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64 Cards in this Set
- Front
- Back
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What is the decussation of the pyramids?
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nerve fibers obliquely cross from one lateral part to the other; they cross at a level other than their origin
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What's is the golgi staining method?
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a microcrystal precipitate of silver salts which deposit on a limited number of cells at random, but throughout their entirety
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What are the tracer methods used to study?
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Tracer molecules are injected into a discrete region of the brain containing cell bodies or axon terminals.
Tracer internalized at cell body and anterogradely transported to the terminals. Tracer internalized at terminals and retrogradely transported to the cell bodies. Tracers are visualized to localize cell bodies, terminals and tracts. |
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Horseradish peroxidase (HRP) : what is it used for?
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A tracer molecule
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What protein makes up microfilaments?
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actin
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What protein makes up microtubules?
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α and β tubulin
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What protein makes up neurofilaments?
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intermediate filament unique to neurons
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How are microfilaments different in neurons than other cells?
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Do not form long stress fibers seen in other cells, in neurons, they form a reticulum of short fibers
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Where are microfilaments concentrated?
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Growth cones, dendritic spines, and below the plasma membrane
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Actin-spectrin membrane complexes: function
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concentrated beneath the membrane. Provides support for membrane and anchorage for membrane proteins.
Spectrin – Cross links microfilaments to support the plasma membrane |
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What is ankyrin?
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Linker protein anchoring transmembrane proteins, e.g., sodium channels to the spectrin- actin network
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Where are actin-spectrin membrane complexes most likely to be found?
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Nodes of Ranvier (support ion channels) and post-synaptic desnsities (basically anywhere where there are a lot of membrane proteins)
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What is responsible for the dynamic properties (shape and volume change etc) of dendritic spines?
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microfilament polymerization and depolymerization
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What regulates microfilament polymerization and depolymerization?
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actin-associated proteins and intracellular calcium levels.
Profilin – elongation Arp 2/3 complex - branching Cofilin/gelsolin – severing |
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What does phosphorylation due to neurofilaments?
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It causes them to repel from the neuron (mostly axon), forming "side arms" that provide additional stability.
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Functions of microtubulin
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pathways for intracellular transport, primarily
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What is the + and - end of microtubules?
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α and β tubulin dimers are ADDED at the + end and SUBTRACTED at the - end.
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What is the polarity of axons vs. dendrites with regard to microtubules?
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Axons: microtubules are oriented with + (growing) end facing distally, away from the nucleus. - end is facing body.
Dendrites: may be either |
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How is the formation of microtubules different in neurons than other cells?
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In non-neuronal cells, MT’s form at the microtubule organizing center (MTOC) and radiate out into the cytoplasm
In neurons, microtubules form at MTOC and released. |
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What are the purpose of the microtubule-associated-proteins?
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Proteins which stabilize microtubules
Differentially distributed between the somato-dendritic and axonal compartments Used experimentally to distinguish axon from dendrite |
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Which microtubule-associated-proteins are associated with
A) Axons B) dendrites and cell body |
A) Tau
B) MAP2 |
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What types of things are carried by anterograde (away from cell body) transport?
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Molecules made in the soma that must be carried out to periphery.
Neurotransmitter vesicles Vesicles for membrane insertion Mitochondria |
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What types of things are carried by retrograde (towards cell body) transport?
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Recycled organelles; endocytic vesicles
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What direction does Kinesin move cargo?
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Towards the + end of the microtubule (may be distally in an axon or distal/proximally in dendrite)
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What direction does dynein move cargo?
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Towards the - end of the microtubule (may be proximally in an axon or distal/proximally in dendrite)
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Which virus takes advantage of axonal transport and how?
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Herpes.
1. Primary infection - In epithelial cells of the skin virus undergoes the lytic cycle: entry, uncoating, viral transcription and DNA replication in the nucleus, particle assembly, exit from the cell. 2. Some virus enters the sensory neuron terminals and travels retrogradely to the nucleus where it establishes latency. 3. Periodic reactivation results in anterograde transport of viral particles, shedding from the neuron, and re-infection of epithelial cells, which leads to recurrent lesions. |
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How might herpes virus be used in treating chronic pain?
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Create replication-deficient HSV containing the DNA for target gene(s):
Enkephalin – endogenous opioid Glutamic acid decarboxylase – GABA synthesis Sodium channel (antisense orientation) Subcutaneous injection, cancer sites, and end organs, pancreas (pancreatitis); bladder (irritatability and hyperactivity) |
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Why does the active zone of the synapse appear more electron dense in electron microscopy?
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Because of the high concentration of proteins/vesicles/ion channels etc. found there
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What is the post-synaptic density?
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Collection of proteins (channels, adapter, linking, cytoskeletal, and adhesion) at the postsynaptic membrane that are visible with the electron microscope.
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What are the three types of vesicles?
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1) Clear vesicles
2) Dense core vesicles - 3) Large dense core vesicles |
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What is contained in clear vesicles?
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ACh, GABA, glutamate
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What is contained in dense core vesicles?
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Appear darker.
Catecholamines (EPI, NE) |
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What is contained in large dense core vesicles?
