Alexei Volkov
Synaptic plasticity is the ability of the brain to adapt and change in response to new information, experiences, and injuries. It refers to the changes in the strength of synaptic connections, which are the junctions between neurons that allow them to communicate. These changes can be short-term, lasting from milliseconds to a few minutes, or long-term, lasting from minutes to hours, days, or years. Synaptic plasticity is influenced by factors such as neurotransmitter release and the activation of neighbouring structures, and it plays a crucial role in learning, memory, and the development of neural circuitry. The concept of synaptic plasticity has important implications for understanding brain functions and treating neuropsychiatric disorders and injuries such as strokes or traumatic brain injuries (TBIs).
| Characteristics | Values |
|---|---|
| Definition | Synaptic plasticity refers to the changes in synaptic strength, or the ability of the brain to change and adapt to new information. |
| Types | Short-term and long-term plasticity |
| Short-term plasticity | Occurs on a sub-second timescale, lasting from tens of milliseconds to a few minutes. |
| Long-term plasticity | Lasts from minutes to hours, days, or years. |
| Role | Controls how effectively two neurons communicate with each other. |
| Underlying mechanisms | Changes in the quantity of neurotransmitters released into a synapse, changes in how effectively cells respond to those neurotransmitters, and postsynaptic calcium release. |
| Importance of location | Biochemical interactions occur at microdomains, such as the exocytosis of AMPA receptors, which is regulated by the t-SNARE STX4. |
| CAMKII signaling | Nanodomain calcium is important for the specificity of signaling. |
| PKA spatial gradient | The spatial gradient of PKA between dendritic spines and shafts influences the strength and regulation of synaptic plasticity. |
| Individual synapses | Biochemical mechanisms altering synaptic plasticity occur at the level of individual synapses of a neuron. |
| LTP and LTD | Long-term potentiation (LTP) refers to the strengthening of a synapse, while long-term depression (LTD) refers to the weakening of a synapse. |
| Regulatory forms | Scaling and metaplasticity provide negative feedback to prevent positive feedback loops from developing. |
| Memory | Synaptic plasticity is thought to play a role in memory storage and formation, particularly in the hippocampus. |
| Neural circuitry | Synaptic plasticity may play a key role in the early development of neural circuitry. |
| Neuropsychiatric disorders | Impairments in synaptic plasticity mechanisms have been implicated in several neuropsychiatric disorders. |
| Neuroplasticity | Synaptic plasticity is a form of neuroplasticity, which involves adaptive structural and functional changes to the brain in response to stimuli or injuries. |
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What You'll Learn
Short-term synaptic plasticity
Synaptic plasticity refers to the brain's ability to change and adapt to new information. It involves changes in the strength of synapses, the junctions between neurons that allow them to communicate. Synaptic plasticity controls how effectively two neurons communicate with each other. The strength of communication between two synapses can be likened to the volume of a conversation.
Short-term plasticity can either strengthen or weaken a synapse. Synaptic enhancement results from an increased probability of synaptic terminals releasing transmitters in response to pre-synaptic action potentials. Synapses will strengthen for a short time due to an increase in the amount of packaged transmitter released in response to each action potential. Synaptic fatigue or depression, on the other hand, is attributed to the depletion of readily releasable vesicles or post-synaptic processes and feedback activation of presynaptic receptors.
Most forms of short-term synaptic plasticity are triggered by short bursts of activity, causing a transient accumulation of calcium in presynaptic nerve terminals. This increase in presynaptic calcium leads to changes in the probability of neurotransmitter release by modifying the biochemical processes underlying the exocytosis of synaptic vesicles. Two types of short-term plasticity, with opposite effects on synaptic efficacy, are Short-Term Depression (STD) and Short-Term Facilitation (STF). STD is caused by the depletion of neurotransmitters consumed during the synaptic signaling process at the axon terminal of a pre-synaptic neuron, while STF is caused by the influx of calcium into the axon terminal, increasing the release probability of neurotransmitters.
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Long-term synaptic plasticity
The concept of long-term synaptic plasticity was first reported in 1973 by Terje Lømo and Tim Bliss, who studied the synapses in the hippocampi of rabbits. They discovered that rapidly and repeatedly activating the synapses made them stronger, a phenomenon known as long-term potentiation (LTP). Conversely, when synapses are less active, they can become weaker over extended periods, a process called long-term depression (LTD). The strength of synapses is bidirectionally modifiable, meaning it can be increased or decreased depending on their activity patterns. Very active synapses are likely to become stronger (LTP), while less active synapses tend to become weaker (LTD).
The molecular mechanisms underlying long-term synaptic plasticity involve the NMDA and AMPA glutamate receptors. The opening of NMDA channels, which is related to the level of cellular depolarization, leads to an increase in post-synaptic Ca2+ concentration. This rise in calcium ions is linked to LTP and the activation of protein kinases, which improve cation conduction and potentiate the synapse. On the other hand, weaker depolarization results in lower Ca2+ concentrations, activating protein phosphatases and inducing LTD.
Synaptic scaling and metaplasticity are regulatory forms of plasticity that provide negative feedback and prevent saturated states of LTP and LTD. Synaptic scaling helps maintain the relative strengths of synapses by adjusting their amplitudes in response to continual excitation or prolonged blockage. Metaplasticity varies the threshold at which plasticity occurs, allowing integrated responses to synaptic activity over time.
