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61 Cards in this Set
- Front
- Back
Neural Doctrine |
Neurons are single units, communicate with each other through contact. Developed by Cajal. Supported by Loewi's work with vagusstof. |
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Reticular Theory |
Neurons are joined together in a continuous reticulum. Developed by Golgi. |
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Nissl Stain |
* looks like lots of little dots |
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Golgi Stain |
* looks like an entire neuron
* stains only some cells (approx 5% of neurons) * shows structure of individual neurons |
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Dendritic Spines |
* primary site of excitation |
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3 Levels of Cytoskeleton |
*microfilaments - 5 nm *microtubules - 20 nm
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Anterograde Transport |
* goes away from soma, towards axon terminal * uses kinesin |
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Retrograde Transport |
* goes away from axon terminal, towards soma * uses dynein |
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What causes Alzheimer's Disease? |
Too much Beta amyloid → different shape of tau → tau is attracted to tau → tau binds to tau instead of microtubules→ tau creates neurofibrillary tangles → neuron dies → tau "infects" other cells |
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What causes herpes and rabies, and how do they affect humans? |
* Viral diseases that infect neurons at axon terminals, hop on a dynin and move towards soma
* Herpes will also use kinesin to migrate back to terminals |
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3 Types of Glia |
Astrocytes, Oligodendroglia, and Schwann Cells |
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Astrocytes |
* found in CNS * protect, support, nourish neuron * help regulate ion concentration |
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Oligodendroglia |
* myelinate more than one cell |
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Schwann Cells |
* insulate Axons
* found in PNS * can only myelinate one axon |
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Why are almost all brain tumors caused by glia? |
glia multiply, neurons do not |
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What is the charge outside the neuron, inside the neuron, and what is the overall voltage at resting potential? |
* Outside: + + + * Inside: – – – |
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What are the ions involved in membrane potentials, and where are they more concentrated at resting potential? |
K+ : more concentrated inside Na+ : more concentrated outside Cl- : more concentrated outside Ca +2 : more concentrated outside |
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What is the Nernst Equation? Describe what happens with different ratios for [Xout]/[Xin] |
* Eion = 2.303(RT)/(F*z) log([Xout]/[Xin]) * ratio < 1 → log is negative |
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What is the equation for ionic current, and what do its varaiables mean? |
Driving Force, I = g(Vm - Eion) where: g is permeability (channels open vs closed) and (Vm - Eion) = driving force
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What are all the channels doing at the resting, rising, overshoot, falling, and undershoot phases of an action potential, respectively? |
* Threshold: all closed (K+ leaking)
* Rising: Na+ open * Overshoot: all closed * Falling: K+ open * Undershoot: K+ open, but starting to close |
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How did Otto Loewi prove that chemical messengers are used for synaptic transmission? |
Two frog hearts, electrically stimulated vagus nerve on one, causing heart rate to slow. Pumped the fluid bathing the first heart and applied it to the second heart, and the second heart also beat slower, proving that some soluble chemical released by the vagus nerve was controlling the heart rate. He called the unknown chemical Vagusstoff. |
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Classification of a NT |
* must be synthesized and packaged |
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Dale’s principle |
There is 1 NT per neuron. There are exceptions to this rule. |
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Catecholamine synthesis |
Tyrosine (hydroxylase)→ Dopa (decarboxylase)→ Dopamine (DA) → Norepinephrine (NE) → Epinephrine
Tyrosine is rate-limiting step |
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What happens if you make a membrane more permeable to a certain ion? |
The membrane potential will move towards the equilibrium potential of that ion. |
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What is the Goldman Equation essentially stating? |
At rest, a neuron's membrane is more permeiable to K+, therefore the resting membrane potential is closest to the equilibrium potential for K+ |
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Amino Acid NT Synthesis |
Glutamate + GAD Enzyme → GABA Glycine occurs naturally in cells that use it as an NT |
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ACh synthesis |
Acetyl CoA + Choline → ACh + CoA |
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Serotonin (5-HT) Synthesis |
Triptophan (hydroxylase)→ 5-HTP (decarboxylase)→ Serotonin |
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Peptide NT Synthesis |
* Made from amino acids, translated in ER
* Bud off from golgi in secretory granules * Transported to the synapse * Called dense core vesicles in synapse |
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Channel-Blocking Toxins |
* TTX - Blocks Na+ channels |
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Monoamine Examples |
ACh, Serotonin (5-HT) |
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Snares |
* Used to attach vesicles to presynaptic membrane * v-snare - grabs vesicle * t snare - grabs membrane (for "target membrane") |
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Charles Sherrington |
Named the synapse |
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Process of NT release (exocytosis) |
*Snares attach *Calcium influx *Vesicle fuses to membrane, releasing NT *Vesicle detaches from membrane, is recycled
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What do various NTs do to ligand-gated ion channels? |
Ach → Na+ → Depolarization Glutamate → Na+/Ca++ → Depolarizaiton GABA → Cl- → Hyperpolarization Glycine → Cl- → Hyperpolarization |
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G-Protein Coupled Receptors - process |
GDP → Exchange GDP for GTP when NT binds → Protein decouples, causes effect → Effect continues until GTP is broken down into GDP, at which point it will recouple with receptor and subunits |
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3 ways to remove NT from synapse |
*Diffusion *Degredation *Reuptake |
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Dura Mater |
Outer layer of meninges, lines skull |
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Subdural Space |
b/w dura mater and arachnoid membrane, vulerable to subdural hematoma |
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Neural Plate → ? → ? (development) |
neural plate → neural crest → neural tube |
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Saltatory Conduction |
The propagation of action potentials along myelinated axons from one node of ranvier to the next , increasing the conduction velocity of action potentials |
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Driving force |
the difference between the membrane potential and the ion’s equilibrium potential |
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What is the best estimate of the maximum number of action potentials your neurons could fire in one second? |
500-1000 |
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Multiple Sclerosis |
Demyelination of axons |
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Lidocaine |
blocks voltage-gated sodium channels to prevent/dull pain |
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Gap junctions |
Another term for electrical synapses |
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Parkinson's disease |
Loss of darkly pigmented cells in the midbrain (substantia nigra) |
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Subdural hematoma |
Blood underneath dura mater, causes increased intracranial pressure/compression of brain tissue |
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Subarachnoid Hemorrhage |
Bleeding into subarachnoid space, a type of stroke; can result from a ruptured aneurysm |
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Alzheimer's Disease (Physiological Symptoms) |
Wider sulci, loss of white and grey matter, enlarged ventricles |
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Spina Bifida |
Failure of neural tube to close at caudal end. Usually not fatal. |
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Anencephaly |
Failure of the neural tube to close at the rostral end. Almost always fatal, very few exceptions. |
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Hydrocephalus |
Swelling of brain due to CSF overflow/increased pressure in ventricles. |
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Arachnoid Membrane |
Spiderweb-like area between dura mater and subarachnoid space |
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Subarachnoid Space |
Between arachnoid membrane and pia mater, contains arteries |
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Pia Mater |
Innermost layer of meninges, lines even the deepest crevices of brain |
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Agonist |
Chemical that binds to a receptor and activates the receptor to produce a biological response |
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Antagonist |
Chemical that binds to a receptor and blocks the action of the agonist. Can be a ligand or drug |
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What stimulates neruogenesis? |
*Physical exercise *Learning *Neuron death |
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What slows neurogenesis? |
*Stress *Aging |