7.3 Synaptic plasticity: LTP and LTD
4 min read•august 15, 2024
Synaptic plasticity is the brain's way of changing connections between neurons. It's crucial for learning and memory. (LTP) strengthens connections, while (LTD) weakens them. These processes help us form new memories and adapt to our environment.
LTP and LTD involve complex molecular changes in neurons. NMDA receptors act as gatekeepers, triggering cascades that add or remove AMPA receptors. This alters how easily signals pass between neurons, shaping our ability to learn and remember.
Synaptic Plasticity in Learning and Memory
Definition and Role
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- Synaptic plasticity enables synapses to strengthen or weaken over time in response to changes in activity
- Serves as a crucial mechanism for learning and memory formation in the brain
- Long-term potentiation (LTP) and long-term depression (LTD) are two forms of synaptic plasticity that can lead to long-lasting changes in synaptic strength
- LTP strengthens synaptic connections and is thought to underlie memory formation and storage (spatial memory, )
- LTD weakens synaptic connections and may play a role in refining neural circuits and eliminating unnecessary connections (sensory adaptation, habituation)
Importance in Brain Function
- Synaptic plasticity allows the brain to adapt and modify its connections based on experience and activity
- Enables the formation of new memories and the modification of existing ones (skill acquisition, knowledge retention)
- Plays a critical role in brain development, allowing the refinement of neural circuits during critical periods (visual cortex development, language acquisition)
- Contributes to the brain's ability to recover from injury or disease through rewiring and reorganization of neural networks (stroke recovery, cognitive rehabilitation)
Mechanisms of LTP and LTD
Long-Term Potentiation (LTP)
- LTP is induced by high-frequency stimulation of presynaptic neurons, leading to a sustained increase in synaptic strength
- Involves the activation of NMDA receptors, which allows calcium influx into the postsynaptic neuron
- Calcium influx triggers a cascade of intracellular signaling events, including the activation of protein kinases (CaMKII) and the insertion of additional AMPA receptors into the postsynaptic membrane
- LTP is associated with the enlargement of , increasing the surface area for synaptic transmission (structural plasticity)
Long-Term Depression (LTD)
- LTD is induced by low-frequency stimulation of presynaptic neurons, leading to a sustained decrease in synaptic strength
- Involves the activation of NMDA receptors and the removal of AMPA receptors from the postsynaptic membrane
- Associated with the activation of protein phosphatases (calcineurin) that dephosphorylate key proteins involved in synaptic transmission
- LTD can lead to the shrinkage of dendritic spines, reducing the surface area for synaptic transmission (structural plasticity)
- May serve as a mechanism for synaptic scaling, preventing excessive excitation and maintaining stable neuronal activity (homeostatic plasticity)
NMDA vs AMPA Receptors in Plasticity
NMDA Receptors
- NMDA receptors are voltage-gated and ligand-gated, requiring both binding and postsynaptic depolarization for activation
- Act as coincidence detectors, allowing calcium influx only when presynaptic glutamate release coincides with postsynaptic depolarization
- Calcium influx through NMDA receptors is essential for triggering the intracellular signaling cascades that lead to LTP and LTD
- Plays a crucial role in the induction of synaptic plasticity and the formation of associative memories (classical conditioning, spatial learning)
AMPA Receptors
- AMPA receptors mediate fast excitatory synaptic transmission and are responsible for the initial depolarization of the postsynaptic neuron
- Insertion or removal of AMPA receptors into/from the postsynaptic membrane is a key mechanism for altering synaptic strength during LTP and LTD
- Phosphorylation of AMPA receptors by CaMKII increases their conductance and promotes their insertion into the postsynaptic membrane, enhancing synaptic strength (LTP)
- Dephosphorylation of AMPA receptors leads to their removal from the postsynaptic membrane, reducing synaptic strength (LTD)
Cellular and Molecular Processes of LTP and LTD
Protein Kinases and Phosphatases
- LTP involves the activation of protein kinases, such as CaMKII and PKA, which phosphorylate key proteins involved in synaptic transmission
- Phosphorylation of AMPA receptors by CaMKII increases their conductance and promotes their insertion into the postsynaptic membrane, enhancing synaptic strength
