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Neuroplasticity

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 Potentiation

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 Potentiation

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.

Long-term Depression

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
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Long-term Depression

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.

MAPK Signaling Cascades

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...

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Related Experiment Video

Updated: May 18, 2026

Implantation of a Cranial Window for Repeated In Vivo Imaging in Awake Mice

Implantation of a Cranial Window for Repeated In Vivo Imaging in Awake Mice

Published on: June 22, 2021

MSK1 regulates homeostatic and experience-dependent synaptic plasticity.

Sonia A L Corrêa¹, Christopher J Hunter, Oleg Palygin

¹School of Life Sciences and Molecular Organisation and Assembly in Cells, University of Warwick, Coventry CV4 7AL, United Kingdom.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|September 21, 2012

Summary

Mitogen- and stress-activated kinase 1 (MSK1) is crucial for synaptic adaptation, learning, and memory. This study demonstrates MSK1

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Last Updated: May 18, 2026

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Area of Science:

Neuroscience
Molecular Biology
Synaptic Plasticity

Background:

Synaptic adaptation is vital for learning, memory, and behavioral responses to environmental stimuli.
Brain-derived neurotrophic factor (BDNF) initiates synaptic adaptation, but its signaling pathways remain unclear.
Mitogen- and stress-activated kinase 1 (MSK1) phosphorylates CREB and histone H3, regulating gene transcription.

Purpose of the Study:

To elucidate the role of MSK1 in BDNF-initiated synaptic adaptation.
To investigate MSK1's necessity in in vivo and in vitro models of synaptic scaling.

Main Methods:

Utilized mice with a kinase-dead knock-in mutation of MSK1.
Assessed synaptic strength upregulation in response to environmental enrichment (in vivo).
Examined synaptic transmission scaling after activity deprivation (in vitro) and rescue experiments.

Main Results:

MSK1 is essential for synaptic strength upregulation during environmental enrichment in vivo.
MSK1-deficient neurons exhibit deficits in homeostatic synaptic scaling following activity deprivation.
MSK1 regulates cell surface GluA1 expression via Arc/Arg3.1 induction, crucial for synaptic scaling.

Conclusions:

MSK1 is an integral component of the BDNF- and MAPK-dependent signaling cascade for homeostatic synaptic scaling.
MSK1 plays a critical role in the adaptive response to synaptic and environmental experiences.
MSK1 functions as a key regulator in activity- and experience-dependent synaptic strength modulation.