Omar Khalid
The dendrites of cortical pyramidal neurons receive synaptic inputs from different pathways, which are organized according to their laminar targets. This architectural scheme provides cortical neurons with a spatial mechanism to separate information, which may support the neural flexibility required during learning. The structural plasticity of dendritic spines is related to changes in synaptic efficacy, learning and memory, and other cognitive processes. Studies have shown that spines that contain SER23,44, or spine apparatus are more prone to plastic changes, possibly due to an additional intracellular calcium release site. Furthermore, the size of a dendritic spine is considered proportional to the size of its postsynaptic density (PSD), the number of glutamate receptors, and synaptic strength. The cadherin-based homophilic cell adhesion system is also involved in spine morphogenesis and regulates synaptic plasticity.
| Characteristics | Values |
|---|---|
| Dendrites | Enable both stable network dynamics and considerable synaptic changes |
| Allow the gating of plasticity in a compartment-specific manner | |
| Mitigate the plasticity-stability dilemma | |
| Help in separating information, supporting neural flexibility during learning | |
| Play a critical role in shaping the growth and structure of spines | |
| Can form in the absence of glutamate release | |
| Are influenced by internal and external stimuli | |
| Are related to changes in synaptic efficacy, learning, memory, and other cognitive processes | |
| Are highly dynamic in nature | |
| Are key specialized structures of neuronal connectivity and signaling in the nervous system | |
| Are influenced by neuronal activity, N-cadherin, and β-catenin | |
| Are implicated in neuropsychiatric disorders |
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What You'll Learn
- The influence of learning and memory-related processes
- The role of dendrites in mitigating the plasticity-stability dilemma
- Structural plasticity and neuropsychiatric disease
- The impact of internal and external stimuli on dendritic spine density and morphology
- The relationship between spine structure and function
The influence of learning and memory-related processes
The structural plasticity of dendritic spines is closely related to learning and memory, as well as other cognitive processes. Early studies showed that tetanic stimulation of hippocampal afferents resulted in increased spine density and enlarged spine heads and necks in granule cells of the dentate gyrus. These morphological changes in dendritic spines are thought to be the anatomical substrates of increased synaptic efficacy.
The dendrites of cortical pyramidal neurons receive synaptic inputs from different pathways, which are organized according to their laminar targets. This architectural scheme provides cortical neurons with a spatial mechanism to separate information, supporting the neural flexibility required during learning. For example, following auditory fear conditioning, auditory-evoked Ca2+ responses were enhanced in tuft, but not basal, dendrites, leading to increased somatic action potential output. This suggests that plasticity can be compartmentalized within cortical pyramidal neurons, with tuft dendrites playing a primary role in driving enhanced somatic output following learning.
Hebbian plasticity, considered a neural hallmark for learning and memory, enables the formation of cell assemblies by strengthening connections between cells with correlated activity. However, it can also cause unstable network dynamics and overwrite stored memories. Dendrites help mitigate this plasticity-stability dilemma by allowing for the gating of plasticity in a compartment-specific manner, maintaining stable network dynamics while enabling considerable synaptic changes.
While the structural changes in dendritic spines are likely both instigators and results of behavioral changes, the exact role of spine dynamics in behavior remains unclear. Improved research tools and methods are needed to directly manipulate spine dynamics and delineate the relationship between spine structure and behavior.
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The role of dendrites in mitigating the plasticity-stability dilemma
The plasticity-stability dilemma refers to the challenge of maintaining stable network dynamics while allowing for synaptic changes. Hebbian plasticity, which is considered a neural hallmark for learning and memory, can cause unstable network dynamics and even overwrite stored memories. While limiting synaptic strengths can solve this issue, it does not resolve the stability-plasticity dilemma.
Dendrites play a crucial role in mitigating this dilemma. They enable both stable network dynamics and significant synaptic changes by allowing the gating of plasticity in a compartment-specific manner. This gating of plasticity influences network stability in plastic balanced spiking networks of neurons with dendrites. The coupling between the dendrite and soma is critical for the plasticity-stability trade-off, and spatially restricted plasticity further enhances stability.
The compartmentalisation of pyramidal cells, which receive synaptic inputs from different pathways, enables dendritic synaptic changes while preserving stability. This architectural scheme provides cortical neurons with a spatial mechanism to separate information, supporting the neural flexibility required during learning.
Furthermore, dendrites allow for the compartmentalisation of learning-related plasticity, increasing the computational power of pyramidal neurons. Fear learning, for instance, enhances somatic action potential output, and computational models suggest that tuft dendrites play a primary role in driving this enhancement. Thus, dendrites enable both stability and plasticity, providing a solution to the plasticity-stability dilemma.
