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61 Cards in this Set
- Front
- Back
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Equilibrium vs steady state
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Steady state - driving forces ating on a substance are constant and net rate of movement is constant
Equilibrium - no net driving force acting on substance and no net transport |
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What ions are higher in ECF than ICF normally?
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Na+, Cl-, Ca2+
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What ions are higher in ICF than ECF normally?
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K+
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Anion gap
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Law of electroneutrality says that a solution must have same number of + and - charges
Anion gap = [Na+] - ([Cl-] + [HCO3-] in plasma) Ignored anions like proteins are at greater concentration than ignored cations |
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Na/K pump
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α subunits mediates transport
β has transmembrane segment and targets ions Extrudes 3 Na+ and uptakes 2 K+ w/ hydrolysis of 1 ATP |
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Osmotic pressure
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π = RTCx
R= gas constant T= temp Cx = # particles in solution |
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Gibbs Donnan effect
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Presence of negatively charged trapped particles (like proteins) on one side of a semi permeable membrane affects distribution of ions across the membrane
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Hematocrit
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Fraction of blood volume occupied by blood cells
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Calculation of membrane potential (Nernst equation and give a descriptive statement of forces)
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E = 60mv * log ([Ion]out/[Ion]in)
When concentration gradient and electrical gradient are equal in magnitude |
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How does current flow effect membrane potential in a passive membrane?
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When current flows into cell it first charges membrane capacitance to new level by displacing charges on the membrane.
Once level is reached all current flows through membrane resistance Higher resistance results in higher change in potential (E=IR) |
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Why do bigger cells have smaller Rm?
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Because there are more open channels for current to flow through
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Length constant definition
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The distance a potential will spread before falling to 1/e (37%_
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Length constant formula (what happens to it as cells get bigger)
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λ = sqrt(Rm/(Ri+Ro))
Increases as cells get bigger |
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Resistance in a cell (3)
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Rm = membrane resistance
Ri = internal resistance imposed by cytoplasm Ro = resistance imposed by extracellular solution |
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What causes the overshoot?
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When cell becomes positive with respect to outside
Dependent on ENa |
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What causes undershoot?
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Due to voltage-gated channels, K+ permeability is higher during action potential than at rest, so following repolarization it is driven closer to EK+
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Hodgkin cycle
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When membrane depolarizes Na+ channels open and Na+ flows in -> further depolarization -> more ion channels -> rapid depolarization
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Inactivation of Na+ channels during action potential (2 causes)
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1. As depolarization takes membrane closer to ENa, influx decreases
2. Inactivating flap causes channel to stay closed for a while after opening due to reorientation of channel protein as polarity of cell changes |
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Refractory periods (2 types)
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As time between stimulus decreases, comes a point where a second action potential cannot be produced unless stimulus is increased
Absolute: no AP possible due to Na inactivation Relative - due to elevated K permeability, a bigger stimulus can overcome |
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Conduction velocity: faster in bigger or smaller cells?
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Since λ is bigger in bigger cells (because Rm decreases slower than Ri as a function of radius), bigger cells conduct faster
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How does myelination increase conductance velocity?
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Myelination vastly increases Rm, which increases λ
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How do Ca2+ channels modulate action potentials?
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Ca++ current in an action potential is high for a long time
Allows time for Ca influx into muscle cells and simultaneous contraction of all muscle fibers so heart acts like a pump |
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3 steps in presynaptic neurotransmitter release
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AP in neuron activates voltage-gated Ca channels in presynaptic terminals
-> Ca influx triggers synaptic vesicle fusion -> neurotransmitter release |
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Relationship between Ca++ entry and neurotransmitter release
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Fourth-power function of Ca++ influx
Implies cooperative event between Ca++ molecules |
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Synapsin
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Tethers vesicles to membrane reducing the # of releasable vesicles
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Synaptic vesicle (SV) core complex
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Synaptobrevin on vesicle
Syntaxin on plasma membrane Interact w/ SNAP-25 creating a 3 protein zipper that brings vesicle in contact w/ membrane |
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Synaptotagmin I
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SV protein tethered to vesicle
Has 2 Ca binding domains Interacts w/ SV core complex |
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Synaptic potential
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At postsynaptic membrane
Declines w/ distance from site |
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Properties of nicotinic Ach receptor
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Sensitive to Ach
Localized to neuron synapse Makes potential a local event that is not regenerative because channel is NOT VOLTAGE-GATED |
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What happens when an Ach receptor channel opens at an NMJ?
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Channel is not selective so K and Na flow along their gradients towards the reversal potential depolarizing the membrane
If enough Ach is released, cell is depolarized past threshold and action potential is generated |
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Basic properties of GABAR (3 and which drug?)