- LTD involves the activation of protein phosphatases, such as calcineurin and PP1, which dephosphorylate key proteins involved in synaptic transmission
- Dephosphorylation of AMPA receptors leads to their removal from the postsynaptic membrane, reducing synaptic strength
Gene Expression and Protein Synthesis
- LTP involves the activation of transcription factors (CREB) that lead to the synthesis of new proteins required for the maintenance of long-term synaptic changes
- Newly synthesized proteins, such as Arc and BDNF, contribute to the stabilization of synaptic modifications and the growth of new synaptic connections (synaptogenesis)
- Protein synthesis inhibitors can block the late phase of LTP and impair long-term memory formation, highlighting the importance of new protein synthesis in synaptic plasticity (anisomycin, cycloheximide)
Structural Changes in Dendritic Spines
- Both LTP and LTD can involve changes in the morphology of dendritic spines, which are small protrusions on dendrites that receive synaptic input
- LTP is associated with spine enlargement and the formation of new spines, increasing the surface area for synaptic transmission and enhancing connectivity (spine growth, synaptogenesis)
- LTD is associated with spine shrinkage and the elimination of spines, reducing the surface area for synaptic transmission and refining neural circuits (spine pruning, synaptic elimination)
Key Terms to Review (18)
Alzheimer's disease: Alzheimer's disease is a progressive neurodegenerative disorder characterized by the gradual decline in cognitive function, memory, and the ability to perform daily activities. It leads to structural brain changes, including the accumulation of amyloid plaques and tau tangles, impacting communication, attention, and overall brain health.
Ampa receptor: The AMPA receptor is a type of ionotropic glutamate receptor that mediates fast synaptic transmission in the central nervous system. It plays a crucial role in synaptic plasticity, particularly in processes like long-term potentiation (LTP) and long-term depression (LTD), which are essential for learning and memory.
Associative learning: Associative learning is a fundamental learning process where an organism learns to associate one stimulus with another, allowing it to anticipate future events based on previous experiences. This type of learning is crucial for adapting to the environment and is often exemplified by concepts like classical conditioning and operant conditioning. In the context of synaptic plasticity, associative learning plays a key role in how experiences can strengthen or weaken synaptic connections in the brain, which is essential for memory formation and behavioral changes.
Axon terminals: Axon terminals are the small structures at the end of an axon that facilitate communication between neurons. They contain synaptic vesicles filled with neurotransmitters, which are released into the synapse to transmit signals to the next neuron. This critical role in neurotransmission connects axon terminals directly to the processes of synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD).
Circuit dynamics: Circuit dynamics refers to the patterns of activity and interaction between neural circuits, particularly in how they process information and adapt over time. This concept is essential for understanding synaptic plasticity, as it highlights how the strength and efficiency of synaptic connections can change, influencing learning and memory through long-term potentiation (LTP) and long-term depression (LTD). These dynamic interactions within circuits are critical for the brain's ability to reorganize itself based on experience.
Dendritic spines: Dendritic spines are small, protruding structures found on the dendrites of neurons that serve as the primary sites for synaptic connections. They play a crucial role in synaptic plasticity, which includes processes like long-term potentiation (LTP) and long-term depression (LTD), impacting how neurons communicate and strengthen their connections based on activity. Dendritic spines can change in size and shape, reflecting the dynamic nature of synaptic strength and memory formation.
Electrophysiology: Electrophysiology is the branch of physiology that studies the electrical properties of biological cells and tissues. This field is crucial for understanding how neurons communicate, how signals are transmitted at synapses, and the overall functioning of the nervous system. By measuring electrical activity, electrophysiology provides insights into cellular functions, synaptic mechanisms, and the basis of complex behaviors and cognitive processes.
