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Related Concept Videos

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
LTP can occur when presynaptic neurons...
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.
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.
Integration of Synaptic Events01:28

Integration of Synaptic Events

Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...

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Related Experiment Video

Updated: Jun 26, 2026

Acquisition of a High-precision Skilled Forelimb Reaching Task in Rats
08:59

Acquisition of a High-precision Skilled Forelimb Reaching Task in Rats

Published on: June 22, 2015

Spred1 is required for synaptic plasticity and hippocampus-dependent learning.

Ellen Denayer1, Tariq Ahmed, Hilde Brems

  • 1Department of Human Genetics and Laboratory of Biological Psychology, University of Leuven, B-3000 Leuven, Belgium.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|January 2, 2009
PubMed
Summary

SPRED1 gene mutations cause a neurofibromatosis type 1-like syndrome with learning difficulties. Spred1-deficient mice exhibit impaired hippocampus-dependent learning and memory due to Ras/ERK pathway hyperactivation.

More Related Videos

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation
09:39

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation

Published on: June 26, 2013

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders
07:43

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders

Published on: May 12, 2015

Related Experiment Videos

Last Updated: Jun 26, 2026

Acquisition of a High-precision Skilled Forelimb Reaching Task in Rats
08:59

Acquisition of a High-precision Skilled Forelimb Reaching Task in Rats

Published on: June 22, 2015

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation
09:39

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation

Published on: June 26, 2013

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders
07:43

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders

Published on: May 12, 2015

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Germline mutations in SPRED1, a Ras regulator, are linked to neurofibromatosis type 1-like syndrome (NFLS).
  • NFLS is part of a group of syndromes affecting neuro-cardio-facial-cutaneous development, often involving learning difficulties.
  • These syndromes share a common genetic basis in the Ras/mitogen-activated protein kinase extracellular signal-regulated kinase (Ras/ERK) pathway.

Purpose of the Study:

  • To investigate hippocampus-dependent learning, memory, and synaptic plasticity in Spred1(-/-) mice, an animal model for NFLS.
  • To elucidate the molecular mechanisms underlying learning deficits associated with SPRED1 deficiency.

Main Methods:

  • Behavioral testing in Spred1(-/-) mice using the Morris water maze and visual-discrimination T-maze.
  • Electrophysiological recordings on brain slices to assess hippocampal synaptic plasticity (LTP/LTD).
  • Biochemical analysis of ERK phosphorylation levels post-LTP induction.

Main Results:

  • Spred1(-/-) mice demonstrated significant deficits in learning and memory performance.
  • Electrophysiology revealed impaired short- and long-term hippocampal synaptic plasticity in mutant mice.
  • Increased ERK phosphorylation was observed in Spred1(-/-) brain slices after LTP induction, indicating pathway hyperactivation.

Conclusions:

  • SPRED1 deficiency leads to impaired hippocampus-dependent learning and memory.
  • These cognitive deficits are associated with aberrant synaptic plasticity in the hippocampus.
  • The findings link SPRED1 deficiency to Ras/ERK pathway hyperactivation, providing a molecular basis for NFLS-related learning difficulties.