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Inhibitory
Erev near -80 = ECl- Cl- is only permeable ion Valium potentiates Cl- current |
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G-protein coupled receptors
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Transmit signal via second messenger or G protein heterodimers
Slower/modulatory response |
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GIRKs (2 with eg)
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G-protein couple inwardly rectifying K+ channel
G-protein coupled channel activates a K+ channel Eg vagus nerve release Ach -> binds muscarinic receptor -> G-protein couple receptor -> GIRK -> K+ current slows pacemaker wave |
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Secretory protein translocation (6 steps)
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1. Protein synthesis w/ signal sequence tag
2. Signal recognition particle (SRP) binds signal sequence 3. SRP stops translation and binds complex to ER membrane 4. Translation resumes w/ synthesis occurring in ER lumen 5. SRP is cleaved 6. Protein is folded and secreted into ER lumen |
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Coatamers (3)
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Involved in trafficking between ER and golgi
Composed of COPS protein Require ATP to form cage |
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Clathrin-coated vesicles (5)
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Trans-golgi -> plasma membrane trafficking
Clathrin associates w/ membrane proteins on vesicles via adaptin that confer specific binding Clathrin coat self assembles Requires ATP to dissemble Vesicle is pinched off via Dynamin FTPase |
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Vesicle docking and fusion and disassembly
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Docking via interactions of t-SNARES and v-SNARES
Fusion is regulated by Rab GTPase SNARE complex disassembly by NSF and SNAP |
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Fast anterograde transport
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Kinesins
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Fast retrograde transport
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dyneins
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Slow anterograde transport
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Episodic dynein and kinesin
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Afferent inputs to ANS (3)
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Visceral (pain)
Somatic (pain, pleasure) Special senses (visual, aud, olf) |
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Motor divisions of ANS (3)
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Sympathetic
Parasympathetic Enteric |
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Compare PNS and SNS ganglia
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PNS:
Preganglionic cell body in CNS Post cell body in ganglion near target tissue SNS: Preganglionic cell body in CNS Post in paravertebral sympathetic chain ganglia |
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Where do PNS nerves exit CNS?
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Cranial or sacral nerve
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Where do SNS nerves exit CNS?
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C8-L3
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Neurotransmitters and receptors of PNS
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Preganglionic neurons release Ach
Post ganglionic neurons have N2 receptors and release Ach Target tissues have muscarinic receptors |
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Neurotransmitters and receptors of SNS
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Preganglionic neurons release Ach
Postganglionic neurons have N2 receptors and release NE Target tissues have adrenergic (α or β) receptors |
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Adrenal medulla as part of SNS
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Some preganglionic sympathetic neurons synapse on adrenal medulla N2 receptors
Adrenal medullary cells release NE and E into circulation Provides generalized/whole body response |
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Atropine
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Muscarinic receptor antagonist
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Joint PNS and SNS action on cardiac pacemaker
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PNS slows firing rate via muscarinic receptors
SNS speeds firing rate via β receptors |
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Adrenergic receptors (which favor NE, which E)
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α : NE > E potency
β : E > NE potency β blockers suppress heart rate and also constrict lung airways due to cross reactivity between β1 + β2 receptors |
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Epinephrine synthesis (enzyme, location, 5 steps)
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N-methyltransferase (NE -> E) is only active in adrenal medulla chromaffin cells
Stress -> steroid (glucocorticoid) release from adrenal cortex -> portal system -> adrenal medulla -> increased epinephrine synth |
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3 responses of PNS muscarinic receptors
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Muscarinic receptors interact w/ heterotrimeric G proteins:
1. Hydrolysis of phosphoinositide -> protein kinase C 2. Inhibition of adenylyl cyclase (decreases cAMP) 3. Modulating K+ channels (GIRK) |
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α1 adrenergic receptors
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Blood vessels to mediate vasoconstriction
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α2 adrenergic receptors
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Presynaptic adrenergic terminals to modulate NT release
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β1 adrenergic receptors
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Only adrenergic receptors in myocardium to mediate increased heart rate and contractility
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β2 adrenergic receptors
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Only adrenergic receptors in bronchial muscle to mediate bronchodilation
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β3 adrenergic receptors
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Fat cells to mediate lipolysis
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2 exceptions to NT and receptor rules in PNS and SNS
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1.Muscarinic receptors can be found on SNS and PNS postganglionic neurons (in addition to N2)
2. Non-cholinergic non-adrenergic transmitters |
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NE and E inactivation
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Via reuptake into postganglionic nurons via active transport
Monoamine oxidase inactivates once inside cell |
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What do botulinum toxins target?
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Synaptic vesicle core complex
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