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Synaptic plasticity and memory
Synaptic plasticity refers to the brain's ability to change and adapt to new information. It involves adaptive changes in the synaptic strength and efficacy, resulting in the strengthening or weakening of synaptic connections. Synaptic plasticity is influenced by factors such as neurotransmitter release and the activation of neighbouring structures. It is believed to be a fundamental mechanism involved in learning and memory.
The concept of synaptic plasticity was first proposed in 1949 by Canadian psychologist Donald Hebb, who suggested that the change in synapses depends on their level of activity. In 1973, Terje Lømo and Tim Bliss described the phenomenon of long-term potentiation (LTP) in the hippocampi of rabbits. This discovery raised questions about the potential role of LTP in information storage and memory.
The hippocampus, a region of the cerebral cortex, has been key in understanding synaptic plasticity and its role in memory. Lesions in the hippocampus prevent the acquisition of new episodic memories, and activity-dependent synaptic plasticity is a prominent feature of hippocampal synapses. This has led to the hypothesis that hippocampus-dependent memory is mediated, at least in part, by hippocampal synaptic plasticity.
The synaptic plasticity and memory hypothesis suggests that activity-dependent synaptic plasticity is induced during memory formation and is necessary for the encoding and storage of memories. This hypothesis has been supported by various techniques in contemporary neuroscience, including optical imaging and molecular-genetic approaches. These studies indicate that changing the strength of connections between neurons is a major mechanism involved in memory storage.
While there is strong evidence for the role of synaptic plasticity in memory, there has been no direct demonstration of it occurring during memory acquisition. However, studies on conditioned fear memory have provided significant insights into the role of synaptic plasticity in memory formation. Additionally, the development of transgenic molecular devices may further enhance our understanding by allowing for the analysis of how networks of neurons encode and represent memory.
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Synaptic plasticity and learning
Synaptic plasticity is a fundamental mechanism involved in learning and memory. It refers to the ability of synapses, the junctions between neurons that allow them to communicate, to strengthen or weaken over time in response to increases or decreases in their activity. This neurochemical foundation of learning and memory is also known as Hebbian theory.
The strength of communication between two synapses can be likened to the volume of a conversation. Some neurons communicate at a low volume, while others are much louder. This "volume setting" of the synapse, or the synaptic strength, is not static but rather can change in both the short term and the long term. Short-term synaptic plasticity acts on a timescale of tens of milliseconds to a few minutes, whereas long-term plasticity can last from minutes to hours, days, or even years. Short-term plasticity can either strengthen or weaken a synapse, depending on the amount of packaged transmitter released in response to each action potential. Synapses will strengthen for a short time due to an increase in the amount of packaged transmitter released in response to each action potential. Synaptic fatigue or depression, on the other hand, is usually attributed to the depletion of readily releasable vesicles or the feedback activation of presynaptic receptors.
Long-term potentiation (LTP) and long-term depression (LTD) in the hippocampus, the hallmark structure for studying synaptic plasticity, have been directly linked to learning and memory. The hippocampus is where memory is initially encoded after learning, before being stabilized in other brain regions such as the cortex. The hippocampus is also involved in certain forms of memory, such as spatial memory. In one study, mice with enhanced NMDAR function displayed enhanced LTP and improved spatial learning. Another study showed that blocking the maintenance of LTP in the hippocampus also abolished the storage of long-lasting spatial memory. These findings suggest that LTP is required for the engram that stores key spatial information.
In addition to spatial learning, synaptic plasticity has also been linked to fear extinction. For example, the administration of D-cycloserine, a partial agonist of NMDARs, has been shown to enhance the extinction of fear in phobic patients. This has led to the potential novel treatment of common psychiatric disorders using D-cycloserine in combination with behavioral therapy.
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Regulatory forms of synaptic plasticity
Synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity. Synapses are the junctions between neurons that allow them to communicate. Synaptic plasticity controls how effectively two neurons communicate with each other. The strength of communication between two synapses can be likened to the volume of a conversation.
The regulatory forms of synaptic plasticity are:
Scaling
Synaptic scaling is a primary mechanism that allows a neuron to stabilize firing rates up or down. It maintains the strengths of synapses relative to each other, lowering amplitudes of small excitatory postsynaptic potentials in response to continual excitation and raising them after prolonged blockage or inhibition. This effect occurs gradually over hours or days, by changing the numbers of NMDA receptors at the synapse.
Metaplasticity
Metaplasticity varies the threshold level at which plasticity occurs, allowing integrated responses to synaptic activity spaced over time and preventing saturated states of LTP and LTD. Since LTP and LTD rely on the influx of Ca2+ through NMDA channels, metaplasticity may be due to changes in NMDA receptors, altered calcium buffering, altered states of kinases or phosphatases, and a priming of protein synthesis machinery.
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Frequently asked questions
Synaptic plasticity refers to the adaptive changes that occur at the synapse, resulting in the strengthening or weakening of synaptic connections. It is a fundamental mechanism involved in learning and memory.
Synaptic plasticity is the ability to make experience-dependent long-lasting changes in the strength of neuronal connections. It is involved in the brain's ability to change and adapt to new information.
Synaptic plasticity is influenced by factors such as neurotransmitter release and activation of neighbouring structures. It can be understood through the concept of long-term potentiation (LTP) and long-term depression (LTD), which refer to the strengthening and weakening of synapses, respectively.
