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77 Cards in this Set
- Front
- Back
neural induction, restriction and patterning are mediated by :
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homeodomain, neurotrophic and transcription factors during development
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in PNS, neural crest cells lead to development of:
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sensory and dorsal root ganglia or intestinal neurons
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in PNS, neural crest cells lead to development of sensory and dorsal root ganglia or intestinal neurons, by expressing what?
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1) NGF --> Trk A and P75 receptors
2) BDNF --> Trk C and P75 receptors |
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what's an ex of CNS developmental disorder?
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ancephaly
spinal bifida |
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what's an ex of PNS developmental disorder?
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hirschsprung disease
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what's so great about notocord?
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tells other genes to differentiate
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when EGF/FGF signal neural stem cells, either _______ or _________
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die or keep growing
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where are the 4 places that neural stem cell pool exists in adult brain?
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1. Subventricular zone
2. Hippocampus--dentate gryrus 3. Olfactory bulb 4. Spinal cord |
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During development
The formation of the forebrain, midbrain, and hindbrain are determined by ?? |
NTF and Transcription factors
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how are neural stem cells isolated?
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using EGF/FGF
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what might result of competition between nerve cells at the level of the target they innervate be?
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apoptosis
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target neurons provide neurotrophic factors to facilitate what?
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the growth and support the survival of the innervating neurons.
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Lack of target support may account for
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some apoptosis
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if apoptosis in large scale, what might it be?
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degeneration
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Nerve fibers may overgrow during what time?
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the embryonic or early postnatal stage.
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the higher than normal adult level of innervation is pruned when? why?
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in the process of maturation.
This process helps to shape the final connections. |
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One of the mechanism of Pruning may be the availability of what?
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Neurotrophic Factor in the target field
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what contributes to what neurons stay and what's leaves in pruning?
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activity! IF YOU DON'T USE IT, YOU LOSE IT!
if talking a lot and playing bingo --> keep it! if in isolation --> lose it |
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when are most of neurons formed?
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before birth
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what area of brain is ex of one that keeps forming new neurons?
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hippocampus
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when are The major neuronal connections formed?
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after birth.
*Particularly, the dendritic complexity including forming spines and postsynaptic connection continue |
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the language cortex increases in complexity during which stage?
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birth to 6 year old
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when learning 2nd language after 18, a lot harder b/c?
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neurons already in place for 1st language... conn b/w broca's area and vocal cords not as strong for 2nd language- is that what he said?
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short term memory starts 1st where?
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hippocampus
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the alpha Ach R is a func unit that binds what?
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2 Ach
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alpha Ach R tends to sit where on nerve terminals?
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right below nerve terminals on muscle
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in development of receptor, what happens to gamma Ach R?
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over time, gamma disappears and alpha stays
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Neuronal receptor formation is also refined throughout what stage?
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development.
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how does cocaine affect AMPA and NMDA?
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Cocaine triggers AMPA receptor redistribution, thus increase NMDA receptor function
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during what time period do The majority of neuronal connections do not change ?
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during normal adulthood
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the dynamic turnover of synaptic contacts and micro-redistribution of receptors and uptake sites may occur during what time frame?
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in everyday life!
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the dynamic turnover of synaptic contacts and micro-redistribution of receptors and uptake sites along with subcellular protein turnover and phosphorylation, may account for WHAT?
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memory, learning, emotional changes, and many psychological and neurological states.
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what's a big difference that can be seen in neurons of young person and old person?
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fewer spines in dendrites of old ppl
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if the Core Blood flow of neuron is <5mi/100g/min, what's the result?
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tissue death in minutes.
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what can help salvage the penumbral tissue.?
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Clot lysis or providing NTF
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when the Blood flow 5-10 mi/100g/min in the penumbra, what can you expect?
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Tissue “stunned” but salvageable
*cell death, degeneration, slow blood flow, salvageable |
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what are the layers to the injury zone?
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1. Core
2. Penumbra 3. uninjured |
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Brain injury causes __________________ depending on the nature and severity of the insult.
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immediate, mid, and long-range plasticity
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what happens at the center of nerve injury w/i the 1st 24 hours?
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neuronal and glial death, invasion of microglia, and proliferation of glial cells
*Throughout the time, stem cells may be trigger to enter to the injury site (such as spinal cord injury). |
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what's a major event a few days after neuronal injury?
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astrocyte activation
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what does these things?
increase transporters to remove toxic molecule, secret extracellular matrix such as laminin attempting to “glue” the broken parts, produce neurotrophic factors to facilitate the growth of health neurons. |
astrocyte
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what does astrocyte do a few days after neuronal injury?
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increase transporters to remove toxic molecule, secret extracellular matrix such as laminin attempting to “glue” the broken parts, produce neurotrophic factors to facilitate the growth of health neurons.
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what effect can break down products of glial cells have?
