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Related Concept Videos

Chemical Synapses01:26

Chemical Synapses

12.1K
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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Chemical Synapses01:26

Chemical Synapses

5.2K
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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Postsynaptic Potential (PSP)01:32

Postsynaptic Potential (PSP)

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Postsynaptic potential (PSP) refers to a change in the electrical potential of a neuron when neurotransmitters released by presynaptic neurons bind to postsynaptic receptors. This potential can either be excitatory, leading to depolarization and ultimately action potential generation, or inhibitory, leading to hyperpolarization and suppression of the postsynaptic neuron.
There are two types of receptors: ionotropic and metabotropic.
The ionotropic receptor is the membrane protein that has an...
6.5K
Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

13.8K
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...
13.8K
Long-term Potentiation01:35

Long-term Potentiation

59.0K
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
59.0K
Long-term Potentiation01:25

Long-term Potentiation

3.7K
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when...
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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

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Neurophysiology of synaptic functioning in multiple sclerosis.

Mario Stampanoni Bassi1, Francesco Mori2, Fabio Buttari2

  • 1Neurology and Neurorehabilitation Units, IRCCS Istituto Neurologico Mediterraneo (INM) Neuromed, Via Atinense 18, 86077 Pozzilli (IS), Italy.

Clinical Neurophysiology : Official Journal of the International Federation of Clinical Neurophysiology
|May 17, 2017
PubMed
Summary
This summary is machine-generated.

Multiple sclerosis (MS) involves immune-mediated CNS inflammation, affecting synapses early. Cytokines disrupt synaptic function and plasticity, influencing disease progression and recovery.

Keywords:
Experimental autoimmune encephalomyelitisInflammatory cytokinesMultiple sclerosisNeurodegenerationSynaptic plasticityTranscranial magnetic stimulation

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Area of Science:

  • Neuroimmunology
  • Neuroscience
  • Central Nervous System (CNS) Disorders

Background:

  • Multiple sclerosis (MS) is an inflammatory immune-mediated disorder of the CNS.
  • It primarily affects the myelin sheath, leading to neurodegeneration.
  • Synaptic alterations are increasingly recognized as key factors in early MS neurodegeneration.

Purpose of the Study:

  • To investigate inflammation-induced alterations in synaptic transmission and plasticity in MS.
  • To explore the role of inflammatory cytokines in synaptic hyperexcitability and excitotoxicity.
  • To understand how synaptic plasticity is affected in MS and its impact on disease course and recovery.

Main Methods:

  • In vitro studies and human MS patient studies using transcranial magnetic stimulation (TMS).
  • Analysis of alterations in glutamatergic and GABAergic transmission.
  • Assessment of long-term potentiation (LTP) and long-term depression (LTD) in experimental autoimmune encephalomyelitis (EAE) and MS.

Main Results:

  • Inflammatory cytokines alter glutamatergic and GABAergic transmission, causing synaptic hyperexcitability.
  • Excitotoxic damage and neurodegeneration occur early in EAE and MS, while inflammation persists in progressive stages.
  • Synaptic plasticity, including LTP and LTD, is altered in EAE and MS, impacting clinical recovery and disease progression.

Conclusions:

  • Cytokine regulation of neuronal activity is crucial in the neuro-immune crosstalk of MS.
  • Inflammation-associated excitotoxicity and compensatory plasticity are influenced by cytokine signaling.
  • Cytokines, neurotransmitters, and neuropeptides form a critical communication system in the CNS during MS.