Neuronal Plasticity
Neuronal Plasticity - Related Videos
12:47
Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
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Cited by 8 •
2014
Here we describe an adaptation of protocols used to induce homeostatic plasticity in neurons for the study of plasticity of astrocytic G protein-coupled receptors. Recently used to examine changes in astrocytic group I mGluRs in juvenile mice, the method can be applied to measure scaling of various astrocytic GPCRs, in tissue from adult mice in situ and in vivo, and to gain a better appreciation of the sensitivity of astrocytic receptors to changes in neuronal activity.
04:53
Compartmentalized Primary Murine Neuron Culture Using Plastic Microfluidic Chips
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2025
This video demonstrates the utilization of a pre-assembled plastic microfluidic chip for the compartmentalized culture of primary rat hippocampal neurons. The neurons are plated into one of the microfluidic compartments, where they attach and grow, extending their axons through the chip's microgrooves into the adjacent compartment. The narrow microgrooves prevent neuronal cell bodies from entering, thereby enabling physical separation between the somatic and axonal compartments.
10:29
Simulating Pancreatic Neuroplasticity: In Vitro Dual-neuron Plasticity Assay
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Cited by 3 •
2014
Neuronal plasticity is an increasingly recognized, but insufficiently understood feature of the gastrointestinal (GI) tract. Here, in the example of human pancreatic disorders, we present an in vitro neuroplasticity assay for the study of neuronal plasticity in the GI tract at both morphological and functional level.
05:01
Inducing Long-Term Plasticity of Intrinsic Neuronal Excitability in Neurons of the Dorsal Lateral Geniculate Nucleus
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2024
Here, we describe a protocol for inducing long-term plasticity of neuronal intrinsic excitability in relay neurons from the dorsal lateral geniculate nucleus maintained in ex vivo brain slices.
00:58
Plasticity
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2023
Plasticity is the property where an object loses its elasticity and undergoes irreversible deformation, even after the deformation forces are eliminated. If a material deforms irreversibly without increasing stress or load, then this is called ideal plasticity. For example, when a force is applied to an aluminum rod, it changes its shape, but it does not return to its original shape once the force is removed. Plastic deformation or ductility is thus a permanent deformation or change in the...
FAQs
Coordinated or repeated neural signaling can shift synaptic strength by changing how much neurotransmitter is released and how responsive the receiving cell becomes. When signaling patterns repeatedly engage a pathway, these activity-dependent adjustments can reinforce communication; different patterns can weaken it. This provides a cellular basis for modifying circuit performance during learning and adaptation.
Several linked changes determine whether a synapse becomes more or less effective. Presynaptic neurotransmitter release alters the signal sent, receptor expression changes the receiving cell’s response, and dendritic spine remodeling changes aspects of synaptic structure. Considering these mechanisms together is important because functional and structural adjustments can occur as coordinated parts of circuit reorganization.
Changes in dendritic spine structure can accompany altered synaptic signaling, helping neural circuits retain activity-dependent modifications. When these adjustments stabilize pathways involved in memory, they may support persistence of learned information rather than only a short-lived change in communication. Studying spine remodeling therefore links cellular structure with the longer-term organization of memory-related circuits.
When damaged pathways lose function, activity-dependent remodeling can help remaining or connected circuitry compensate. This does not imply that every change is beneficial: remodeling may also become maladaptive, meaning it reinforces an unfavorable circuit state. Neuroscience therefore examines both compensation and harmful reorganization when considering how plasticity shapes outcomes after injury.
Studies can focus on changes in structure, function, and connectivity, with particular attention to neurotransmitter release, receptor expression, and dendritic spine structure. Examining these levels together helps relate cellular synaptic events to broader circuit changes. The resulting picture can connect activity-dependent remodeling with learning, memory, adaptation, or responses to injury.
Learning research asks how activity-dependent strengthening and weakening helps stabilize circuits involved in memory. Rehabilitation research applies the same framework to compensation after damaged pathways lose function, seeking to understand which circuit changes support recovery. Together, these areas use plasticity as a basis for studying how experience or intervention can reinforce beneficial neural adaptations.
The same capacity for circuit remodeling that supports adaptation can also produce maladaptive changes. This makes plasticity relevant to neurological disorders because research can distinguish beneficial compensation from reorganization that limits function or reinforces an unfavorable state. Such distinctions guide efforts to encourage useful circuit changes while limiting changes that may worsen neural outcomes.