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238 Cards in this Set
- Front
- Back
What are the two types of active transport?
|
Primary- energy directly from ATP hydrolysis
Secondary- energy provided indirectly via chemical gradients |
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What are the examples of primary active transport?
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Na+/K+ pump
Ca2 pump and H+ pump |
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What is the most highly studied active transport?
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Na+/K+ pump
|
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What does the sodium potassium pump transfer into and out of the cell and in what ratio?
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pumps 3 Na+ out of the cell and 2 K+ into the cell
|
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T/F The sodium potassium pump is a unidirectional system
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False- it can run the other way depending on [ATP], [ADP], and Na+/K+ gradients
|
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What percentage of total energy do neurons use to power Na+/K+ pumps?
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up to 70%
|
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What are the two types of Calcium pumps?
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cell membrane pump and
intracellular pump (on organelles) |
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Which calcium pump drives Calcium into the ECF and results in low cytosolic [Ca2+]?
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cell membrane pump
|
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Which calcium pump concentrates internal stores of Calcium?
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intracellular pump
|
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Where are the two examples of proton pumps located?
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gastric glands of stomach and
renal tubules/cortical collecting ducts of kidney (in intercalated cells) |
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What does the proton pump in the stomach do?
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Hydrogen ions are co-secreted with Cl- to produce HCL which maintains the low stomach pH, optimizing enzyme activity
|
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What is a symporter?
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two substances binding EC surface of carrier protein and are transported in the SAME direction (into cell)
|
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What is an antiporter?
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two substances binding opposite surfaces of carrier protein and are transported in OPPOSITE directions (one into and one out of cell)
|
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What are examples of symporters?
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glucose transporter
amino acid transporter and others (chloride, iodine,iron and urate) |
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What are examples of antiporters?
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calcium transporter and
proton transporter |
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What is the glucose transporter coupled with and what provides the energy?
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Sodium transport
High extracellular (EC) [Na+] provides energy |
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What is the amino acid transporter coupled with and what provides the energy?
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Sodium transport
High extracellular (EC) [Na+] provides energy |
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What is the calcium transporter coupled with and in which direction do the ions move?
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Sodium transport
Na+ transported into cell and Ca+ out |
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Where is the proton transporter located and in which direction are the ions moved?
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in proximal tubules of kidney
Na+ transported into cell from lumen and H+ transported into lumen |
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What occurs during active transport through cellular sheets?
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active transport and diffusion are combined to transport substances across a sheet or membrane
|
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Where does active transport through cellular sheets occur?
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intestinal epithelium
renal tubule epithelium exocrine gland epithelium gallbladder epithelium choroid plexus and other membranes |
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Is there more sodium inside or outside of the cell?
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Outside
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Is there more potassium inside or outside of the cell?
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inside
|
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What are the charges of the cell membrane inside and outside?
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Inside is negative, outside is positive
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What accounts for 95% of resting membrane potential?
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passive diffusion of ions through leak channels due to Electron motive force (Donnan Equilibrium)
|
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T/F the membrane is more permeable to Na+
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False it's less permeable to Na+
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T/F the membrane is more permeable to K+
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True
|
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Can large ions diffuwse through leak channels?
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No
|
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What accounts for 5% of resing membrane potential?
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active Na+/K+ pump which adds (+) charge to outside
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What is Ohm's law?
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V=IR
|
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What is the definition of voltage (V)?
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difference in electrical potential (charge) between two points
|
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What is the definition of current (I)?
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flow of charge
|
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What is the definition of resistance (R)?
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resistance to current flow
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What is the definition of voltage for cells?
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difference in potential (voltage)across membrane (ECF/ICF)
|
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What is the definition of current for cells?
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flow of ions across membrane
(through ion channels) |
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What is the definition of resistance for neurons?
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Rm= resistance across membrane
Ra= resistance along length of axon |
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What is the definition of capacitance?
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storage or separation of charge across barrier
Cm= membrane capacitance |
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What is capacitance important for?
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to determine conduction speed
|
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Is the current in cells normally high or low?
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low
|
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Is the Rm of a cell usually high or low?
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high- membrane is a good insulator
|
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Conductance is the reciprocal value of what?
