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162 Cards in this Set
- Front
- Back
What is the main goal of a Negative Feedback System?
|
Diminish the Difference
(thermostat: match the set and actual temperature) |
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When does baroreceptor firing increase, when BP is low or high?
|
BP high
(more firing with higher BP) |
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What is the main goal with positive feedback system?
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Excentuate the change
|
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What are the effectors of maintenance of blood glucose levels?
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insulin/ glucagon
negative feedback system |
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What is the purpose of an effector?
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to bring about a change
|
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What unit is missing from positive feedback compared to negative feedback?
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a controller
sensor directly affects the effector |
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What is an example of a positive feedback system?
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LH surge during a menstrual cycle
estrogen is the effector and ovaries are the sensors |
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What is the downfall of a feedforward system?
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no back pathway
|
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What is the purpose of feedforward system?
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respond in anticipation of a disturbance
|
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What are two methods for movement of molecules?
|
diffusion
bulk flow |
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What is needed for bulk flow?
List 2 examples |
Driving Force
Lungs - air movement Heart - blood movement |
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Factors that determine membrane permeability
|
-size
-charge -lipid solubility |
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Factors of Rate of diffusion
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Area available
Concentration Difference Lipid solubility (size and charge) |
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Hydrophobic
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permeable
|
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Frick's Law
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rate of diffusion is proportional to concentration difference
J = P.A. (C1-C2) net rate of membrane transport = permeability coefficient* concentration difference |
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Secondary active transport
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co-transport with Na+ ions
(symport or antiport) |
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How does a parietal cell utilize channels, transporters and pumps?
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transports Cl from the blood to the stomach lumen and H+ with utilization of the bicarbonate ion
|
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What does the drug omeprazole inhibit?
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H+/K+ ATPase in the parietal cell
(inhibiting H+ secretion into the stomach lumen) |
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3 diseases from disordered cell membrane transport
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1. hexo-malabsorption
2. cystic Fibrosis (lung consolidation) 3. diabetes insipidus (unable to reabsorbe H2O) |
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Amount and % of total body water
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42 L
60% |
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Amount and % of Intracellular water
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28L
40% |
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Amount and % of interstital/ lymph water
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10.5L
15% |
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Amount and % of plasma water
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3.5L
5% |
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Amount and % of extracellular water
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14L
20% |
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What is unique about transcellular water
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contained within an epithelial layer
(ex. cerebrospinal fluid, ocular fluid, joint fluid) |
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Equation for Volume distribution
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V distribution = (m. of indicator injected - m. of indicator lost)/ concentration in plasma
|
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Equation for mass of indicator excreted (lost)
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mass of indicator excreted = urine volume*indicator concentration in urine
|
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Indicator for total body water
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antipyrine, D2O, HTO
|
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Indicator for plasma H2O
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Evans blue, I-Albumin
|
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Indicator for extracellular H2O (PW & ISW)
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Impermeate ions (overestimate H2O)
Inert sugars (underestimate H2O) |
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Determine intracellular Fluid Volume
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total body water - extracellular body water
|
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Determine interstitial fluid volume
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extracellular body water - plasma water
|
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tonicity
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effective osmolality with regard to a reference solution
|
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Adrenal Insufficiency
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decrease in aldosterone -> decrease in Na reabsorption
Hyposmotic volume contration (loss of Na and water, but kidneys excrete more Na than water) |
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SIADH
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Syndrome of Inappropriate Antidiuretic Hormone
Hyposmotic Volume Expansion too much ADH secreted -> not much urine, instead reabsorbing lots of H2O |
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Sweating, fever, diabetes insipidus
|
Hyperosmotic volume contraction
|
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High NaCl intake
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Hyperosmotic volume expansion
|
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Diarrhea
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Isomotic volume contraction
|
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Isotonic NaCl infusion
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Isosmotic volume expansion
|
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4 responses to decrease in blood volume
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1. inc. RAAS
2. inc. sympathetic outflow (SNS) 3. inc. Arginine vasopressin AVP... ADH 4. dec. atria natriutetic peptide (ANP) ->all reabsorb sodium |
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Ways to regulate ECF osmolality
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1. release of AVP or ADH
2. trigger thirst |
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Ion movement depends on ______ ______ and ______ _____
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electrical gradient and concentration gradient
|
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What 2 factors constitute the net 'driving force'?
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Concentration gradient and electrical gradient
|
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How does the Nernst Potential relate to the driving force
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Nernst Potential is where there is ZERO driving force
|
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Nernst Equation
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Eion = 61/z * log[ion]o/[ion]i
|
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[K+] inside and outside of cell
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[K+]inside = 140mM
[K+]outside = 5mM |
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[Na+] inside and outside of cell
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[Na+]inside = 10mM
[Na+]outside = 140mM |
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[Ca2+] inside and outside of cell
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[Ca2+]inside = 0.0001mM
[Ca2+]outside = 1mM |
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[Cl-] inside and outside of cell
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[Cl-]inside = 20mM
[Cl-]outside = 116mM |
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Equilibrium potential (Ek)
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-88mV
|
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Equilibrium potential for sodium (Ena)
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+70 mV
|
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Equilibrium potential for calcium (Eca)
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+122 mV
|
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Equilibrium potential for chloride (Ecl)
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-47 mV
|
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What causes a membrane to be selectively permeable to a specific ion
|
an open channel
|
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A membrane at rest is most permeable to _____ ions
|
K+ (potassium)
|
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2 factors that determine membrane potential
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1. Nernst Potential
2. Permeabilities |
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What does the Goldman- Hodgkin-Katz equation determine
|
membrane potential (Em)
|
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How permeable is Cl- in neurons and skeletal muscle cell
|
neurons -> negligible permeability
skeletal m. cell -> significant |
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What structure maintains the membrane potential?
