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Related Concept Videos

Biological Effects of Radiation02:59

Biological Effects of Radiation

All radioactive nuclides emit high-energy particles or electromagnetic waves. When this radiation encounters living cells, it can cause heating, break chemical bonds, or ionize molecules. The most serious biological damage results when these radioactive emissions fragment or ionize molecules. For example, α and β particles emitted from nuclear decay reactions possess much higher energies than ordinary chemical bond energies. When these particles strike and penetrate matter, they produce ions...
Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

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 specific...
Disorders of the Nervous Tissue01:28

Disorders of the Nervous Tissue

Nervous tissue is a vital component of the human body's communication system, enabling us to perceive and respond to stimuli. However, like all other tissues, it is vulnerable to disorders and diseases that can significantly impact our neurological functioning.
Homeostatic Imbalances:
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Parkinson's disease arises from the...
Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
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 21, 2026

Functional Interrogation of Adult Hypothalamic Neurogenesis with Focal Radiological Inhibition
11:45

Functional Interrogation of Adult Hypothalamic Neurogenesis with Focal Radiological Inhibition

Published on: November 14, 2013

Radiation induces acute alterations in neuronal function.

Peter H Wu1, Steven Coultrap, Chelsea Pinnix

  • 1Department of Psychiatry, University of Colorado Denver, Anschutz Medical Campus, Aurora, Colorado, United States of America.

Plos One
|June 5, 2012
PubMed
Summary

Radiation acutely impairs brain function by altering neurotransmitter receptors in neurons. This study reveals early synaptic changes after radiation, offering new targets for cognitive protection in brain tumor patients.

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Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress
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Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress

Published on: May 7, 2014

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Last Updated: May 21, 2026

Functional Interrogation of Adult Hypothalamic Neurogenesis with Focal Radiological Inhibition
11:45

Functional Interrogation of Adult Hypothalamic Neurogenesis with Focal Radiological Inhibition

Published on: November 14, 2013

Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress
09:51

Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress

Published on: May 7, 2014

Area of Science:

  • Neuroscience
  • Radiation Oncology
  • Cellular Biology

Background:

  • Brain radiation therapy affects nearly 200,000 patients annually, with cognitive impairment being a major adverse effect.
  • Existing research on radiation-induced brain injury primarily focuses on late-stage parenchymal changes, neglecting acute synaptic effects.
  • Understanding the acute cellular mechanisms of radiation damage is crucial for developing effective neuroprotective strategies.

Purpose of the Study:

  • To investigate the acute effects of radiation on neuronal function and synaptic plasticity using ex vivo hippocampal brain slices.
  • To identify alterations in the cellular localization and functional status of excitatory and inhibitory neurotransmitter receptors post-radiation.
  • To explore potential therapeutic interventions targeting radiation-induced synaptic dysfunction.

Main Methods:

  • Utilized ex vivo hippocampal brain slices for radiation exposure experiments.
  • Employed immunoblotting to assess the cellular localization of neurotransmitter receptors.
  • Performed electrophysiological recordings to evaluate neuronal function and synaptic responses, including long-term potentiation (LTP).

Main Results:

  • Radiation exposure induced rapid decreases in tyrosine phosphorylation and reduced surface expression of N-methyl-D-aspartate receptors (NMDARs).
  • Concurrently, radiation increased the surface expression of inhibitory gamma-aminobutyric acid receptors (GABA(A)Rs) in the dentate gyrus.
  • These receptor alterations correlated with impaired synaptic responses and inhibited LTP, effects partially reversed by memantine.

Conclusions:

  • Demonstrated acute, radiation-induced alterations in neuronal synaptic function within isolated brain slices.
  • Identified specific changes in NMDAR and GABA(A)R localization as key early events following radiation.
  • Findings suggest novel therapeutic avenues for mitigating acute cognitive deficits in patients undergoing brain radiation therapy.