freely moving conscious rats. The extracellular concentrations of NE and fEPSP amplitudes in the DG were significantly increased during MWM test, while these responses were suppressed in SD rats. When fEPSP amplitudes in the DG were measured after local injection of isoproterenol (an agonist of β-AR), SD rats significantly alleviated the fEPSP impairment and rescued deficits of spatial L&M. In addition, the reduced expression of N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors in SD rats significantly increased by activation of β-AR by isoproterenol in the DG. In conclusion, we propose that β-adrenergic signaling can improve memory impairment in sleep-deficient rats by regulating synaptic efficiency and glutamatergic receptor expression.

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    Heeyoung An, Hyowon Lee, Seulkee Yang et al.

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Subcortical structures in elderly subclinical depression

Structural changes in the subcortical area can affect cognitive function and cause increased vulnerability to mood symptoms such as anxiety and subclinical depression. However, studies on changes in subcortical structures show inconsistencies. This research shows the structural differences in segmented subcortical regions between control and subclinical depression groups and visualizes the pathway between structures based on their connection strength through tractography analysis.