The ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity.
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Changes in cytosolic calcium are crucial for numerous processes including neuronal plasticity.
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Membrane depolarization leads to changes in gene expression that modulate neuronal plasticity.
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HDAC3 is an essential negative regulator of neuronal plasticity and memory formation.
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Translational control at the synapse is thought to be a key determinant of neuronal plasticity.
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Synapses are particularly prone to dynamic alterations and thus play a major role in neuronal plasticity.
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The peptide may therefore be expected to regulate regeneration and synaptic plasticity.
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Furthermore, loss of Triad3A mimics and occludes Arc-dependent forms of synaptic plasticity.
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Altogether, our results reveal novel molecular and cellular mechanisms of synaptic plasticity.
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Some of them may also contribute to synaptic plasticity, learning, and memory.
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Specific contributions of SKF83959 to synaptic plasticity have not been well elucidated.
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Lingo-1 is a potent negative regulator of axonal outgrowth and synaptic plasticity.
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Transcriptional activation is a key link between neuronal activity and long-term synaptic plasticity.
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These results suggest that long-term synaptic plasticity has distinct presynaptic and postsynaptic modules.
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This property is called synaptic plasticity and is implicated in learning and memory.
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Activity-dependent gene transcription and protein synthesis underlie many forms of learning-related synaptic plasticity.
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Transcription is a molecular requisite for long-term synaptic plasticity and long-term memory formation.
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Protein synthesis is crucial for the maintenance of long-term-memory-related synaptic plasticity.
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These signaling scaffold complexes may function to regulate receptor phosphorylation in synaptic plasticity.
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PAC1-mediated signaling has been implicated in neuronal differentiation and synaptic plasticity.
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This abnormal synaptic plasticity might cause the movement disorders observed in Parkinson's disease.
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Furthermore, synaptic plasticity and neuro-immune system may be two principal affected areas by dioxin.
