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130 Cards in this Set
- Front
- Back
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What layer does all neural tissue develop from?
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ectoderm
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When does nervous system start to develop?
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embryologic week 4
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T/F The early development of nervous system is dominated by events that occur prior to formation of synapses and is therefore activity-indpt
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T
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What process proceeds neurulation?
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Gastrulation
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What type of cells form notochordal process?
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mesoderm
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What induces the overlying ectoderm to become neural plate?
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The axial mesoderm/notochordal process
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Process by which CNS is formed
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neurulation
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The entire CNS develops from ____________
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neural tube
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What fuses to form neural tube?
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Neural groove folds in to make neural folds which form neural tube
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What is the order of neurulation?
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Neural plate --> Neural groove (with neural crest cells at top) --> Folds in to form Neural tube
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What gives rise to neural structures in PNS?
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neural crest. It pinches off dorsolateral to neural tube
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What induces the cells to become neural tissue?
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morphogens
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BMP
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bone morphogenetic protein
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Influence differntiation of dorsal part of cord and hindbrain
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BMPs (Part of TGF-β family)
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Molecule Important in establishing motor neurons in ventral part of spinal cord. Released by notochord.
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Sonic hedgehog (Shh)
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influences both dorsal and ventral cell identity in spinal cord and has roles in neuronal differentiation thru the CNS
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retinoic acid
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What are the embryonic structures that are critical for the initial induction and patterning of the CNS?
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notochord, floorplate, roofplate, and neural ectoderm itself (contain morphogens)
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How is retinoic acid (ie, accutane) exposure teratogenic?
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Retinoic acid activates gene expression in a SMALL SUBSET of cells at a time in the developing forebrain. If mother consumes it, it gets ectopically activated throughout the forebrain.
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What causes medulloblastoma?
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Lack of Shh-mediated regulation of a transcription factor causes subset of granule precursor cells in cerebellum transforms and divides uncontrollably.
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What is holoprosencephaly? What causes it?
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Prosencephalon (forebrain) fails to develop due to failure of certain genes (Shh) to guide placement of embryologic structures.
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what is derived from neural crest cells?
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1) Sensory ganglia
2) Autonomic ganglia 3) Neurosecretory cells 4) Melanocytes |
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CNS is derived from neural _____ while PNS derived from neural ______
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tube; crest
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When does neural tube close?
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4th week (day 21-24)
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Elevated levels of ___________ seen in amniotic fluid/maternal blood when neural tube defects occur.
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Alpha-fetoprotein
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Failure of anterior end of neural tube to close causes ___________
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anencephaly
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Failure of posterior end of neural tube to close causes ___________
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spina bifida
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rachischisis
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Neural folds fail to fuse.
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What is spina bifida occulta?
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outer part of some of the vertebrae are not completely closed. asymptomatic in most cases, may have a slight tuft of hair or dimple.
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What is meningocele?
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vertebrae develop normally, however the meninges are forced into the gaps between the vertebrae. As the nervous system remains undamaged, individuals with meningocele are unlikely to suffer long-term health problems.
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What is myelomeningocele?
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unfused portion of the spinal column allows the spinal cord to protrude through an opening. The meningeal membranes that cover the spinal cord form a sac enclosing the spinal elements.
More serious than meningocele, where just the meninges come out. |
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what is encephalocele?
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a neural tube defect characterized by sac-like protrusions of the brain and the membranes that cover it through openings in the skull. These defects are caused by failure of the neural tube to close completely during fetal development.
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Three primary brain vesicles resulting from cephalization of neural tube
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1) Prosencephalon - Forebrain
2) Mesencephalon - Midbrain 3) Rhombencephalon - hindbrain |
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What does the hollow canal inside the neural tube become?
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ventricles
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What are the 3 locations where the neural tube folds sharply?
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1) Mesencephalic flexure
2) Pontine flexure 3) Cervical flexure |
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When does the neural tube fold sharply?
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Between 4th and 8th weeks
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What day does cephalization occur?
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Day 26
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What are the 5 secondary vesicles?
