Exam 3 Short Answers Flashcards
Identify the role of myelin in the regeneration of central neurons
Myelin, produced by oligodendrocytes in the central nervous system, plays a crucial role in the regeneration of central neurons. Recent studies have shown that modulating these inhibitory signals or targeting specific signaling pathways can promote axonal regeneration and functional recovery. Remyelination by oligodendrocytes not only restores conduction velocity but also provides trophic support for regenerating axons.
Identify the role of myelin and nerve sheaths in the regeneration of peripheral neurons.
- Schwann cells and myelin debris clearance: Schwann cells proliferate and migrate to the injury site, secreting enzymes to degrade myelin debris, and facilitating axon regeneration.
- Remyelination: Schwann cells remyelinate new axons as regenerating axons grow, restoring saltatory conduction and nerve function.
- Extracellular matrix remodeling: Schwann cells and nerve sheath cells produce and remodel the extracellular matrix, providing a supportive environment for axon regeneration.
- Promotion of target reinnervation: The bands of Büngner and nerve sheaths guide regenerating axons, facilitating target reinnervation and functional recovery.
- The central nervous system lacks robust regenerative response due to inhibitory factors and limited intrinsic regenerative capacity.
Briefly describe Hebb’s rule.
It states that when a presynaptic neuron repeatedly participates in firing a postsynaptic neuron, the strength of the synaptic connection between them increases. This is often summarized as “neurons that fire together, wire together.”
In a sentence describe how NMDA receptors are activated and what type of current results
NMDA receptors are activated by the simultaneous binding of glutamate and the removal of magnesium block by depolarization of the postsynaptic membrane. This results in the influx of calcium ions, producing an excitatory current.
What is the source of inhibitory signals in central axon regeneration, and how do we know?
The primary sources of inhibitory signals in central axon regeneration are myelin-associated inhibitors (e.g., Nogo, MAG, OMgp) and components of the extracellular matrix in the glial scar, particularly chondroitin sulfate proteoglycans (CSPGs).
Describe the basic concept behind the synaptic tagging hypothesis.
The synaptic tagging hypothesis proposes that the induction of long-term potentiation (LTP) or long-term depression (LTD) at a synapse creates a local “tag” or signal that marks the synapse for subsequent capture of plasticity-related proteins (PRPs). The synthesis of these PRPs is thought to be triggered by a separate event, such as strong neuronal activity or neuromodulatory signals. The synapse can only undergo long-lasting changes if both the tag and PRPs are present.
Briefly explain the difference between E-LTP and L-LTP. What are the cellular events that differentiate them?
E-LTP lasts for 1-3 hours and results from the modification of existing proteins and receptors at the synapse.
L-LTP lasts for several hours to days and requires gene transcription, new protein synthesis, and the growth of new synaptic connections.
The primary cellular events differentiating E-LTP and L-LTP are the involvement of new protein synthesis and structural changes in L-LTP, whereas E-LTP mainly relies on the modification of existing proteins and receptors.
On an average neuron with a dendritic tree and a single un-branching axon, an action potential is initiated on the soma by a large sudden depolarization. Where does the action potential travel?
Action potentials are generated on the neuron’s soma when membrane potential reaches the threshold for triggering an action potential.
Once initiated, the action potential propagates towards the dendrites and the axon.
Dendrites have a lower density of voltage-gated sodium channels, limiting the regenerative propagation of action potentials.
The axon, with a high density of voltage-gated sodium channels, efficiently propagates action potentials over long distances.
The action potential travels a significant distance along the axon, enabling the release of neurotransmitters at synapses.
What must be true about a mechanism for plasticity for it to be modeled by the binomial distribution?
Binary outcome: The mechanism must involve a process with two possible outcomes: “success” and “failure.”
Constant probability: The probability of success or failure must remain constant across all trials.
Binomial distribution: Models the number of “successful” events out of the total number of trials.
When studying the mechanism of hippocampal plasticity, what is commonly used for an induction protocol to ensure that LTP is induced?
Post tetanic potentiation
Describe the classical conditioning in Aplysia.
Classical conditioning in Aplysia involves a neutral stimulus (conditioned stimulus) and a reinforcing stimulus (unconditioned stimulus) eliciting a natural reflex response (unconditioned response).
The process involves three steps: baseline response, acquisition (pairing), and conditioned response.
Classical Conditioning:
* Sensory neuron action potential precedes shock for calmodulin to be activated, activating facilitated interneuron and serotonin release.
*Action potential in sensory neurons causes more CA2+ to enter the cell, leading to Calmodulin activation and Adenylyl cyclase 4 primed, enhancing AP and bigger PKA.
*Adenylyl Cyclase is a coincidence detector
* Calmodulin, associated with Adenylyl cyclase, enhances Action potential and bigger PKA activation.
* MAP K inhibits CREB 2 and activates CREB 1, directing gene transcription and PKA activation.
Describe the prototypical process of NMDA-dependent LTP (Schaffer collateral or direct perforant). Be sure to include short- and long-term mechanisms mediating this phenomenon. Be precise.
NMDA-dependent LTP is a form of synaptic plasticity that enhances synaptic strength.
The process involves Presynaptic glutamate release, postsynaptic depolarization, and NMDA receptor activation.
Short-term mechanisms include calcium influx, activation of CaMKII, and AMPA receptor phosphorylation.
Long-term mechanisms include gene expression and protein synthesis, dendritic protein synthesis, and structural changes.
ΔT—positive and negative meaning
ΔT (delta T): The time difference between the pre- and postsynaptic spikes. A positive ΔT means the presynaptic spike preceded the postsynaptic spike (pre-post pairing), while a negative ΔT means the postsynaptic spike preceded the presynaptic spike (post-pre pairing).
