neurobio 920 the genesis of the nervous system part 3 (proliferation neural tube neuroblasts filo

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mikepl103
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274067
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neurobio 920 the genesis of the nervous system part 3 (proliferation neural tube neuroblasts filo
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2014-05-12 08:51:52
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neurobio 920 genesis nervous system part proliferation neural tube neuroblasts filopodia synapse formation 34
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neurobio 920 the genesis of the nervous system part 3 (proliferation, neural tube, neuroblasts, filopodia, synapse formation) #34
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  1. describe the process in which synapse elimination in the neuromuscular junction occurs
    the first change is the loss of postsynaptic AChRs, followed by the dissasembly of the presynatpic terminal and retraction of the axon branch
  2. what causes the post-synaptic receptors to disappear during the reduction in synapses?
    insufficient receptor activation in an otherwise active muscle
  3. how is the synapse formed between a pre-synaptic neuron and a post-synaptic neuron strengthened?
    when the presynaptic axon is active and, at the same time, the postsynaptic neuron is strongly activated under the influence of other inputs, then the synapse formed by the presynaptic neuron is strengthened
  4. how is the synapse formed between a pre-synaptic neuron and a post-synaptic neuron weakened?
    when the presynaptic axon is active and, at the same time, the postsynaptic neuron is weakly activated by other inputs, then the synapse formed by the presynaptic axon is weakened.
  5. True or false? the magnitude of sodium ion flux passing through the NMDA receptor channel specifically signals the level of pre- and postsynaptic coactivation
    false, the magnitude of calcium ion flux passing through the NMDA receptor channel specifically signals the level of pre- and postsynaptic coactivation
  6. excitatory synaptic transmission i nthe immature visual system is mediated by which neurotransmitter and which receptor(s)?
    Glutamate is the neurotransmitter and the two receptors are NMDA and AMPA
  7. true or false? in the immature visual system, when a glutamatergic synapse first forms, only NMDA receptors appear in the postsynaptic membrane.
    true
  8. true or false? research indicates that a consequence of strong potassium receptor activation is a strengthening of synaptic transmission
    false, research indicates thata a consequence of strong NMDA receptor activation is a strengthening of synaptic transmission
  9. in what two ways is LTP accounted for?
    1. by the insertion of new AMPA receptors into the synaptic membrane

    2. synapses can split in half following LTP induction
  10. what is the molecular basis for the reduced visual responsiveness that results in an eye that is closed for an extended period of time?
    closing one eye replaces well-correlated pre-synaptic action potentials with less correlated noise. The noise weakly activates NMDA receptors, and the resulting modest increase in Ca ions cause internalization of AMPA receptors. On the other hand, the well-correlated activity strongly depolarizes the postsynaptic neurons and stimulates large increases in Ca ion concentration, which stimulate AMPA receptor delivery to the synapse
  11. Describe the three phases of pathway formation. In which phase (or phases) does neural activity play a role?
    The three phases of pathway formation are pathway selection, target selection, and address selection. The growing retinal axon makes several “decisions” to find its correct target. During pathway selection, the axon chooses the correct path. During target selection, the axon chooses the correct structure to innervate. During address selection, the axon chooses the correct cells to synapse with in the target structure. Synaptic rearrangement is the final step in the process of address selection. Synaptic rearrangement occurs as a result of neural activity and synaptic transmission. Therefore, neural activity plays a role in the phase of address selection.
  12. What are three ways that Ca2+ is thought to contribute to the processes of synapse formation and rearrangement?
    According to the model of synapse formation provided by the neuromuscular junction, interaction between growing axon and target occurs in both directions; induction of a presynaptic terminal involves proteins in the basal lamina. Basal lamina factors provided bythe target cell evidently stimulate Ca2+ entry into the growth cone, which triggers neurotransmitter release. Besides mobilizing transmitter and Ca2+ entry into the axon, Ca2+ also triggers changes in the cytoskeleton that cause it to assume the appearance of a presynaptic terminal and to adhere tightly to its postsynaptic partner. Ca2+ may also play a role during synapse rearrangement. A specific type of glutamate receptor, known as NMDA receptor, can only be activated when glutamate is released by the presynaptic element and the postsynaptic membrane is sufficiently depolarized to dislodge an Mg ion from the NMDA receptor. The NMDA receptor conducts Ca2+ ions. It is the magnitude of the Ca2+ flux passing through the NMDA receptor channel that specifically signals the level of pre- and postsynaptic coactivation. This occurs only when there is highly correlated activity—the necessary condition for synaptic enhancement during development.
  13. How are the elimination of polyneuronal innervation of a muscle fiber and the segregation of retinal terminals in the LGN similar? How do these processes differ?
    The similarities are that in the process of polyneuronal innervation of a muscle fiber, eventually each muscle fiber receives synaptic input from a single alpha motor neuron. In the process of segregating retinal inputs from the two eyes, axons from the two eyes intermingle in the LGN layers at first and then segregate into the eye-specific layers characteristic of the adult nucleus. In both the neuromuscular junction and the LGN, synaptic segregation is a consequence of neural activity and synaptic transmission. Silencing neural activity disrupts segregation. On the other hand, the synapses at the neuromuscular junction and LGN use different neurotransmitters. In addition, the innervation of muscle by alpha motor neurons in the peripheral nervous system may regenerate after injury but damaged retinogeniculate connections in the central nervous system that are established during development are permanent, and cannot regenerate.
  14. Not long ago, when a child was born with strabismus, the defect was usually not corrected until after adolescence. Today, surgical correction is always attempted during early childhood. Why? How does strabismus affect the connections in the brain, and how does it affect vision?
    Strabismus is a common visual disorder in humans in which the eyes are not perfectly aligned. As a result, the fovea in each eye is not focused on the same point in the visual field. Ocular misalignment must be corrected in early childhood, as soon as surgically feasible, to avoid permanent visual disability. This is because strabismus prevents corresponding binocular input to cortical neurons (input from both the right and left eye to cortical neurons representing the same point in space). This noncorrespondence prevents the development of binocular cortical neurons, which are essential for stereopsis, the ability to discriminate fine differences in three-dimensional spaces. In addition, people with strabismus often favor one eye over the other. The nonprefered eye is at a disadvantage during the critical period of visual cortical development when the process of binocular competition determines which eye wins synaptic space in visual cortex. The preferred eye establishes more than its share of synaptic contacts in visual cortex, and after the critical period ends, the unequal distribution becomes permanent. Corrective surgery for strabismus during adolescence may realign the eyes, but the cortical connections will not change. Establishing the correct cortical circuitry requires that corrective surgery be done early, before the critical period for cortical development ends.

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