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From Prosencephalon:
1) Telecephalon - cerebral cortex 2) Diencephalon - thalamus From mesencephalon - 3) Mesencephalon From rhombencephalon 4) Metencephalon 5) Myelencephalon |
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What does telencephalon become?
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Cerebral hemispheres
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What does diencephalon become?
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Thalamus
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What does mesencephalon become?
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Midbrain
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What cavities/ventricles are the following associated with:
1) Telecephalon 2) Diencephalon 3) Mesecephalon 4) Metencephalon 5) Myelencephalon |
1) Lateral ventricles
2) Third ventricle 3) Cerebral aqueduct 4) Upper part of 4th ventricle 5) Lower part of 4th ventricle |
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What does metencephalon become?
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Pons and Cerebellum
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What does myelencephalon become?
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Medulla
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What is derivative of mantle of neural tube?
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Gray matter
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What is the relative location (closer to PIA or closer to NEURAL TUBE LUMEN/VENTRICLE) of nucleus of neurons during the following cells stages:
A) G1 B) S C) G2 D) Mitosis |
A) Near ventricular surface/lumen
B) Migrate towards pial surface for DNA replication C) Cell grows and nucleus migrates back to ventricular surface D) Cells lose connection to pial surface and divide close to ventricle. |
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Where are the firstborn cells of cerebral cortex located?
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Deepest layers
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Where are the layer generations of cells in cerebral cortex located
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Superficial to older layers. They get piled on in an "inside-out" fashion
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What does the mantle layer (Primordial gray matter) of neural tube divide into?
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Alar and basal plates
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What separates alar and basal plates?
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Sulcus limitans
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What does the alar plate become?
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Sensory nuclei (dorsal horn of spinal cord)
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What does the basal plate become?
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Motor nucleu (ventral horn)
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Which grows faster?
1) Vertebral column 2) Spinal cord |
1) Vertebral column. This is why the spinal cord does not go the entire length of the vertebrae and the cauda equina is necessary.
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What does the dorsal part of the alar plates become?
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Rhombic lip which becomes thickened to form primordium of cerebellum
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How is cerebellum formed?
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The dorsal part of the alar plate become the rhombic lip that forms primordial cerebellar cortex
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In midbrain, what does alar plate give rise to?
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Superior and inferior colliculi
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In midbrain, what does basal plate give rise to?
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Oculomotor and trochlear nuclei (GSE) and Edinger-Westphal nuclei (GVE)
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How does telencephalon develop?
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It swells and grows posteriorly and laterally and eventually envelops the diencephalon
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Does the prosencephalon arise from alar or basal plate?
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Alar
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Progenitor of corpus callosum and other commissures
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Lamina terminalis thickens to becmoe commissural plate
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Hernia of brain where brain protrudes thru congenital skull opening
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Encephalocele
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Convolutions of cerebral cortex aren't fully formed and brain surface is smooth.
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Lissencephalia
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Cause of lissencephalia
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Defective neuronal migration
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Developmental defect in which convolutions are abnormally small, resulting in structural malformation of cortex
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Microgyria
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Disorder involving cyst or cavity in cerebral hemisphere, communicating by a pore in subarachnoid space. Signs include delayed growht, spastic paresis, hypotonia, seizures
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Porencephaly
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Agenesis of corpus callosum
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Disorder where corpus callosum fails to form. May have mild to severe abnormalities. May have normal intelligence with compromise of skills requiring matching of visual patterns
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Communicating hydrocephalus
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Impaired CSF reabsorption in arachnoid granules leading to obstruction of flow in subarachnoid space
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Non-Communicating hydrocephalus
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Caused by obstruction of flow within ventricular system
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What are the steps for forming a neural circuit?
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1) Neural induction and patterning
2) Specification of neural type 3) Neuronal migration 4) Neuronal polarization 5) Circuit formation 6) Circuit refinement |
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What protein sets the direction of the growth cone?
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Actin
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What protein drives outgrowth (fwd or bwd movement) of growth cone?
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Tubulin
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Regional changes in ________ steer growth cone?