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resistance
|
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What is recorded with a current clamp?
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voltage
|
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What is altered with a current clamp?
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current
|
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What are current clamps used for?
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to record graded membrane potentials or action potentials
|
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What is altered with a voltage clamp?
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voltage
|
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What is measured with a voltage clamp?
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current flow from membrane ion channels
|
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What is the membrane potential for a single ion?
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NONE
|
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Is there an equilibrium potential for single ions?
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yes
|
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What is equilibrium potential?
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the membrane potential that exactly opposes net diffusion of that ion across the cell membrane
|
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The equilibrium potential is also referred to as what?
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electron motive force (EMF)
|
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In the equation
Eion= RT/ZF ln([ion]o/ [ion]i) what does the R, T, Z and F stand for? |
R- gas constant
T- temperature in kelvins Z- ion valence F- Faraday's constant |
|
What is the simplified equation for positive univalent ions?
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Eion= +61 log ([ion]o / [ion]i)
|
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What is the simplified equation for negative univalent ions?
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Eion= -61 log ([ion]o / [ion]i)
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If E(Na+)= + 61mV what does that tell you?
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Assuming free diffusability, Sodium would flow into cell until the charge inside was 61mV more positive than the outside
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Each tenfold increase in ion concentration produces what change in equilibrium potential? (in mv)
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61mV
|
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Why can't the Nernst equation be used to calculate membrane potential?
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1) the equation only accounts for a single ion whereas the membrane has multiple ions crossing it
2) it assumes the ion is freely permeable when most of the time they're not |
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What equation is used to determine the resting membrane potential of real cells?
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Goldman equation (Goldman-Hodgkin-Katz eq)
|
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What is a permeability constant?
|
P= measure of the ease by which an ion or molecule crosses a unit area of membrane in response to a 1 M difference in concentration
|
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What is the order of permeability constants for sodium, potassium, and chloride from greatest to least?
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P(k+) >> P(cl-) > P(na+)
|
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By convention, how does one account for difference in charge using the Goldman equation?
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[cation] out is placed in the numerator and [anion] in is placed in the numerator
(so [cation]in and [anion]out is in denominator) |
|
EQUATION:
What is the Vm using the information listed below? [Na+]i= 14mmol/L; [Na+]o=142mmol/L [K+]i=140mmol/L; [K+]o= 4mmol/L [Cl-]i=4mmol/L; [Cl-]o=108 mmol/L P(k+)= 5.0 * 10^-7 cm/sec P(cl-)= 1.0 * 10^-8 cm/sec P(na+)= 5.0 * 10^-9 cm/sec |
Vm= 61 log ((5.0 * 10-7)(4)+ (5.0 * 10-9)(142)+ (1.0 * 10-8)(4)) /
((5.0 * 10-7)(140) + (5.0 * 10-9)(14) + (1.0 * 10-8)(108) Vm= 61 log (.039) = -86mV |
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What is the primary contributor to resting membrance potential?
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potassium because the Vm of passive diffusion is closer to E(k+)
|
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T/F During an action potential the rate of diffusion is constant
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False
|
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Vm can change in response to a stimuli, what types of stimuli are there?
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electrical, chemical, or mechanical
|
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Are graded potentials a passive or active response?
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passive
|
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Are action potentials a passive or active response?
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active
|
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What are the important characteristics of a graded potential?
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1) magnitude of potential change is directly proportional to current (increase mag. of stimulus = bigger response)
2) may summate 3) local 4) decremental (not propagated): magnitude inversely proportional to distance from stimulus (due to leaky channels) |
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T/F Some neurons can only use graded potentials
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True
|
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T/F Summation always results in an additive effect
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False- a positive potential can summate with a negative potential and may have a (+) effect if (+)>(-), cancel each other out if (+)=(-), or have a (-) effect if (+)<(-)
|
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What are the specific types of graded potentials?
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1)receptor (generator) potentials
2) pacemaker potential 3) postsynaptic membrane potentials 4) EPP- end plate potential |
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What are receptor potentials and what are some examples?
