regulation of long-term neuronal synaptic plasticity

Definition

Target type: biologicalprocess

A process that modulates 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]

Long-term neuronal synaptic plasticity, a fundamental mechanism underlying learning and memory, involves persistent changes in synaptic strength. This intricate process is regulated by a complex interplay of molecular events that occur at the synapse, the specialized junction where neurons communicate.

**Induction of Long-Term Potentiation (LTP):**
* **Early LTP:** This phase is triggered by high-frequency stimulation (HFS) of presynaptic neurons, leading to increased glutamate release and activation of postsynaptic NMDA receptors. NMDA receptor activation allows calcium influx into the postsynaptic neuron, initiating a cascade of signaling events.
* **Late LTP:** This phase requires protein synthesis and involves structural changes at the synapse. It is driven by the activation of various signaling pathways, including:
* **Calcium/calmodulin-dependent protein kinase II (CaMKII):** Phosphorylates AMPA receptors, enhancing their sensitivity to glutamate.
* **Protein kinase A (PKA):** Activates CREB (cAMP response element-binding protein), a transcription factor that regulates gene expression involved in synapse strengthening.
* **Mitogen-activated protein kinases (MAPKs):** Contribute to gene expression and structural remodeling of the synapse.

**Induction of Long-Term Depression (LTD):**
* **LTD:** This process involves a decrease in synaptic strength, often triggered by low-frequency stimulation. It is mediated by the activation of specific receptors and signaling pathways, including:
* **mGluR1 receptors:** Activate signaling pathways that lead to internalization of AMPA receptors, reducing synaptic strength.
* **Tyrosine kinases:** Phosphorylate proteins involved in LTD, including the protein tyrosine phosphatase (PTP).

**Molecular Mechanisms:**
* **Synaptic Protein Synthesis:** The production of new proteins is crucial for late LTP and LTD. This process involves the activation of ribosomes and the translation of mRNA into proteins.
* **Structural Remodeling:** Long-term plasticity involves alterations in the size and morphology of synapses. This includes changes in the number and distribution of dendritic spines, the postsynaptic structures where synapses form.
* **Gene Expression:** Specific genes are activated during LTP and LTD, leading to the production of proteins that contribute to synaptic plasticity.

**Regulation of LTP and LTD:**
* **Homeostatic Plasticity:** This process ensures that synaptic strength is maintained within a specific range. It involves mechanisms that counteract excessive synaptic strengthening or weakening.
* **Age-related Changes:** Synaptic plasticity undergoes age-related changes, with a decline in LTP and an increase in LTD observed in aging neurons.
* **Neurological Disorders:** Impairment of synaptic plasticity is implicated in neurodevelopmental disorders and neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease.

**Conclusion:**
Regulation of long-term neuronal synaptic plasticity is a complex and multifaceted process that involves intricate molecular mechanisms, including receptor activation, signaling pathways, protein synthesis, and structural remodeling. This intricate regulation is essential for learning, memory, and the overall function of the nervous system.'
"

Proteins (8)

Compounds (1,149)