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neuropeptides
(substance P, somatostatin) |
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Spherical vesicles (e.g., acetylcholine, glutamate)
Large active zone Prominent postsynaptic density Wide synaptic cleft Are characteristics of what type of synapse? |
Excitatory/type I
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Oval vesicles (GABA)
Restricted active zone Less conspicuous postsynaptic density Narrower synaptic cleft Are characteristics of what type of synapse? |
Inhibitory/type II
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What are the advantages/disadvantages of chemical vs. electrical synapses?
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Chemical synapses are slower, but they allow for plasticity.
Electrical synapses, while fast, don't allow for much ability to change/adapt. |
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Oval vesicles are found in what type of synapse?
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inhibitory
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What type of proteins are associated with gap junctions/electrical synapses?
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Connexins/Connexons
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Small molecule neurotransmitters mediate what kind of synaptic actions?
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Rapid
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Neuropeptides (larger neurotransmitters) mediate what kind of synaptic actions?
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slower, ongoing functions
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Where does the synthesis of small-molecule neurotransmitters occur?
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Locally, within presynaptic terminals. The enzymes needed to make these are produced in neuronal cell body and transported via slow axonal transport
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Where does the synthesis of neuropeptides occur?
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Cell body (a long way away from site of secretion). Transported via fast axonal tarnsport
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What is the end plate potential?
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Depolarization of the muscle cell that is brought on by presynaptic release of ACh
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What is a mini-end plate potential? (MEPP?)
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The change in potential that occurs postsynaptically as a result of fusion of ONE vesicle of ACh. The summation of these is the EPP
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What happens to the fused vesicle membrane after the NT is released?
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Although it seems like a bout of exocytosis could drastically increase the size of the surface area of presynaptic terminals, the vesicles are actually retrieved (called the <b>synaptic vesicle cycle</b>).
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Synaptotagmin
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protein found in membrane of synaptic vesicles.
Acts as a sensor to detect when Ca2+ is present. When it binds Ca2+, it also binds lipids which pulls the vesicle and cell membrane together to promote fusion and vesicle content release. |
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Clathrin
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protein involved in endocytotic budding of vesicles from plasma membrane. Structures form pits that initiate membrane budding.
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Components of synaptic vesicle cycle
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Vesicle formation and filling
Movement into vesicle pools Docking at presynaptic membrane Priming Fusion (neurotransmitter release) Budding and Recycling |
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What are Congenital myasthenic syndromes?
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inherited diseases of neuromuscular transmission.
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What are symptoms of congenital myasthenic syndromes?
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Clinical features: Weakness which increases with exertion and starts in childhood.
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What causes Presynaptic congenital myasthenic syndromes (CMS) with episodia apnea?
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Defect in choline acetyltransferase [ChAT] leads to inefficient resynthesis of ACh
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Lambert Eaton myasthenic syndrome (LEMS)
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Syndrome in which autoantibodies are generated against voltage-gated calcium channels (VGCCs) (and other synaptic proteins)
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What are symptoms of Lambert Eaton myasthenic syndrome (LEMS)?
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Weakness affecting proximal muscles most. Exertion worsens symptoms. Reduced reflexes at rest, with muscle use reflex strength increases (Characteristic feature). 75% of patients have autonomic disruption as well (dry mouth, constipation, impaired sweating).
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What are SNAREs?
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The primary role of SNARE proteins is to mediate vesicle fusion, that is, the exocytosis of cellular transport vesicles with the cell membrane.
Two types: 1) v-SNARES:incorporated into the membranes of transport vesicles during budding 2) target or t-SNAREs, which are located in the membranes of target compartments. |
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What are v-SNARES?
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proteins that mediate vesicle fusion that are in the membranes of the transport vesicles
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synaptobrevin
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a v-SNARE protein involved in formation of the SNARE complexes.
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SNAP25 and Syntaxin
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t-SNARE proteins
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How are synaptic vesicle contents released?
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1) Vesicle docks on membrane
2) SNARE complexes (v-SNARE synaptobrevin and t-SNARE SNAP25 and syntaxin) form to pull vesicle and cell membrane together. 3) Entering Ca2+ binds to synaptotagmin. 4) Ca2+-bound synaptotagmin catalyzes membrane fusion --> release of vesicle contents |
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How does <b>tetanus</b> toxin affect neurotransmitter release?
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It cleaves v-SNARE synaptobrevin, but only affects inhibitory neurons of spinal cord.
These neurons are unable to release their contents, thus their function (selective inhibition) is diminished, resulting in phenotype of tetanus/lockjaw (hypertonic muscles) |
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Clostridial toxins: what are they and what diseases do they cause?
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Anearobic bacterial toxins (botulinum and tetanus toxins)
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How does <b>botulism </b> toxin affect neurotransmitter release?
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Botulinum toxins cleave all three SNARE proteins
Preferentially affects neuromuscular junction leading to muscle weakness and in extreme cases respiratory failure. Also affects synapses innervating smooth muscle leading to visceral motor dysfunction |
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How does α-Latrotoxin
affect neurotransmitter release? |
Venom from widow spiders (Latrodectus), particularly female black widows
Induces massive neurotransmitter release, even in the absence of calcium Binds neurexin, a presynaptic membrane protein that binds intracellularly to synaptotagmin |
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What determines whether an EPSP or IPSP occurs?
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1)Types of channels coupled to receptor
2) The concentration of ions inside and outside of the membrane (depends on reversal potential) |
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What is the reversal potential?
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the Nernst potential
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