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calcium
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T/F Growth cone must be attached to cell bodies to move
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False! A severed growth cone will still move and steer
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What regulates the assembly/disaseembly of subunits of growth cone?
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Changes in intracellular Ca via voltage regulated Ca channels as well as transient receptor potential channels (TRPs)
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Acts from a distance on a pioneer growth cone to reorient growth towards it
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chemoattractant
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Difference between fasciculated and pioneer growth cones
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fasciculated growth cones just follow the pioneers
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Where do chemorepulsants act? (2)
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1) At a distance
2) Regions where axons must defasciculate from a nascent nerve in order to change trajectory of avoid inappropriate target. |
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Support the further growth and differentiation of axon and parent nerve cell
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trophic signals
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What are the major classes of axon guidance molecules? (4)
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1) EC matrix molecules - ligands for multiple integrin receptors
2) CAMs 3) Soluble ligands and receptors 4) Repulsive cues (e.g., semaphorins) |
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What other functions are the axon guidance molecules conserved in?
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Angiogenesis, cell migration (tumor formation)
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Difference between TROPIC and TROPHIC
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Tropic - guide axons towards a source
Trophic - support survival and growth once target has been contacted |
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What is the chemoaffinity hypothesis?
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Chemical tags (Such as CAMs, ECMs, etc) on the target cell creates an affinity for the selective binding by the receptive part of growth cone. This is activity independent.
Demonstrated in the famous Sperry frog tectum experiments |
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T/F Target selection by chemoaffinity is activity independent
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T
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Congenital Cranial Dysinnervation Disorders (CCDDs): What are they?
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Congenital, non-progressive
• Sporadic or familial • Developmental abnormalities of one or more cranial nerves/nuclei • Primary dysinnervation - absence of normal innervation - neurons do not develop or are misguided • Secondary dysinnervation - aberrant innervation during development by branches of another nerve |
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What is congenital fibrosis of EOM type 3?
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Pt presents with unilateral ptosis and inability to elevate eye. Due to a mutation in tubulin.
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What is Duane retraction syndrome?
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Predominantly horizontal disorder of ocular motility.
most commonly characterized by the inability of the eye to abduct or move outwards. Due to mutations in CHN1, an axon pathfinding gene. This stalls growth of some axons, leads to mistargeting of others. |
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T/F The synapse is the same size as the neurotransmitter release site
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F. The true release site may be much smaller than the synapse.
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What must happen for initiation of synapse to occur?
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Adhesion. This involves recognition between pre and post synaptic membranes mediated by adhesive factors (cadherins)
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Once the initial specialization of a synapse is established, what happens?
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Additional adhesion molecules are recruited including Synaptic CAM (SynCAM). These are considered INDUCTIVE factors. Adhesive signaling between these molecules initiates differentiation of the presynaptic active zone and postsynaptic density.
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What is agrin?
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A molecule derived from motor neurons responsible for initiating assembly of postsynaptic apparatus in muscle.
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Where does agrin come from?
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From the motor neuron.
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What signal is necessary for assembly of postsynaptic apparatus in muscle to form NMJ?
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Agrin
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Without agrin what happens?
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No agrin means no NMJ. No NMJ means death.
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What are supernumerary neurons?
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Neurons that fail to successfully interact with intended targets. They're eliminated by apoptosis.
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What are neurotrophins?
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Signals that provide trophic support to neurons once they find their targets. They prevent death by apoptosis.
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Why are neurotrophins a therapeutic target?
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They promote neuronal survival. Mutations in these have been linked to neurodegenerative diseases and memory problems.
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Examples of neurotrophins
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Nerve growth factor (NGF); Brain derived neurotrophic factor (BDNF), NT3and4
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T/F Synaptic elimination is the process by which supernumerary inputs are eliminated.
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T
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T/F The initial formation of synapses is activity driven
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FALSE. Synapse elimination (the pruning of supernumerary inputs) is activity driven. Initial formation is genetically driven.