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stimulation of sensory receptors
Ex: photoreceptors, mechanoreceptors, chemoreceptors, thermoreceptors, and nocireceptors |
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What are pacemaker potentials and what is its effect?
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special cells in the heart's pacemaker have leaky channels which leads to autonomously generated graded potentials
-responsible for cardiac autorhythmicity |
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What are postsynaptic membrane potentials involved in?
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synaptic transmission of nerve impulses
|
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What are end plate potentials?
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synaptic transmission at neuromuscular junction
|
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Where are action potentials generated?
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at the axon hillock
|
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What are characteristics of action potentials?
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1) self-sustained change in membrane potential
2) all-or-none 3) does NOT summate 4) regenerative- propagated over long distances without decrement 5) results from threshold level of depolarization 6) magnitude of AP is much greater than mag. of stimulus |
|
What are the importances of action potentials?
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1) nerve signal transmission- the elctrical portion of nerve signal transmission is carried in an AP
thought, sensation, motor pathways 2) muscle contraction- the contraction of all muscle is initiated by a muscle AP |
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What is the sodium hypothesis?
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AP is due to Na+ influx through transiently permeable membrane
|
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What led to the sodium hypothesis?
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[Na+]out reduction experiments using squid giant axon
|
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What is the basis for the sodium hypothesis?
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when permeability of membrane increases for a specific ion, Vm moves toward Eion
Ex: at rest: K+ permeable, Vm close to E(K+)= -91mV during AP: Na+ permeable, Vm moves towards E(Na+) = +65mV |
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What are the primary stages of an action potential?
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1) resting stage (polarized stage)
2) depolarization stage 3) repolarization stage |
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What is the resting stage of an AP?
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the normal resting membrane potential
|
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What is the depolarization stage of an AP?
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cell membrane becomes depolarized as Na+ flows into the cell and it occurs when Vm exceeds threshold for voltage gated Na+ channels
|
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What is the repolarization stage of an AP?
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cell mebrane repolarizes as K+ ions flow out of the cell and it occurs when voltage gated K+ channels are opened (Vm moves back toward the resting membrane potential)
|
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What are the characteristics of voltage-gated ion channels?
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1) voltage changes alter the teriary structure of the protein channel
2) channels will close after some time but takes 10x longer than opening 3) must be reset before they can open again 4) different channels have different activation kinetics |
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What are the conformations of the voltage-gated Na+ channels?
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open, closed, or inactivated
|
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What are the conformation of the voltage-gated K+ channels?
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open or closed
|
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How many gates do voltage-gated Na+ channels have?
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2: fast gate (activation gate) on extracellular region and slow gate (inactivation gate) on intracellular region
|
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Which gate of the voltage-gated Na+ channels is closed at resting Vm?
|
activation gate
|
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Each channel of the voltage-gated Na+ channels allows how many sodium ions to move into the cell?
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5-6
|
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Which gate of the voltage-gated Na+ channels is closed at the peak of the AP?
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inactivation gate
|
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Threshold triggers the rapid opening of the _________ gate and slow closing of the ___________ gate (of Sodium).
|
activation gate
inactivation gate |
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When can the inactivation gate reopen?
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when the membrane repolarizes near resting Vm
|
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How many gates do the voltage-gated K+ channels have?
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one activation gate on intracellular region
|
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Is the activation gate of the voltage-gated K+ channel open or closed at resting Vm?
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closed
|
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When is the voltage-gated K+ channels open?
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from +35mV to -90mV
|
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Where are voltage-gated Ca2+ channels located?
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cardiac and smooth muscle
|
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Which of the voltage-gated channels have slow activation kinetics?
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potassium and calcium
|
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What is the Hodgkins cycle and what does it do?
|
It sustains the membrane depolarization (+ feedback)
-depolarization opens more Na+ channels -more Na+ influx leads to greater depolarization -more depolarization opens further Na+ channels - continues until all voltage-gated Na+ channels are activated |
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During the rising phase of an AP the Vm approaches what?
|
E(Na+)
|
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What is the overshoot of an AP due to?
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due to the delayed Na+ channel inactivation and K+ channel activation
|
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What 3 mechanisms determine the timing and magnitude of the AP peak?
