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Related Concept Videos

Neuroplasticity01:01

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
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.
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
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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.
Brain Imaging01:14

Brain Imaging

Brain imaging technologies provide critical insights into both the structure and function of the human brain, enabling medical professionals and researchers to diagnose, study, and treat neurological disorders or psychiatric disorders more effectively.
These technologies include computerized axial tomography (CAT or CT scans), positron-emission tomography (PET scans),  magnetic resonance imaging (MRI),  functional magnetic resonance imaging (fMRI), and Transcranial Magnetic Stimulation (TMS).

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Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis
14:58

Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis

Published on: February 13, 2014

Exercise influences hippocampal plasticity by modulating brain-derived neurotrophic factor processing.

Q Ding1, Z Ying, F Gómez-Pinilla

  • 1Department of Integrative Biology and Physiology, UCLA Brain Injury Research Center, University of California, Los Angeles, CA 90095, USA.

Neuroscience
|July 16, 2011
PubMed
Summary
This summary is machine-generated.

Voluntary exercise boosts brain plasticity by increasing brain-derived neurotrophic factor (BDNF) and its processing via tissue-type plasminogen activator (tPA). This enhances TrkB receptor signaling and neuronal function in the hippocampus.

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Area of Science:

  • Neuroscience
  • Exercise Physiology

Background:

  • Exercise influences brain plasticity and function through brain-derived neurotrophic factor (BDNF).
  • Two forms of BDNF, precursor (proBDNF) and mature (mBDNF), have distinct roles.
  • Understanding exercise-induced BDNF processing is key for therapeutic applications.

Purpose of the Study:

  • To investigate how exercise affects BDNF processing and signaling pathways in the rat hippocampus.
  • To determine the role of tissue-type plasminogen activator (tPA) in exercise-mediated BDNF changes.

Main Methods:

  • Rats underwent 7 days of voluntary exercise.
  • BDNF levels, tPA activity, and downstream signaling molecules (TrkB, phospho-ERK, phospho-Akt, phospho-CaMKII) were measured.
  • tPA activity was blocked to assess its role.

Main Results:

  • Exercise increased both proBDNF and mBDNF in the hippocampus.
  • Exercise enhanced tPA activity, facilitating proBDNF to mBDNF conversion.
  • Blocking tPA reduced exercise-induced BDNF changes and inhibited TrkB receptor activation and downstream signaling.
  • tPA blockade also counteracted exercise effects on plasticity markers like phospho-synapsin I and GAP-43.

Conclusions:

  • Exercise-induced hippocampal plasticity is dependent on BDNF processing via tPA.
  • Subsequent TrkB receptor signaling is crucial for mediating these effects.
  • These findings have implications for understanding neuronal function and developing exercise-based therapies.