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Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
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Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...
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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.
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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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Author Spotlight: Advancing Understanding Through Technological Innovations in Psychoneuroimmunology
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Synaptic elimination by microglia and disturbed higher brain functions.

Kazuya Miyanishi1, Arisa Sato2, Nanako Kihara2

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Microglia actively shape neural circuits by removing synapses in mature brains. Impaired microglial function disrupts synaptic balance, impacting cognitive functions and various neurological disorders.

Keywords:
Cognitive functionComplementE/I balanceEat-me signalMemoryPruning

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Neuroimmunology

Background:

  • Microglial cells were traditionally viewed as quiescent immune cells in the brain, activated only by pathology.
  • Recent research reveals microglia are dynamic, actively participating in neural circuit formation and maintenance in mature brains.

Purpose of the Study:

  • To review current understanding of microglial roles in mature brains, focusing on synaptic phagocytosis.
  • To explore the connection between microglial synaptic pruning and higher brain functions.

Main Methods:

  • Literature review of recent findings on microglial function.
  • Analysis of the impact of microglial phagocytosis on synaptic transmission and neural circuits.

Main Results:

  • Microglia actively phagocytose synapses, contributing to neural circuit development and maintenance.
  • Impaired microglial synaptic elimination disrupts the excitatory/inhibitory (E/I) balance in the brain.

Conclusions:

  • Microglial phagocytosis is crucial for maintaining E/I balance, essential for normal cognitive functions, sleep, and behavior.
  • Dysfunctional microglial phagocytosis is linked to various neurological and psychiatric disorders, including Alzheimer's, autism, and schizophrenia.