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1) Na+ influx diminished as Vm approaches ENa+
2) Na+ channels inactivate 3) K+ channels activate |
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What causes the undershoot (after-hyperpolarization)?
|
some K+ channels remain open after Na+ channels close
|
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Na+ and K+ electrochemical gradients must be re-established which requires what?
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Na+/K+ ATPase pump
|
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A deficit in [Ca2+]E does what to the threshold for Na+ channel activation
|
lowers the threshold
|
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Why can't AP summate?
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the membrane must recover for a period of time before noather AP can be generated at the same location
|
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What is it called when it is impossible for another AP to be generated during this time?
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absolute refractory period
(Na+ channels are still inactivated) |
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What is it called when new AP generation is possible but more difficult?
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relative refractory period- requires greater depolarizing stimulus (K+ channels still activated)
|
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Explain a "tonic" firing pattern
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(non-accomodation) AP's persist throughout duration of stimulus
|
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Explain a "phasic" firing pattern
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(accomodation) initial burst of 1 or more AP's at beginning of stimulus, then no response
|
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High resistance = ______current
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low
|
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T/F there is little conductance through the lipid bilayer
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true
|
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What does membrane resistance depend on?
|
ion channel density and conductance
|
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at rest, gm is ____ and Rm is _____
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low; high
|
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What part of the cell acts as a capacitor?
|
cell membrane
|
|
Cm affects timecourse for change in Vm, what does that mean?
|
Cm determines the steepness of slope in AP, or in other words the speed of AP generation
|
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T/F resistors and capacitors respond differently to current injection
|
true
|
|
pure resistors do what to Vm?
|
cause an instantaneous change in Vm
|
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pure capacitors do what to Vm?
|
cause a linear rate change of Vm
|
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what does a true cell do to the rate of Vm?
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cause a changing (rounding) rate of change of Vm
|
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What is the time constant?
|
the amount of time to reach 63% of the total Vm
|
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what is the equation for time constant?
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t= Rm * Cm
|
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Why is the time constant important?
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it's an important determinant of AP propagation rate and synaptic integration
|
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what does a low time constant mean?
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the change in Vm occurs more quickly
|
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What does a high time constant mean?
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AP regenerated at faster rate
|
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What is Ra or Rc?
|
Axial (cytoplasmic) resistance- the resistance to ionic current through cytoplasm along longitudinal axis
|
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When does axial resistance increase?
|
with increased distance of longitudinal current flow
|
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When does cytoplasmic resistance decrease?
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with increasing cross-sectional area of cell
|
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The rate of Vm decays exponentially with distance from site of initial Vm. This rate of decay is due to what?
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1) leak of current through ion channels in membrane
2) change (increase) in Ra with distance from injection site 3) current follows path of least resistance |
|
what is the space constant?
|
distance from site of inital Vm at which Vm declines by 63%
|
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What does diameter affect, Rm or Ra?
|
Ra
|
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What does myelin affect, Rm or Ra?
|
Rm
|
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What is the space constant important for?
|
it's an important determinant of AP propagation and synaptic integration
|
|
what does a high space constant mean?
|
change in Vm travels greater distance before decaying and the AP is regenerated at a faster rate
|
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What is the equation for conduction velocity?
|
CV= change in conduction distance/ change in conduction time
|
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What is the alternate equation for conduction velocity?
|
CV= space constant/ time constant
|
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How can you increase conduction velocity?
|
by increasing space constant (w/o affecting Ra) or decrease time constant (theoretically)
|
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How does a larger axon diameter affect Ra, CV, and space constant?
|
lower Ra, increase CV, increase space constant
|
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How does axon myelination affect Rm, Cm, and space constant?
|
higher Rm, lower Cm, increase space constant
|
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How do faster ion channel kinetics affet Rm,and time constant?
|
lower Rm, decrease time constant
|
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What does higher ion channel density do to Rm and time constant?
|
lower Rm, lower time constant
|
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T/F An AP can propagate in any direction
|
True- membrane has no inherent directionality
|
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T/F AP propagation is bidirectional
|
False- its unidirectional
local current flows bidirectionally but cannot generate AP in reverse direction |
|
What prevents reverse propagation of an AP?