GABA: GABA, or gamma-aminobutyric acid, is a neurotransmitter that plays a crucial role in inhibiting neural activity in the brain. It is primarily responsible for reducing the excitability of neurons, thus helping to regulate muscle tone and prevent excessive firing of neurons that can lead to anxiety and seizures. Understanding GABA's function is key to exploring synaptic transmission, motor coordination, and mechanisms of synaptic plasticity.
Glutamate: Glutamate is the most abundant excitatory neurotransmitter in the brain, crucial for synaptic transmission and communication between neurons. It plays a significant role in various neurological functions, including learning, memory, and motor coordination, as well as influencing reward systems and addiction.
Long-term depression: Long-term depression (LTD) is a persistent decrease in synaptic strength that occurs following certain patterns of activity between neurons. This process plays a crucial role in refining neural circuits and is essential for learning and memory, as it helps to decrease the efficacy of synapses that are less important, allowing the brain to adapt and reorganize itself based on experiences.
Long-term potentiation: Long-term potentiation (LTP) is a lasting increase in synaptic strength following high-frequency stimulation of a synapse. This phenomenon is critical for learning and memory, as it enhances the communication between neurons, making it easier for them to transmit signals over time. It relates to various processes in the brain, including synaptic transmission, memory consolidation, and the formation of new connections between neurons.
Memory consolidation: Memory consolidation is the process by which newly acquired information is transformed into a stable and long-term memory representation. This process is essential for the retention of memories over time and involves the strengthening of synaptic connections in the brain, often facilitated by both synaptic plasticity mechanisms and the reactivation of memory traces during retrieval.
Neural network modulation: Neural network modulation refers to the processes that influence the activity of neural networks, altering their behavior and connectivity in response to various stimuli. This modulation can enhance or inhibit synaptic connections, playing a crucial role in synaptic plasticity mechanisms like long-term potentiation (LTP) and long-term depression (LTD). By adjusting the strength of these connections, neural network modulation facilitates learning, memory formation, and adaptation to new experiences.
Nmda receptor: The NMDA receptor is a specific type of glutamate receptor that plays a crucial role in synaptic plasticity and memory function by allowing the flow of ions, particularly calcium, into the neuron when activated. This receptor is unique because it is both ligand-gated and voltage-dependent, meaning it requires the binding of glutamate and a change in membrane potential to open. Its function is particularly important for processes like long-term potentiation (LTP) and long-term depression (LTD), which are essential for learning and memory.
Patch-clamp technique: The patch-clamp technique is a sophisticated electrophysiological method used to measure the ionic currents flowing through individual ion channels in cells. This technique allows researchers to study the properties of specific ion channels, providing crucial insights into their roles in synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD). By isolating a tiny patch of membrane, scientists can analyze how different conditions affect channel behavior, which is essential for understanding mechanisms underlying synaptic changes.
Schizophrenia: Schizophrenia is a chronic and severe mental disorder that affects how a person thinks, feels, and behaves. It is characterized by symptoms such as delusions, hallucinations, disorganized thinking, and impaired functioning, which can significantly disrupt daily life. Understanding the biological underpinnings of this disorder involves examining aspects like neural migration during brain development, the role of synaptic plasticity in learning and memory, and the distinct features of psychotic disorders.
Synaptic strengthening: Synaptic strengthening refers to the process by which the efficacy of synaptic transmission is enhanced, leading to increased communication between neurons. This phenomenon is often associated with learning and memory, as it allows for the more efficient processing of information in neural circuits. Key mechanisms involved include long-term potentiation (LTP), where synaptic connections are strengthened through repeated stimulation, and various molecular changes that support sustained enhancements in synaptic responses.
Synaptic weakening: Synaptic weakening refers to the process by which the strength of synaptic connections between neurons is decreased, often resulting in reduced neurotransmission efficiency. This phenomenon is a critical aspect of synaptic plasticity, balancing the mechanisms of long-term potentiation (LTP) that enhance synaptic strength. Synaptic weakening is primarily associated with long-term depression (LTD), which helps in refining neural circuits and is essential for learning and memory processes.