Nonsynaptic plasticity
Nonsynaptic plasticity is a form of neuroplasticity that involves modification of ion channel function in the neuron's membrane, as opposed to synaptic plasticity, which involves a change in the efficacy of the synapses. This form of plasticity is thought to play a role in learning and memory, as well as in the development of certain neurological disorders.
Overview[edit | edit source]
Nonsynaptic plasticity is a type of cellular learning that occurs in the neurons of the brain. Unlike synaptic plasticity, which involves changes in the strength of synapses, nonsynaptic plasticity involves changes in the function of ion channels in the neuron's membrane. This can result in changes in the neuron's excitability, or ability to fire action potentials.
Mechanisms[edit | edit source]
The mechanisms of nonsynaptic plasticity are not fully understood, but it is thought to involve changes in the function of various types of ion channels, including voltage-gated ion channels and ligand-gated ion channels. These changes can be brought about by various factors, including changes in the neuron's environment, such as changes in the concentration of certain ions, and changes in the neuron's activity, such as increased or decreased firing of action potentials.
Role in Learning and Memory[edit | edit source]
Nonsynaptic plasticity is thought to play a role in learning and memory. This is because changes in the function of ion channels can affect the neuron's excitability, which can in turn affect the strength of synaptic connections. This can result in changes in the patterns of neural activity, which are thought to underlie the formation of memories.
Role in Neurological Disorders[edit | edit source]
Nonsynaptic plasticity is also thought to play a role in the development of certain neurological disorders. For example, changes in the function of ion channels can result in increased neuronal excitability, which can lead to the development of seizures. Similarly, changes in the function of ion channels can result in decreased neuronal excitability, which can lead to the development of neurodegenerative diseases.
See Also[edit | edit source]
References[edit | edit source]
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