|
the refractory state of the membrane
|
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When does continuous conduction occur?
|
in non-myelinated neuronal fibers
|
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T/F AP's do not decay
|
False- they do decay because of leaky currents
|
|
Where does saltatory conduction occur?
|
in myelinated axons
|
|
what are myelin sheaths made out of and what are its other characteristics?
|
concentric layers of plasma membranes
1) highly enriched for lipids but contains less protein than most cell membranes 2) lack channels and carrier proteins 3) very good insulator 4) helps to protect axons |
|
myelin sheath membranes are made out of what cell?
|
glial cells
in CNS- oligodendrocytes in PNS- Schwann cells |
|
myelin sheaths are interrupted by what?
|
nodes of Ranvier
|
|
nodes of ranvier occur at what interval?
|
1-3mm intervals along the sheath
|
|
Where are most ion channels?
|
concentrated at the nodes of Ranvier
|
|
Where are the APs regenerated?
|
only at the nodes of Ranvier
|
|
What does multiple sclerosis and Guillain-Barre syndrome cause?
|
demyelination- loss of myelin sheath (neurodegenerative disease)
|
|
What are the characteristics of Group A fiber?
|
1)largest diameter
2) highly myelinated 3) max CV=150 m/s 4) mostly somatic sensory and motor fibers |
|
What are nerve fibers typed by?
|
diameter, degree of myelination, and conduction speed
|
|
What are the characteristics of Type B fibers?
|
1) intermediate diameter
2) less myelinated 3) avg CV=15 m/s 4) autonomic sensory and motor fibers; somatic sensory fibers |
|
What are the characteristics of Type C fibers?
|
1)smallest diameter
2) unmyelinated 3) avg CV=1 m/s 4) autonomic sensory and motor fibers; somatic sensory fibers |
|
T/F Each nerve has one type of fiber
|
False- many nerves contain multiple types of fibers
|
|
how are neuronal networks assembled?
|
by connecting multiple neurons
|
|
what does it mean when a network exhibits convergence?
|
many neurons input onto one
|
|
What does it mean when a network exhibits divergence?
|
one neuron outputs onto many
|
|
What is it called when neurons synapse with other tissue types?
|
chemical synapses
|
|
what is it called when a neuron synapses with another neuron?
|
internuncial synapse
|
|
what is it called when an axon synapses with a soma?
|
axosomatic synapse
|
|
what is it called when an axon synapses with a dendrite?
|
axodendritic synapse
|
|
what is it called when an axon synapses with another axon?
|
axoaxonic synapse
|
|
what is it called when a neuron synapses with a muscle cell?
|
neuromuscular junction
|
|
what is it called when a neuron synapses with a gland cell?
|
neuroglandular junction
|
|
what is it called when a muscle cell synapses with another muscle cell?
|
electrical synapses
|
|
Where are electrical synapses found?
|
cardiac and smooth muscle
|
|
How do electrical synapses work?
|
through gap junctions which allows direct electrical coupling (ionic currents) and exhange of other small cytoplasmic solutes
|
|
T/F Unlike chemical synapses, electrical synapses don't degrade during transmission, in other words the post synaptic potential change stays the same
|
False- electrical potentials do degrade during transmission and post synaptic potential change is always reduced
|
|
Is electrical transmission unidirectional or bidirectional?
|
Both bidirectional (non-rectifying synapse) or unidirectional (rectifying)
|
|
Where are electrical synapses found?
|
cardiac muscle, smooth muscle, nervous system (less common in vertebrates, more common in developing NS)
|
|
Transmission at _______________ synapses is faster than than at __________ synapses.
|
electrical; chemical
|
|
What are the disadvantages of electrical synapses?
|
1) less plasticity compared to chemical syn.
