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Related Concept Videos

Long-term Potentiation01:35

Long-term Potentiation

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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.
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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
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Nuclear protein sorting regulates nucleus composition and gene expression, crucial for determining the fate of a eukaryotic cell. Hence, the entry and exit of molecules across the nuclear envelope is a tightly controlled process. Nuclear protein sorting can be inhibited by one of the following ways: 1) masking cargo signal sequences, 2) modifying the nuclear receptor's affinity for cargo, 3) controlling the nuclear pore size, 4) retaining the cargo during its transit to the cytosol or the...
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Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
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LPS Primes Brain Responsiveness to High Mobility Group Box-1 Protein.

Verena Peek1, Lois M Harden2, Jelena Damm1

  • 1Institute of Veterinary Physiology and Biochemistry, Justus Liebig University Giessen, 35392 Giessen, Germany.

Pharmaceuticals (Basel, Switzerland)
|July 2, 2021
PubMed
Summary

High mobility group box 1 (HMGB1) released during sepsis exacerbates brain inflammation, particularly after lipopolysaccharide priming. This mediator enhances inflammatory responses in brain cells, contributing to sustained sepsis symptoms.

Keywords:
circumventricular organscytokineshigh mobility group box-1 proteinlipopolysaccharideseptic-like inflammation

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • High mobility group box 1 (HMGB1) is implicated in sepsis pathogenesis.
  • The specific role of HMGB1 in brain inflammation during sepsis remains unclear.

Purpose of the Study:

  • To investigate the role of HMGB1 in the brain during lipopolysaccharide (LPS)-induced inflammation in rats.
  • To determine the direct effects of HMGB1 on neuro-glial cells in the area postrema (AP).

Main Methods:

  • Rats were injected with LPS to induce a septic-like state.
  • HMGB1 levels were measured using RT-PCR, immunohistochemistry, and ELISA.
  • In vitro studies used primary neuro-glial cell cultures from the AP exposed to disulfide-HMGB1 and LPS.

Main Results:

  • LPS injection led to elevated HMGB1 plasma levels and increased HMGB1 translocation in brain and AP cells.
  • Disulfide-HMGB1 stimulated nuclear factor (NF)-κB activation and interleukin-6 release in AP cells.
  • LPS priming significantly increased the responsiveness of AP cells to HMGB1.

Conclusions:

  • HMGB1 acts as both a humoral and local mediator that enhances brain inflammatory responses.
  • LPS priming potentiates HMGB1-induced neuroinflammation, potentially contributing to sustained sepsis symptoms.