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 Experiment Videos

Transient synaptic potentiation in the visual cortex. II. Developmental regulation

K Harsanyi1, M J Friedlander

  • 1Department of Neurobiology, University of Alabama at Birmingham 35294, USA.

Journal of Neurophysiology
|March 1, 1997
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

A comparative analysis exposes an amplification delay distinctive to SARS-CoV-2 Omicron variants of clinical and public health relevance.

Emerging microbes & infections·2022
Same author

Development and implementation of a scalable and versatile test for COVID-19 diagnostics in rural communities.

Nature communications·2021
Same author

Structure and projections of white matter neurons in the postnatal rat visual cortex.

The Journal of comparative neurology·2001
Same author

LTD induction in adult visual cortex: role of stimulus timing and inhibition.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2001
Same author

Arginine analogs modify signal detection by neurons in the visual cortex.

The Journal of neuroscience : the official journal of the Society for Neuroscience·1999
Same author

Dynamic modulation of cerebral cortex synaptic function by nitric oxide.

Progress in brain research·1999

Synaptic potentiation in the visual cortex develops with age, becoming less frequent but stronger in younger animals. This plasticity relies on postsynaptic calcium but not NMDA receptors in neonates, with NMDA receptor linkage occurring during development.

Area of Science:

  • Neuroscience
  • Developmental Neurobiology
  • Synaptic Plasticity

Background:

  • Previous studies identified pairing-induced transient synaptic potentiation in the visual cortex of mature guinea pigs.
  • Understanding the developmental trajectory and underlying mechanisms of this plasticity is crucial for comprehending neural circuit maturation.

Purpose of the Study:

  • To investigate the developmental changes in visual cortical transient synaptic potentiation from postnatal day 5 to 180.
  • To elucidate the cellular mechanisms mediating this plasticity across different developmental stages.

Main Methods:

  • Electrophysiological recordings in guinea pig visual cortex at various postnatal ages (PND 5-180).
  • Pharmacological manipulations including Lidocaine, gamma-aminobutyric acid (GABA) blockade, N-methyl-D-aspartate (NMDA) receptor antagonists (APV), and intracellular calcium chelators (BAPTA).

Related Experiment Videos

  • Assessment of potentiation likelihood and magnitude under different experimental conditions.

    • Main Results:

    • Synaptic potentiation is more reliably evoked and has a greater magnitude in younger animals (PND 5-30) compared to older ones.
    • Potentiation occurs at direct excitatory synaptic sites, independent of local recurrent cortical circuits or inhibitory GABAergic transmission.
    • In young animals (PND 11-27), potentiation is induced independently of NMDA receptors, suggesting a developmental shift in its mechanism.
    • Postsynaptic intracellular calcium plays a critical role in inducing potentiation across all ages studied.
    • Nitric oxide synthase inhibition did not significantly affect potentiation in young animals.

    Conclusions:

    • Visual cortical transient synaptic potentiation exhibits significant developmental changes, with enhanced expression in younger animals.
    • The NMDA receptor becomes functionally integrated into the potentiation cascade during development, replacing an earlier APV-insensitive mechanism.
    • Postsynaptic calcium signaling is a conserved and critical mediator of this synaptic plasticity throughout development.