Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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.

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The cost-effectiveness of vaccination against COVID-19 in at-risk populations and older adults in the United Kingdom: Projections using a dynamic transmission model.

Vaccine·2026
Same author

Pituitary Stalk Lesion Sampling by Transsphenoidal Posterior Lobe Biopsy: A Case Series.

Journal of neurological surgery. Part B, Skull base·2026
Same author

Linking Breastfeeding Support Training and Certification to Knowledge, Self-Efficacy, and Attitudes among Alabama Healthcare Professionals.

Southern medical journal·2026
Same author

Brain-wide mapping and synaptic localization of C1QL3 using a novel epitope-tagged knock-in mouse.

bioRxiv : the preprint server for biology·2026
Same author

Severe neurotoxicity from accidental tetrabenazine ingestion in a child, with laboratory confirmation.

Clinical toxicology (Philadelphia, Pa.)·2026
Same author

Postoperative Visual Outcomes in Pediatric Craniopharyngioma: A Comparison of Endoscopic Endonasal and Transcranial Approaches.

Journal of pediatric hematology/oncology·2026

Related Experiment Video

Updated: May 7, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
14:57

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Surface L-type Ca2+ channel expression levels are increased in aged hippocampus.

Félix Luis Núñez-Santana1, Myongsoo Matthew Oh, Marcia Diana Antion

  • 1Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.

Aging Cell
|September 17, 2013
PubMed
Summary

Age-related cognitive decline is not due to overall L-type Ca(2+) channel (LTCC) changes. Instead, increased LTCCs on the plasma membrane may drive age-related cognitive deficits in hippocampal neurons.

Keywords:
Cav1.2Cav1.3biotinylationcalciumphosphorylationqRT-PCR

More Related Videos

Fluorescence and Bioluminescence Imaging of Subcellular Ca2+ in Aged Hippocampal Neurons
13:24

Fluorescence and Bioluminescence Imaging of Subcellular Ca2+ in Aged Hippocampal Neurons

Published on: December 1, 2015

Minimizing Hypoxia in Hippocampal Slices from Adult and Aging Mice
08:58

Minimizing Hypoxia in Hippocampal Slices from Adult and Aging Mice

Published on: July 2, 2020

Related Experiment Videos

Last Updated: May 7, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
14:57

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Fluorescence and Bioluminescence Imaging of Subcellular Ca2+ in Aged Hippocampal Neurons
13:24

Fluorescence and Bioluminescence Imaging of Subcellular Ca2+ in Aged Hippocampal Neurons

Published on: December 1, 2015

Minimizing Hypoxia in Hippocampal Slices from Adult and Aging Mice
08:58

Minimizing Hypoxia in Hippocampal Slices from Adult and Aging Mice

Published on: July 2, 2020

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Aging Research

Background:

  • Age-related cognitive deficits are linked to changes in hippocampal pyramidal neurons.
  • Increased L-type Ca(2+) channel (LTCC) expression was hypothesized to cause these deficits.

Purpose of the Study:

  • To re-examine LTCC (Cav 1.2 and Cav 1.3) expression in young and aged rat hippocampi.
  • To determine if altered LTCC expression underlies age-related cognitive impairments.

Main Methods:

  • Western blot analysis of total Cav 1.2 and Cav 1.3 expression.
  • Surface biotinylation to assess plasma membrane expression.
  • Immunohistochemistry to evaluate Cav 1.2 immunoreactivity.

Main Results:

  • Total Cav 1.2 and Cav 1.3 levels were reduced in aged rats.
  • Plasma membrane expression of Cav 1.2 and Cav 1.3 was higher in aged rats (CA1/CA3).
  • Increased Cav 1.2 phosphorylation was observed in the aged dentate gyrus.

Conclusions:

  • Age-related cognitive deficits are not caused by global LTCC expression changes.
  • Increased plasma membrane LTCCs, particularly Cav 1.2 in CA1 neurons, may contribute to age-related cognitive decline.