|
Na+/K+ ATPase
|
|
Hyperkalemia
|
depolarize membrane potential
increase sodium channel inactiviation -> inexcitability |
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Hypokalemia
|
hyperpolarization
increase concentration gradient |
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Excitable cells
|
nerves and all three muscle types
|
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Start and stop of action potential duration
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start: threshold
stop:upon return to resting potential (before hyperpolarize phase) |
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What produces an electrical current
|
flow of ions across a membrane
|
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g(Na) > g(K)
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ion conductance for upstroke of AP
|
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g(Na) = g(K)
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conductance at the peak of an AP
|
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g(Na) < g(K)
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conductance for the downstroke of an AP
|
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What causes the threshold?
|
voltage-gated Na+ channels
|
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Na+ channels open in a fast, _______ feedback process
|
positive
|
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To initiate an AP, the resting ____ efflux must be overcome
|
K+
potassium moving out tries to keep the cell negative |
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Hyperparathyroidism
|
Hypercalcemia
reduced excitability -> muscle weakness |
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Hypoparathyroidism/ Chronic Renal Failure
|
Hypocalcemia
increased excitability -> spontanous m. twitching |
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What happens to the sodium driving force at the peak of an AP?
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decreases
|
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Where in the AP is the inactivation gate closed?
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peak and downstroke of an AP
|
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Where in an AP is the activation gate open?
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upstroke and peak of an AP
|
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What explains the refractory period?
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recovery from inactivation
|
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___________ can increase Na+ channel inactivation and cause inexcitability
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Hyperkalemia
|
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What 2 channels contribute to the cell K+ efflux
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inward rectifier - open at negative potentials (resting)
Voltage gated - open at depolarized potentials (causes repolarization) |
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What does a smaller K+ current do to the AP duration
|
makes it longer
|
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What happens to a passive current as it passes down an excitable cell?
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magnitude of current decreases due to leakiness
|
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Passive current spreak triggers ____ ____ _______
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action potential regeneration
|
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What affects how far a current spreads passively?
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the extent of leakiness
|
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length or space constant
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measure of the leakiness of a cell
(37% of initial voltage) |
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What does increasing the radius do to the internal resistance?
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decreases the internal resistance
|
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large space constant = _____ ______ velocity
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faster conduction
|
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What does myelination do?
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increases membrane resistance -> reducing leakiness
|
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2 types of synapses
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electrical and chemical
|
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What is needed at an electrical synapse?
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direct connection - connexon make a gap junction
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What 3 things possess gap junctions
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neurons, cardiac myocytes, and smooth muscle
|
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What does ischemia do to gap junctions?
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gap junction become uncoupled/ closed
|
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What would decreasing the pH and increasing the intracellular [Ca2+] do to a gap junction?
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cause it to close
|
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What causes an increase in [Ca2+] within the terminal of an axon?
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opening of voltage gated calcium channels due to depolarization caused by open sodium channels
|
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What does the drug SSRI affect?
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neurotransmitter reuptake channel on the pre-synaptic axon
|
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Difference between ionotropic and metabotropic receptors?
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ionotropic receptor is permeable to ions upon ligand binding
metabotropic receptor is a G coupled receptor, slower response |
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Which neurotransmitter produces effect through both ionotropic and metabotropic receptors?
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Acetylcholine
|
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Nicotinic receptor
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ionotropic receptor
|
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Muscarinic receptor
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metabotropic receptor
|
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What movement of ions cause an inhibitory postsynaptic respose?
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Cl- ions in
K+ ions out |
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Acetylcholine
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parasympathetic Neurotransmitter
|
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Nitric oxide
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parasympathetic Neurotransmitter
|
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Norepinephrine
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sympathetic neurotransmitter
|
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Epinephrine
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sympathetic neurotransmitter
|
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3 Neurotransmitters found in the brain
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Dopamine
Histamine Serotonin |
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2 excitatory amino acid neurotransmitters
|
Glutamate
Aspartate |
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2 inhibitory amino acid neurotransmitters
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Glycine
GABA |
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Where does neuromuscular transmission occur?
