positive regulation of long-term neuronal synaptic plasticity

Definition

Target type: biologicalprocess

A process that increases long-term neuronal synaptic plasticity, the ability of neuronal synapses to change long-term as circumstances require. Long-term neuronal synaptic plasticity generally involves increase or decrease in actual synapse numbers. [GOC:jid, PMID:11891290]

Positive regulation of long-term neuronal synaptic plasticity is a complex biological process that underlies learning and memory formation. It involves a series of molecular and cellular events that strengthen the connections between neurons, allowing for more efficient communication and information processing. This process is characterized by long-lasting changes in synaptic strength, which are often referred to as long-term potentiation (LTP) and long-term depression (LTD).

LTP is an increase in synaptic strength, typically induced by high-frequency stimulation of a synapse. This increase in strength is mediated by the insertion of new AMPA receptors into the postsynaptic membrane, leading to increased sensitivity to glutamate, the primary excitatory neurotransmitter in the brain. LTD, on the other hand, is a decrease in synaptic strength, typically induced by low-frequency stimulation. LTD is often mediated by the removal of AMPA receptors from the postsynaptic membrane.

The process of positive regulation of long-term neuronal synaptic plasticity involves several key players, including:

1. **Glutamate receptors:** These receptors are activated by the neurotransmitter glutamate and play a crucial role in synaptic transmission. AMPA receptors are primarily responsible for fast excitatory transmission, while NMDA receptors are involved in LTP induction and plasticity.
2. **Calcium signaling:** Calcium ions play a central role in regulating synaptic plasticity. Upon glutamate release, calcium influx through NMDA receptors triggers a cascade of downstream signaling pathways, leading to changes in gene expression, protein synthesis, and cytoskeletal remodeling.
3. **Signaling pathways:** Several signaling pathways, such as the MAPK and PI3K pathways, are activated by calcium signaling and contribute to the regulation of LTP and LTD. These pathways regulate the expression of genes involved in synaptic plasticity and the trafficking of proteins required for synapse formation and function.
4. **Transcription factors:** These proteins bind to DNA and regulate gene expression. Transcription factors, such as CREB, are activated by signaling pathways and play a role in the long-term changes in gene expression associated with synaptic plasticity.
5. **Cytoskeletal proteins:** These proteins form the structural framework of the synapse. Changes in cytoskeletal organization, mediated by proteins like actin and tubulin, contribute to the structural modifications associated with LTP and LTD.

In addition to these key players, numerous other factors, including neuronal activity, neurotrophic factors, and epigenetic modifications, can also influence the process of positive regulation of long-term neuronal synaptic plasticity.

Overall, positive regulation of long-term neuronal synaptic plasticity is a highly dynamic and regulated process that ensures the flexibility and adaptability of the nervous system. This process is essential for learning, memory, and other cognitive functions.'
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Proteins (3)

Compounds (337)