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Ruminating on replay during the awake state 清醒状态下的回放反思
IF 34.7 1区 医学 Q1 Neuroscience Pub Date : 2024-11-20 DOI: 10.1038/s41583-024-00885-z
Anna K. Gillespie
In this Journal Club, Anna Gillespie discusses how the discovery of hippocampal replay during the awake state reshaped our understanding of its role in memory function.
在本期 "期刊俱乐部 "中,安娜-吉莱斯皮(Anna Gillespie)将讨论清醒状态下海马回放的发现如何重塑了我们对海马在记忆功能中作用的认识。
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引用次数: 0
Structural neural plasticity evoked by rapid-acting antidepressant interventions. 速效抗抑郁剂干预诱发的结构性神经可塑性。
IF 34.7 1区 医学 Q1 Neuroscience Pub Date : 2024-11-18 DOI: 10.1038/s41583-024-00876-0
Clara Liao, Alisha N Dua, Cassandra Wojtasiewicz, Conor Liston, Alex C Kwan

A feature in the pathophysiology of major depressive disorder (MDD), a mood disorder, is the impairment of excitatory synapses in the prefrontal cortex. Intriguingly, different types of treatment with fairly rapid antidepressant effects (within days or a few weeks), such as ketamine, electroconvulsive therapy and non-invasive neurostimulation, seem to converge on enhancement of neural plasticity. However, the forms and mechanisms of plasticity that link antidepressant interventions to the restoration of excitatory synaptic function are still unknown. In this Review, we highlight preclinical research from the past 15 years showing that ketamine and psychedelic drugs can trigger the growth of dendritic spines in cortical pyramidal neurons. We compare the longitudinal effects of various psychoactive drugs on neuronal rewiring, and we highlight rapid onset and sustained time course as notable characteristics for putative rapid-acting antidepressant drugs. Furthermore, we consider gaps in the current understanding of drug-evoked in vivo structural plasticity. We also discuss the prospects of using synaptic remodelling to understand other antidepressant interventions, such as repetitive transcranial magnetic stimulation. Finally, we conclude that structural neural plasticity can provide unique insights into the neurobiological actions of psychoactive drugs and antidepressant interventions.

重度抑郁障碍(MDD)是一种情绪障碍,其病理生理学特征之一是前额叶皮层的兴奋性突触受损。耐人寻味的是,氯胺酮、电休克疗法和非侵入性神经刺激等不同类型的治疗方法具有相当快的抗抑郁效果(数天或数周内),似乎都能增强神经的可塑性。然而,将抗抑郁干预与兴奋性突触功能的恢复联系起来的可塑性形式和机制仍然未知。在这篇综述中,我们重点介绍了过去15年的临床前研究,这些研究表明氯胺酮和迷幻药能促使大脑皮层锥体神经元树突棘的生长。我们比较了各种精神活性药物对神经元重接线的纵向影响,并强调了快速起效和持续时间过程是潜在速效抗抑郁药物的显著特征。此外,我们还考虑了目前对药物诱发体内结构可塑性认识的不足之处。我们还讨论了利用突触重塑来理解其他抗抑郁干预措施(如重复经颅磁刺激)的前景。最后,我们得出结论:神经结构可塑性可以为精神活性药物和抗抑郁干预措施的神经生物学作用提供独特的见解。
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引用次数: 0
Innate immune control of synapse development 突触发育的先天免疫控制
IF 34.7 1区 医学 Q1 Neuroscience Pub Date : 2024-11-18 DOI: 10.1038/s41583-024-00887-x
Katherine Whalley
Innate lymphoid cells regulate inhibitory synapse formation in the mouse cortex during early postnatal life.
先天性淋巴细胞在小鼠出生后早期调节大脑皮层抑制性突触的形成
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引用次数: 0
Issues of parcellation in the calculation of structure-function coupling. 结构-功能耦合计算中的解析问题。
IF 34.7 1区 医学 Q1 Neuroscience Pub Date : 2024-11-14 DOI: 10.1038/s41583-024-00877-z
Adam Turnbull, Feng Vankee Lin, Zhengwu Zhang
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引用次数: 0
Reply to 'Issues of parcellation in the calculation of structure-function coupling'. 对 "结构-功能耦合计算中的分割问题 "的答复
IF 34.7 1区 医学 Q1 Neuroscience Pub Date : 2024-11-14 DOI: 10.1038/s41583-024-00878-y
Panagiotis Fotiadis, Dani S Bassett
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引用次数: 0
A new target for leptin 瘦素的新目标
IF 34.7 1区 医学 Q1 Neuroscience Pub Date : 2024-11-13 DOI: 10.1038/s41583-024-00884-0
Michael Attwaters
Tan et al. identify a population of leptin-responsive neurons that regulate food intake and body weight.
Tan 等人发现了一个瘦素反应神经元群体,它能调节食物摄入量和体重。
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引用次数: 0
Understanding Parkinson's disease. 了解帕金森病。
IF 34.7 1区 医学 Q1 Neuroscience Pub Date : 2019-12-11 DOI: 10.1038/s41583-019-0254-x
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引用次数: 0
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Nature Reviews Neuroscience
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