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Questions and Answers
In the context of cortical plasticity, what does altered synaptic functioning refer to?
In the context of cortical plasticity, what does altered synaptic functioning refer to?
- Changes in the number of neurons
- Changes in the speed of action potentials
- Changes in neurochemical concentrations
- Changes in the structure and function of synapses (correct)
Which process underlies learning, memory, and recovery/reorganization processes?
Which process underlies learning, memory, and recovery/reorganization processes?
- Synaptic modulation (correct)
- Axon growth inhibition
- Myelin sheath disintegration
- Neurotransmitter depletion
What is the basis of cortical plasticity?
What is the basis of cortical plasticity?
- Blood flow alterations
- Neuronal firing rate changes
- Brain size increase
- Altered synaptic functioning (correct)
How is cortical plasticity related to learning and memory?
How is cortical plasticity related to learning and memory?
What is the role of synaptic modulation in cortical plasticity?
What is the role of synaptic modulation in cortical plasticity?
How does altered synaptic functioning contribute to recovery and reorganization processes?
How does altered synaptic functioning contribute to recovery and reorganization processes?
What is the pivotal finding mentioned in the text regarding cortical plasticity?
What is the pivotal finding mentioned in the text regarding cortical plasticity?
What is the key point related to glutamate synapses in the experimental model?
What is the key point related to glutamate synapses in the experimental model?
Which phase of long-term potentiation identified by Bliss & Collingridge is protein kinase independent and lasts up to one hour?
Which phase of long-term potentiation identified by Bliss & Collingridge is protein kinase independent and lasts up to one hour?
In the context of cortical plasticity, what effect does high-frequency stimulation have on glutamate synapses?
In the context of cortical plasticity, what effect does high-frequency stimulation have on glutamate synapses?
What is the role of NMDAR & AMPAR in the short and long term effects mentioned in the text?
What is the role of NMDAR & AMPAR in the short and long term effects mentioned in the text?
What kind of synaptic changes are associated with an experimental model typically involving 100Hz for 1 second on glutamate synapses?
What kind of synaptic changes are associated with an experimental model typically involving 100Hz for 1 second on glutamate synapses?
What neurotransmitter is downregulated while glutamate is upregulated?
What neurotransmitter is downregulated while glutamate is upregulated?
Which process involves changes in synaptic structure including dendrites and spines growing and contracting?
Which process involves changes in synaptic structure including dendrites and spines growing and contracting?
What controls the excitability of horizontal connections involved in cortical map modeling?
What controls the excitability of horizontal connections involved in cortical map modeling?
In the context of adaptations to retinal lesions, what leads to disinhibition in the peri-lesion zone?
In the context of adaptations to retinal lesions, what leads to disinhibition in the peri-lesion zone?
Which factor promotes dendritic growth and is increased in the context of adaptations to retinal lesions?
Which factor promotes dendritic growth and is increased in the context of adaptations to retinal lesions?
What rapid changes are observed in the context of inhibitory alterations around lesion zones?
What rapid changes are observed in the context of inhibitory alterations around lesion zones?
What is the term used to describe the alteration in synaptic strength due to changes in release probability or receptor properties?
What is the term used to describe the alteration in synaptic strength due to changes in release probability or receptor properties?
Which process involves the formation or loss of dendritic spines and modification of synapse number?
Which process involves the formation or loss of dendritic spines and modification of synapse number?
What is a characteristic of late LTP (Long-Term Potentiation) as mentioned in the text?
What is a characteristic of late LTP (Long-Term Potentiation) as mentioned in the text?
Which area serves as a site for research on neuroplasticity according to the text?
Which area serves as a site for research on neuroplasticity according to the text?
What is involved in cortical plasticity as a result of altered afferent input, training, or pathology according to the text?
What is involved in cortical plasticity as a result of altered afferent input, training, or pathology according to the text?
Which process in plasticity involves unmasking or disinhibition of pre-existing cortical connections through GABA's role?
Which process in plasticity involves unmasking or disinhibition of pre-existing cortical connections through GABA's role?
What is the main effect of LTP on AMPAR according to the text?
What is the main effect of LTP on AMPAR according to the text?
Which molecular process leads to the formation of new dendritic spines in the context of cortical plasticity?
Which molecular process leads to the formation of new dendritic spines in the context of cortical plasticity?
What is the role of calmodulin in the context of LTP?
What is the role of calmodulin in the context of LTP?
What happens when the same stimulus activates two receptors in LTP?
What happens when the same stimulus activates two receptors in LTP?
In the context of long-term potentiation, what is the consequence of AMPAR diffusion across the membrane?
In the context of long-term potentiation, what is the consequence of AMPAR diffusion across the membrane?
What is the primary mechanism through which LTP induces pre- and post-synaptic effects according to Kandel et al. 2013?
What is the primary mechanism through which LTP induces pre- and post-synaptic effects according to Kandel et al. 2013?
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