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release inhibitory protein (such as Nogo by oligodendrocyte) prevent neurite outgrowth
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what happens on day 0 and day 7 of injury that are in common?
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glutamate is released!
also released: toxic peptides @ day 7 |
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what is :regrowth of the damaged nerve fibers. Require cytoskeleton e.g. microtubule for rebuild.?
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regeneration
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what is regrowth of the intact nerve fibers.?
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sprouting
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what is regrowth of the intact nerve fibers which carry the same transmitter as the damaged one?
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homotypic sprouting
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what is regrowth of the intact nerve fibers which carry a different transmitter from the damaged one?
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heterotypic sprouting
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what is synapses formation in response to the damage of adjacent nerve terminals. This event accounts for the most occurring process in the daily wear & tear.?
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reactive synaptogenesis
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what do glial cells and Dr. Zhou's 1st girlfriend have in common?
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they're both unpredictable! he could never tell what they're going to do!
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who am I? Injury cause demyelination; its fragment can release anti-regeneration molecule.
Remyelination is critical for repairing. .e.g. Spinal cord injury. who am I? |
OLIVER THE OLIGODENDROCYTE : CNS
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In addtion to Basal lamina scaffolds,can also produce many Extracellular matrix, neurotrophic factors & Mitogens
who am I? |
SCHWANN CELLS: PNS
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if denervated, what's the result?
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either more receptors
or if have same # of receptors, --> hypersensitivity ex: Long-term medication of a transmitter blocking agent can also cause this process : blocking of dopamine in Schizophrenia patient --> tardive dyskinesia |
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what happens when you give L-dopa to parkinsonism dosage response?
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turns into uncontrolled mvmnt b/c receptor very sensitive
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how do you reverse cocaine effects?
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Cocaine triggered AMPA receptor redistribution is reversed in vivo by mGluR-dependent
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Activation of metabotropic glutamate receptors (mGluR1s) by intraperitoneal injection of a positive modulator depotentiated synapses and abolished rectification in slices of cocaine-treated mice, revealing a mechanism to reverse cocaine-induced synaptic plasticity in vivo.
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reverse cocaine effects!
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how can receptors be redistributed after injury?
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gamma Ach R reappear
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what are exs of neuronal functional reorganization?
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Blind person with acute hearing
Phantom limb |
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what is this: In response to peripheral injury, such as amputation, the brain regions that control or response to the peripheral, through training over time, can be reassigned to control or respond to the adjacent area to the injured peripheral. ?
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Somatosensory Reorganization after injury
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Trimming of the whisker during early development deprive sensation to the trimmed whisker, but their neurons were reassigned to do what?
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response to remaining adjacent whisker which become highly sensitive.
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what might neuronal reengineering look like in future?
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1. Prevention of Neuronal Death
2. Recruit and replenish stem cells 3. Cellular therapy through Neuronal Transplantation 4. Neurite Promotion and Axonal Guiding |
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what prevents neuronal death?
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1)antioxidant
2)anti-excitatory agents/ anti-apoptotic agents- Anti- glutamate 3)neurotrophic factors 4)anti-degeneration |
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what antioxidant is used to prevent neuronal death?
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supraoxide dismutase: SOD
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what anti-excitatory agents/ anti-apoptotic agents- Anti- glutamate are used to prevent neuronal death?
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Riluzole partial protection against Glu in synapsis used in stroke, motor neuron disease
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what neurotrophic factors are used to prevent neuronal death?
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GDNF
BDNF CNTF IGF |
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what neurotrophic factor acts on dopamine neurons?
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GDNF
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what neurotrophic factor acts on spinal motor neurons?
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BDNF
CNTF |
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what anti-degeneration methods are there for prevention of neuronal death?
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anti-nogo
anti-alpha synuclein anti-amyloid increase astrocyte gene expression |
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what antidegeneration method is key for alzheimer's disease?
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anti-amyloid
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what antidegeneration method is good for spinal cord injury?
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anti-nogo
*spinal cord injuries are a "no go"! |
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what anti degeneration method is there for prevention of neuronal death in PD?
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anti alpha synuclein
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how do you engineer non-neuronal cells?
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making iPS (induced progenitor cells)
by converting skin cells into stem cells through introducing stem cell genes, Oct4 and Sox |
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what part of brain grows in number comparing couch potato rats w/ running rats?
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hippocampus
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what are the key points involved in neurite production and axonal guiding?
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anti-inhibitor factor
increase remyelination neurotrophic factor neuronal bridging |
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what anti-inhibitor injury is involved in neurite production and axonal guiding?
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anti-nogo for spinal cord injury
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what neurotrophic factors are involved in Neurite Promotion and Axonal Guiding?
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BDNF
NGF CNTF |
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if damage substantia nigra, how can it be fixed?
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transplant dopamine neuron into nigra
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