2) less capability for integrative/combinatorial signaling 3) no inhibitory signaling 4) lack variability of multiple chemical transmitters |
|
What does an AP stimulate?
|
neurotransmitter release
|
|
Nerve impulses are transduced into what which are then transduced back into what?
|
chemical signals; electrical signals
|
|
Are chemical impulses unidirectional or bidirectional?
|
always unidirectional
|
|
Which are more common in the NS, electrical or chemical synapses?
|
chemical
|
|
Is transmission at chemical synapses slow or fast?
|
slow
|
|
What are the advantages of chemical synapses?
|
1) greater ability for long term modification
2) capable of complex integrative/combinatorial signaling 3) both excitatory and inhibitory signaling 4) many chemical transmitters allow for complex regulation 5) modulation of signal gain |
|
Separation of pre- and post synaptic membrane is called what?
|
synaptic cleft
|
|
What recieve 80-90% of presynaptic terminals?
|
dendrites
|
|
electrical signals are conducted towards what?
|
the soma
|
|
What recieves 5-20% of presynaptic terminals?
|
the soma
|
|
What connects the soma with the axon?
|
the axon hillock
|
|
Where is the spike initation zone (SIZ)?
|
the axon hillock
|
|
What does the axon hillock contain?
|
high density of voltage-gated Na+ channels
|
|
What are the steps for the mechanism of chemical neurotransmission?
|
1) depolarization of Vm at axon hillock generates AP
2) AP propagates down axon to depolarize presynaptic terminals (PST's) 3) depolarization results in localized influx of Ca2+ into PST's 4) influx of Ca2+ stimulates synaptic vesicle exocytosis 5) Neurotransmitters diffuse across synaptic cleft and bind specific receptors on postsynaptic membrane 6) activated receptor mediates specific effect in postsynaptic cell 7) synaptic delay |
|
What is the signaling cascade order starting with what calcium activates?
|
1)Calcium activates calmodulin
2)calmodulin activates protein kinase 3)protein kinase phosphorylates membrane bound tethering proteins 4) tethering proteins release synaptic vesicles |
|
Synaptic delay occurs in chemical neurotransmission due to what?
|
migration and fusion of vesicles
diffusion of Neurotransmitters receptor binding/activation postsynaptic response |
|
What are the types of post-synaptic receptor proteins?
|
ionotropic and metabotropic
|
|
What are the characteristics of ionotropic receptor proteins?
|
1) receptor is also an ion channel
2) ligand binding opens channels (some are voltage-gated) 3) fast acting 4) may produce excitatory or inhibitory postsynaptic potentials |
|
Do ionotropic receptor proteins allow the flow of cations or anions?
|
both
|
|
What are the characteristics of metabotropic receptor proteins?
|
1) receptor is coupled w/ second messenger system
2) ligand binding activates signaling cascade 3) slow acting 4) may result in synaptic excitation or inhibition ( by changing conductance oc cationic or anionic protein channels or increasing/decreasing density of ion channels) 5) common G-protein 2nd messenger system |
|
How does the common G-protein 2nd messenger system work?
|
1) a membrane-bound trimeric GTP binding protein exchanges GDP for GTP upon ligand binding
2) alpha subunit dissociates and diffuses through cytoplasm to activate membrane-bound adenylate cyclase (AC) 3) AC catalyzes the conversion fo ATP to cAMP and PPi 4) cAMP effects other cellular changes such as changing ion channel permeability, activating other pathways, or activating gene transcription |
|
What are the types of postsynaptic potentials?
|
Excitiatory (EPSP) or inhibitory (IPSP)
|
|
What are the characteristics of EPSPs?
|
Excitatory postsynaptic potentials
1) postsynaptic membrane is depolarized so Vm approaches/exceeds threshold 2) multiple EPSPs are required to reach threshold 3) mechanism is ually activation of Na+ channels |
|
What are the charactersitics of IPSPs?
|
Inhibitory post synaptic potentials
1) postsynaptic membrane is hyperpolarized so Vm moves farther from threshold 2) 2 common mechanisms a) activation of K+ channels (outward K+ current) b) activation of Cl- channels (inward Cl- current) |
|
During synaptic integration, what does the total Vm result from?
|
the additive effects (summation) of multiple passive membrane potentials, both excitatory and inhibitory
|
|
What are the types of summation?
|
spatial and temporal
|
|
What is spatial summation?
|
occurs when multiple PSPs are simultaneously generated from different synapses
- may be from terminals arising from same neuron (less common) - may arise from different neurons (more common) |
|
What is temporal summation?
