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Related Concept Videos

Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Long-term Potentiation01:35

Long-term Potentiation

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.
Long-term Potentiation01:25

Long-term Potentiation

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 presynaptic neurons...
Long-term Depression01:03

Long-term Depression

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
If over time, all...
Long-term Depression01:05

Long-term Depression

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.
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...

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Related Experiment Video

Updated: May 11, 2026

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins
09:07

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

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Synaptic plasticity in hepatic encephalopathy - a molecular perspective.

Shuping Wen1, Annett Schroeter, Nikolaj Klöcker

  • 1Institute of Neural and Sensory Physiology, Medical Faculty, University of Düsseldorf D-40225 Düsseldorf, Germany.

Archives of Biochemistry and Biophysics
|April 30, 2013
PubMed
Summary

Hepatic encephalopathy (HE) impairs cognitive functions by affecting glutamatergic neurotransmission and synaptic plasticity. Animal models reveal molecular mechanisms impacting learning and memory, highlighting AMPA-receptor signaling disruptions.

Keywords:
AMPA receptorFunctional proteomicsHepatic encephalopathyMembrane protein complexNMDA receptorSynaptic plasticity

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Last Updated: May 11, 2026

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Area of Science:

  • Neuroscience
  • Hepatology
  • Molecular Biology

Background:

  • Hepatic encephalopathy (HE) is a frequent neuropsychiatric complication of liver disease, causing cognitive dysfunction and motor disturbances.
  • Existing animal models of HE replicate cognitive deficits, including impaired learning and memory, offering a basis for molecular investigation.

Purpose of the Study:

  • To explore the molecular mechanisms by which hepatic encephalopathy (HE) impacts cognitive functions.
  • To investigate the effects of acute and chronic HE models on glutamatergic neurotransmission and synaptic plasticity.

Main Methods:

  • Review of existing literature on HE animal models and their impact on cognitive performance.
  • Focus on molecular pathways and signal transduction involved in long-term potentiation (LTP) and long-term depression (LTD).
  • Discussion of the role of ionotropic glutamate receptors, particularly AMPA-subtype, in HE-related cognitive deficits.
  • Introduction of functional proteomic analysis as a novel strategy for investigating membrane protein complex dysfunction.

Main Results:

  • Both acute and chronic HE models demonstrate constrained plasticity of glutamatergic neurotransmission.
  • Long-term potentiation (LTP) and long-term depression (LTD), crucial for synaptic plasticity, are significantly impeded in HE models.
  • Experimental HE targets specific molecules and signaling pathways involved in LTP and LTD, with a notable impact on AMPA-subtype receptors.

Conclusions:

  • Hepatic encephalopathy (HE) molecularly disrupts synaptic plasticity and glutamatergic neurotransmission, underlying cognitive impairments.
  • Targeting ionotropic glutamate receptors, especially AMPA-subtype, represents a potential therapeutic avenue for HE.
  • Functional proteomic analysis offers a promising approach to elucidate molecular dysfunctions in HE, particularly concerning receptor signaling complexes.