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motor end plate
|
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motor neuron
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1 motor axon with corresponding muscle fibers it innervates
|
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What is the neurotransmitter and receptor at the neuromuscular junction
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receptor: nicotinic ACh receptor
neurotransmitter: acetylcholine |
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End plate potential (EPP)
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results in muscle fiber upon motor nerve stimulation and can possibly lead to an AP
|
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What determine the magnitude of an EPP
|
dependent upon the extent of ACh release
|
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What make up the end plate current?
|
mixture of Na+(in) and K+(out) => net flow of ions
|
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What terminates an EPP
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degradation of ACh by acetylcholinesterase
|
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How is ACh resynthesized?
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choline is transported back into the nerve terminal via Na+/choline symport -> then choline is connected to acetyl group via choline-acetyl transferase
|
|
Myasthenia Gravis
|
autoimmune disease affecting ACh receptors
(antibodies that block ACh receptors) treatment: Neostigmine - block AChesterase |
|
Lambert-Eaton syndrome
|
autoimmune disease that attacks presynaptic Ca2+ channels
-> decreasing ACh release |
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Cobra Venom
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paralysis via blocking nicotinic ACh receptors
|
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2 v-SNARES
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synaptotagmin - calcium sensor
synaptobrevin - intertwine |
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2 t-SNARES
|
SNAP-25
Syntaxin |
|
How does Botulinum toxin reduce vesicle release
|
cleave SNARE proteins
unable to dock vesicles |
|
How does Tetanus toxin reduce vesicle release
|
cleaving synaptobrevin
unable to dock vesicle |
|
How does tetanus toxin reduce vesicle release?
|
cleaves synaptobrevin -> vesicle unable to dock
|
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How does tetanus toxin cause 'lock jaw'?
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inhibits vesicle release in the inhibitory internueron -> motor axon active all of the time
|
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Spatial Summation
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postsynaptic potentials sum when they collide within the soma
different inputs that fire at the same time |
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Temporal Summation
|
rapid EPSPs from a single input that sum if close enough in time
|
|
Synaptic Facilitation
|
increase in EPSP magnitude caused by repetitive synaptic transmission
|
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Skeletal m.: velocity, duration, fatigability
|
rapid velocity
relatively long duration variable fatigability |
|
Cardiac m.: velocity, duration, fatigability
|
rapid velocity
short duration no fatigue |
|
Smooth m.: velocity, duration, fatigability
|
slow velocity
long duration no fatigue |
|
myogenic
|
no axon is needed for initiation
|
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A Band
|
entire myosin molecule
|
|
I Band
|
only actin, including Z line
|
|
H Band
|
only myosin, including M line
|
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What does Myosin Light chain kinase do?
|
phosphorylates myosin -> allowing myosin to bind to actin
|
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Where does the triad fall in skeletal m.?
|
along A-I junction
|
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Where does the Dyad fall in cardiac m.?
|
along the Z line
|
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What do Ryanodine receptors (RyR) span?
|
t-tubule and SR
|
|
Dihydropyridine receptors (DHPR)
|
Ca2+ voltage gated channels within the t-tubule
|
|
__ DHPR : ___ RyR in skeletal and cardiac m.
|
2:1 in skeletal m.
1:~4 in cardiac m. |
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How does Ca2+ cause contraction
|
by binding to Troponin C
|
|
3 ways of removing Ca2+ from the cell
|
1. SERCA pump
2. Na-Ca exchanger 3. Ca-ATPase |
|
Malignant Hyperthermia
|
mutation that prevents termination of Calcium release by high [Ca]
|
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How is contractile force increased in a single skeletal muscle fiber?
|
increase twich frequency
|
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How is contractile force increased in whole skeletal muscle?
|
increase number of motor units
|
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How is contractile force increased in cardiac muscle?
|
increase [Ca] in cytosol from SR
|
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What do Golgi Tendon Organs sense?
|
Tension
|
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What do muscle spindles sense?
|
length
|
|
Afferent neuron of GTOs
|
Ib
|
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Afferent neurons of Muscle Spindles
|
II and Ia
|
|
Myotatic (Stretch) Reflex
|
muscle stretch triggers contraction of the stretched muscle
|
|
Major players in control of posture
|
muscle spindles and stretch reflex
|
|
Inverse Myotatic Reflex
|
muscle tension triggers muscle relaxation
|
|
Flexor Reflex
|
produces coordinated responses in ipsilateral and contralateral limbs
|
|
Importance of Muscle Spindles
|
sense muscle length
-stretch reflex -posture -position sense |
|
2 Main types of Smooth Muscle
|
1. Single Unit (phasic)
2. Multi-unit (tonic and fine control) |
|
Smooth m. in the bladder
|
well coupled, 1 functional unit
|
|
smooth m. in blood vessels
|
less coupling, lots of small units
|
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Difference in cross-bridges in smooth m. compared to skeletal m.
|
smooth m. cross bridges have a longer attachment time due to lower contration velocity and more force/ cross-bridge
|
|
2 examples of tonic smooth muscle
|
spincter and blood vessels
|
|
2 examples of phasic smooth m.
|
intestines and bladder
|
|
What is the electrical activity of phasic smooth m.?
|
action potentials
|
|
electrical activity of tonic smooth m.?
|
graded changes in Em or Independent of Em
|
|
Myosin Light Chain Phosphatase
|
dephosphorylates myosin causing relaxation
|