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Structural plasticity and neuropsychiatric disease
The structure of neuronal circuits that support cognitive functions in the brain is shaped and refined throughout development and into adulthood. Evidence from human and animal studies suggests that the cellular and synaptic substrates of these circuits are atypical in neuropsychiatric disorders, indicating that altered structural plasticity may be an important part of the disease biology.
Genetics has redefined our understanding of neuropsychiatric disorders and revealed a spectrum of risk factors that impact pathways known to influence structural plasticity. Genetic studies of common and rare variants in neuropsychiatric disorders have discovered a range of genes and chromosomal regions involved in disease risk. For example, genome-wide association studies (GWAS) of common risk variants in schizophrenia and bipolar disorder have identified a growing number of synaptic genes related to the disease.
Exome sequencing studies of de novo variants are particularly useful for uncovering genetic risk networks involved in different disorders. While many genes discovered in exome sequencing studies are individually insignificant, they can collectively reveal a mutational spectrum for each disorder and provide insights into the underlying pathways and networks involved in pathogenesis. Genes with de novo mutations for which the protein products localize to the postsynaptic density (PSD) are excellent candidates for future studies on the dysfunctional pathways altering structural plasticity in neuropsychiatric disorders.
Each neuropsychiatric disorder is associated with a distinct pattern of dendritic spine pathology, and altered structural plasticity of spines is considered a central disease mechanism in these disorders. Neuropsychiatric disorders are a heterogeneous group of mental disorders that manifest psychiatric symptoms and demonstrable brain pathology. They are thought to arise from disruptions of the synaptic circuits that support cognitive, social, and emotional processing.
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The impact of internal and external stimuli on dendritic spine density and morphology
Internal stimuli, such as local calcium release in dendritic spines, have been found to be required for long-term synaptic depression, indicating a role in neuronal plasticity. The size of a dendritic spine is considered proportional to the size of its postsynaptic density (PSD) and the number of glutamate receptors, influencing synaptic strength. Following learning, the PSD-core growth exceeds dendritic spine growth, indicating a long-lasting structural alteration. Additionally, the presence of SER in dendritic spines has been associated with profound remodelling, further influencing spine volume and PSD-core volume correlation during synaptic plasticity.
External stimuli, such as fear learning, have been shown to enhance somatic action potential output without changing the auditory-evoked subthreshold voltage response. This suggests that plasticity can be compartmentalized within cortical pyramidal neurons, leading to increased somatic output. The architectural scheme of cortical neurons provides a spatial mechanism to separate information, supporting neural flexibility during learning.
The specific contribution of internal and external stimuli to dendritic spine density and morphology is complex and requires further investigation. While studies have provided insights into the relationship between structural plasticity and behavioural changes, improved research tools and methods are needed to directly manipulate spine dynamics and establish causality.
In conclusion, both internal and external stimuli influence dendritic spine density and morphology. While the impact of these stimuli is not yet fully understood, ongoing research continues to enhance our understanding of the complex relationship between structural plasticity and behavioural changes.
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The relationship between spine structure and function
The size of a dendritic spine is thought to be proportional to the size of its postsynaptic density (PSD), the number of glutamate receptors, and synaptic strength. However, this correlation is not yet fully understood, and it is unclear if it holds true for all dendritic spine volumes and during synaptic plasticity. The structural plasticity of dendritic spines is influenced by both internal and external stimuli, and their morphology, number, density, and motility can change rapidly.
Studies have shown that spines with specific proteins, such as SER23,44, or the spine apparatus, are more prone to plastic changes due to the additional intracellular calcium release site. The presence of perforated synapses, which are larger and contain more receptors, is also associated with spines containing SER. These structural differences may contribute to the profound remodelling observed in large spines with SER.
The investigation of layer-specific plasticity in the auditory cortex of mice provides insights into the spatial mechanisms of neurons. The findings suggest that dendrites enable the separation of information, supporting neural flexibility during learning. This challenges the traditional hypothesis that neurons function as a single compartment.
Additionally, the gating of plasticity in a compartment-specific manner within dendrites helps maintain stable network dynamics while allowing for considerable synaptic changes. This gating is influenced by neuromodulators such as acetylcholine and noradrenaline, which regulate neural excitability. Overall, the relationship between spine structure and function is multifaceted, and further research is needed to fully understand the underlying mechanisms and their implications for behaviour and cognitive processes.
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Frequently asked questions
The structural plasticity of dendritic spines is related to changes in synaptic efficacy, learning, memory, and other cognitive processes.
Dendritic spines are multifunctional integrative units of the nervous system. They are highly dynamic and diverse in nature.
The size of a dendritic spine is considered proportional to the size of its postsynaptic density (PSD), the number of glutamate receptors, and synaptic strength.
The dendritic compartmentalization of learning-related plasticity may act to increase the computational power of pyramidal neurons.
Dendrites enable both stable network dynamics and considerable synaptic changes by allowing the gating of plasticity in a compartment-specific manner.
