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Long-term Depression01:03

Long-term Depression

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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
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Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders01:27

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

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Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within...
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Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

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When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of...
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Antidepressant Drugs: MAOIs and Other Agents01:23

Antidepressant Drugs: MAOIs and Other Agents

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Atypical antidepressants, including bupropion (Wellbutrin), mirtazapine (Remeron), nefazodone (Serzone), trazodone (Desyrel), and vilazodone (Viibryd), offer unique mechanisms of action. Bupropion weakly inhibits dopamine and norepinephrine reuptake, aiding depression treatment and smoking cessation, with a low risk of sexual dysfunction. Mirtazapine enhances serotonin and norepinephrine neurotransmission, leading to sedation, increased appetite, and weight gain. As a result, it helps treat...
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Chemical Synapses01:26

Chemical Synapses

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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
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G-protein Coupled Receptors01:21

G-protein Coupled Receptors

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G-protein coupled receptors are ligand binding receptors that indirectly affect changes in the cell. The actual receptor is a single polypeptide that transverses the cell membrane seven times creating intracellular and extracellular loops. The extracellular loops create a ligand specific pocket which binds to neurotransmitters or hormones. The intracellular loops holds onto the G-protein.
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相关实验视频

Updated: Jul 2, 2025

DetectSyn: A Rapid, Unbiased Fluorescent Method to Detect Changes in Synapse Density
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DetectSyn: A Rapid, Unbiased Fluorescent Method to Detect Changes in Synapse Density

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血清激素调节发育前额叶皮层中刺激性突触成熟的过程.

Roberto Ogelman1, Luis E Gomez Wulschner1, Victoria M Hoelscher1

  • 1Department of Pharmacology, University of Colorado School of Medicine, Aurora, CO, 80045, USA.

Nature communications
|February 16, 2024
PubMed
概括

血清素 (5-HT) 通过改变刺激性突触强度和存活率来影响前额叶皮层 (PFC) 的发育. 早期的fluoxetine治疗增强了PFC突触,突出了血清激素信号传递的关键发育窗口.

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科学领域:

  • 神经科学是一个神经科学.
  • 发展生物学 发展生物学
  • 分子生物学分子生物学

背景情况:

  • 在前额叶皮层 (PFC) 发育中的血清激素 (5-HT) 失衡与行为缺陷有关.
  • 5-HT在PFC发育中的作用的精确突触机制尚不清楚.

研究的目的:

  • 为了研究由血清素介导的前额叶皮层发育的突触机制.
  • 探索血清素对激发性突触可塑性在PFC发育中的影响.

主要方法:

  • 在出生后的早期发育过程中利用化学遗传学来操纵小鼠PFC中的5-HT释放.
  • 在层2/3的金字塔神经元上检查了刺激性脊柱突触的结构和功能变化.
  • 研究了5-HT2A和5-HT7受体在突触可塑性中的作用.
  • 在特定的产后周内进行慢性西治疗.

主要成果:

  • 调节5-HT释放改变了刺激性脊柱突触密度和强度.
  • 在单个脊柱中,5-HT诱导的长期增强 (LTP),依赖于5-HT2A和5-HT7受体.
  • 5-HT信号通过5-HT7受体激活促进了新的长期存活.
  • 产后早期的西治疗增强了PFC激发性突触,这种效应被受体对抗剂阻断.

结论:

  • 血清素直接调节发育中的PFC中的单个棘中的激发性突触可塑性.
  • 特定的血清素受体 (5-HT2A,5-HT7) 调解这些突触变化.
  • 通过这些机制,早年暴露在像fluoxetine这样的SSRI可能会影响PFC突触发育.