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representation of the sensory receptor surface, preserving orderly arrangements from periphery
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topographic map
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area of receptor surface (skin) that when stimulated causes neural response
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receptive field
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T/F The same relative locations of the body map are true for different individuals, but the exact borders and shapes vary between individuals
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T
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T/F Activity independent restructuring of visual ocular dominance columns occurs
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F. Activity DEPENDENT
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Experience-dept plasticity: what happens?
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Afferent inputs compete for synaptic spacec within cortex
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Reduced vision in one eye due to brain not acknowledging images in that eye
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Amblyopia
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What is treatment for amblyopia?
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Patch the unaffected eye. This forces brain to respond to the weaker eye. Over time they become equal. MUST be done at young age.
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T/F Development of normal sensory perception requires sensory experience.
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T
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What are the mechanisms of critical period plasticity?
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Has to do with changes in thalamocortical afferents. Initially they are spread over a relatively large region and have simple branching patterns. During development these branches become focused/pruned.
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What are the molecular mechanisms of thalamocortical afferent changes?
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Dept on NMDA glu receptors.
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Blockage of NMDA receptors can result in __________ of ocular dominance columns, while NMDA agonists result in ______ of OD columns
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elimination/blurring ; sharpening
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What is the "memory molecule" that is necessary for LTP and has autophosphorylation properties?
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Calcium-calmodulin protein-kinaseII (CKII)
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T/F LTP and LTD only occur during critical period.
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F. LTD only occurs during critical period. LTP occurs beyond.
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T/F Loss of LTD mechanisms is what causes the end of the critical period.
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Maybe. There is a correlation.
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What layer is thalamocortical projection?
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Layer IV
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Main serine protease in brain
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tissue plasminogen activator
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What is the role of proteases in plasticity?
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Proteases like TPA can degrade the ECM surrounding individual spines, allowing them greater motility
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T/F Even though ocular dominance columns and thalamocortical afferents are fixed by adulthood, you can still change topographic maps in adults by affecting intracortical connections.
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T
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What happens in phantom limb syndrome?
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Reorganization of the somatotopic map occurs after amputation such that the neighboring regions in S1 take over the deafferented cortex. However, association-cortices still "think" the missing part is there. This can lead to pain.
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When will there be no phantom limb pain after amputation?
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When there is no reorganization
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Why does reorganization after amputation occur in some people but not others, resulting in phantom limb pain?
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It has to do with how much the adjacent cortical area is getting used. If it's getting used a lot, there's a higher likelihood that it will take over the deafferented areas.
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T/F The degree of cortical reorganization is not correlated with severity of phantom limb pain
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F. It IS correlated.
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T/F In phantom limb syndrome, only S1 is remapped, not association cortices
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T
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What is the inhibitory mechanism by which sensory deprivation leads to expansion of adjacent representations?
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Some excitatory cortical neurons (say from digit 1, D1) send axons into the representation for D2. These are normally inhibited by GABAergic interneurons that fire when the D2 representation is activated. However, when there is no stimulation to D2, the inhibitory interneuron is no longer excited. The excitatory D1 can encroach on its territory.
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What is the timeframe of inhibitory mechanism?
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Within seconds
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T/F The pattern of thalamic input to cortical layer IV can only be altered during the critical period
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T
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T/F The larger a representation for a body part, the finer the control
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T
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What is BMI/bicuculline?
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Antagonist for the GABA
Receptor, (blocks inhibition). |
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What is importance of BMI/bicuculline in studying plasticity?
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It blocks the effects of the inhibitory interneuron in somatosensory cortices, thereby allowing the excitatory input from adjacent fields to be unmasked.
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What is cross modal plasticity?
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Phenomenon whereby input from one sensory system (ie., vision) causes changes in another (ie., somatosensation). This is the basis of mirror visual feedback.
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What happens in mirror visual feedback for an amputated hand?
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Getting the visual input of looking at the intact body part in a mirror tells the mind (aka association cortices) that the amputated hand’s representation is located within the brain at the site of intact hand representation within primary somatosensory cortex.
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Why does blindfolding sighted adults increase ability to learn Braille?
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Blindfolding increases recruitment of visual cortex. This is an example of cross-modal plasticity. This shows there are connections between sensory cortices that can be unmasked.
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