|
occurs when multiple PSPs are simultaneously generated from teh same synapse in rapid succession
|
|
Where is presynaptic inhibition mediated?
|
at axoaxonic synapses
|
|
What are the types of modulation of postsynaptic responses?
|
1) facilitation
2) synaptic fatigue 3) synaptic potentiation |
|
What is facilitation of postsynpatic responses?
|
occurs when neurons are depolarized to subthreshold level
- facilitated neurons are more easily excited by successive EPSPs |
|
What is synaptic fatigue of postsynaptic responses?
|
loss of neuron excitability resulting from excessive excitation due to rapid firing rate
- due mainly to exhaustion of presynaptic neurotransmitter stores |
|
What is synaptic potentiation of postsynaptic responses?
|
repeated presynaptic firing results in increased effect of presynaptic activity on postsynaptic cell
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What are the primary mechanisms of synaptic potentiation?
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1) residual Ca2+ levels in presynaptic terminal following AP generation enhances neurotransmitter release
2) Ca2+ influx into postsynaptic terminals (via voltage-gated Ca2+ channels) enhances postsynaptic response |
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Where are neurotransmitters synthesized?
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in presynaptic terminals
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How do neurotransmitters get into the vesicles?
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active transport from presynaptic terminals
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What neurotransmitters don't utilize vesicular transport? What do they do instead?
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gases diffuse directly through cell membrane
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What are the classifications of neurotransmitters?
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1) cholinergic
2) biogenic amines a) catecholamines b) indoleamines 3) amino acids 4) purinergic 5) gases |
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What are the examples of cholinergic neurotransmitters?
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Acetylcholine- excit. or inhib.
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What are the examples of catecholamine neurotransmitters?
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dopamine, epinephrine, or norepinephrine- excit. or inhib.
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What are the examples of indoleamine neurotransmitters?
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serotonin- inhibitory
histamine- excitatory |
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What are the examples of amino acid neurotransmitters?
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GABA, glycine- inhibitory
glutamate- excitatory |
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What are the examples of purinergic neurotransmitters?
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ATP- excit. or inhib.
adenosine- inhib |
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What are the examples of gas neurotransmitters?
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nitric oxide and carbon monoxide - excitatory
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Where are neuropeptides synthesized?
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in soma
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What are neuropeptides classified as?
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peptidergic
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What are the types of peptidergic neuropeptides?
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endorphins, tachykinins and others
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What are some examples of endorphins?
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dynorphin and enkephalin - inhibitory
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What are some examples of tachykinins?
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substance P, neurokinin A- excitatory
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How are neurotransmitters metabolized?
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1) enzymatically degraded in synaptic cleft (acetylcholinesterease)
2) reabsorbed by presynaptic cell or glia (norepinephrine) |
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What are the types of receptor interactions?
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agonists and antagonists
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What is an agonist receptor interaction?
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exogenous substances mimic effect of endogenous NT's
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What are the examples of agonist recepter interactions?
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1) nicotine, muscarine- (+) ACh receptors (stimulants)
2) ethanol, valium- (+) GABA receptors (depressants) |
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What are the examples of antagonist receptor interactions?
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1) curare, atropine- block ACh at nicotinic receptors
2) propranolol- blocks NE at beta adrenergic receptors 3) caffeine- blocks adenosine |
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What are antagonist receptor interactions?
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block neurotransmitter activation of receptors
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What are the types of presynaptic modulation?
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1) inhibitory- blocks NT release
2) stimulatory- increases NT release |
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What are some examples of inhibitory presynaptic modulation?
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1) botulinum toxin- blocks ACh release
2) some conotoxins- block Ca2+ release |
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What are some examples of stimulatory presynaptic modulations?
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1) amphetamines- increase NE release
2) some spider venom- increase ACh release |
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What are the types of postsynaptic modulation?
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1) block NT destruction
2) reuptake inhibition |
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What are the examples of blocking NT destruction?
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cocaine- block NE destruction
nerve gas- block acetylcholinesterase |
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What is an example of reuptake inhibition?
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SSRI's- block reuptake of serotonin, commonly prescribed as antidepressants
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