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83 Cards in this Set
- Front
- Back
Conduction Velocity
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V= λ/T
Velocity = Length constant/Time constant |
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Length constant
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λ = square root of (Rm/Ri)
Length constante equals the square root of Membrane resistance over Internal resistance membrane resistance is inversely related to speed current flows across membrane (how far depolarizing current will spread along a fiber Internal resistance is inverseley proportional to the ease current passes thru cytoplasm and inversely proportional to the cross sectional area of the fiber |
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Time constant
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T = Rm Cm
Time constant = Membrane resistance times membrane capacitance Time constant refers to the amount of time it takes reach 63% of its final value (100% would be the total change from RMP to threshold) Membrane capacitance is the ability of the cell membrane to store a charge |
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contiguous conduction
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AP spreads across every portion of membrane because it is an unmyelinated fiber
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Saltatory conduction
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Generates APs 50 times faster than unmyelnated fibers of comparable size
myelination via schwann cells in PNS & oligodendrocytes in PNS |
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Multiple sclerosis
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most common demyelinating disease of the CNS
(oligodendrycytes) |
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Hyponatremia
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-Plasma Na levels below normal
-Reduces concentration gradient and driving force for Na -causes decrease in magnitude of overshoot & rate of rise of upstroke |
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Hyperkalemia
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-Plasma K levels below normal
-Depolarizes RMP -continuous depolarization innactivates some of the VG-Na channels -because fewer Na channels are available to initiate APs a greater stimulus will be needed |
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Hyperparathyroidism
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If plasma concentration of phosphate decreases there will be an increase in free Ca to reduce neuron excitability
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Hypoparathyroidism
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If plasma concentration of phosphate increaes ther will be a decrease in free Ca to increase neuron excitability
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effect of free ionized Ca on neuron excitability
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greater Free Ca stabalizes plasma membrane and makes it less excitable
less free Ca makes threshold potential more negative and neuron becomes more excitable |
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background channels
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These channels spontaneously open in the absence of an external stimulus.
They are generally largely responsible for generating the resting membrane potential. |
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Hyponatremia
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-Plasma Na levels below normal
-Reduces concentration gradient and driving force for Na -causes decrease in magnitude of overshoot & rate of rise of upstroke |
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Mechanosensitive channels
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These channels, also known as stretch-activated channels, respond to membrane deformation, pressure of touch, and also other sensory inputs (e.g. sound, blood pressure, temperature).
Stimulating mechanosensitive channels generates graded potentials. |
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Hyperkalemia
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-Plasma K levels below normal
-Depolarizes RMP -continuous depolarization innactivates some of the VG-Na channels -because fewer Na channels are available to initiate APs a greater stimulus will be needed |
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Ligand-gated channels
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Also known as chemically-gated channels, these channels respond to chemical signals.
Opening ligand-gated channels generates graded potentials. |
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Hyperparathyroidism
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If plasma concentration of phosphate decreases there will be an increase in free Ca to reduce neuron excitability
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Voltage-Gated Channels
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these channels have a voltage sensor that alters the channel conformation when membrane potential changes over a specific range.
opening of voltage-gated ion channels initiate action potentials, not graded potentials. |
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Hypoparathyroidism
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If plasma concentration of phosphate increaes ther will be a decrease in free Ca to increase neuron excitability
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Examples of graded potentials:
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Postsynaptic potentials
End-plate potentials Pacemaker potentials Slow-wave potentials |
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effect of free ionized Ca on neuron excitability
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greater Free Ca stabalizes plasma membrane and makes it less excitable
less free Ca makes threshold potential more negative and neuron becomes more excitable |
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background channels
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These channels spontaneously open in the absence of an external stimulus.
They are generally largely responsible for generating the resting membrane potential. |
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Mechanosensitive channels
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These channels, also known as stretch-activated channels, respond to membrane deformation, pressure of touch, and also other sensory inputs (e.g. sound, blood pressure, temperature).
Stimulating mechanosensitive channels generates graded potentials. |
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Ligand-gated channels
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Also known as chemically-gated channels, these channels respond to chemical signals.
Opening ligand-gated channels generates graded potentials. |
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Voltage-Gated Channels
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these channels have a voltage sensor that alters the channel conformation when membrane potential changes over a specific range.
opening of voltage-gated ion channels initiate action potentials, not graded potentials. |
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Examples of graded potentials:
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Postsynaptic potentials
End-plate potentials Pacemaker potentials Slow-wave potentials |
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Temporal summation
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summation of several ESPS occurring very close together in time by successive firing of a single presynaptic neuron
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Spatial summation
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summation of several ESPS ocurring simultaneously from several different presynaptic imputs
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Generation of Action Potentials: Summary
Step 1: Resting State |
Voltage-gated Na+ and K+ channels are closed
Leakage accounts for all movement of Na+ and K+ |
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Generation of Action Potentials: Summary
Step 2: Depolarization |
At threshold ALL voltage-gated channel gates (both Na+ and
K+) are triggered or activated Activation gates of voltage-gated Na+ channels open quickly More voltage-gated Na+ channels open by positive feedback mechanism Na+ ions rush into cytoplasm causing rapid depolarization Inner membrane changes from negative to positive |
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Generation of Action Potentials: Summary
Step 3: Repolarization |
At peak (+30 mV) Na+ inactivation gates close (Na+ channel inactivation) and K+ channels open.
Na+ channels begin to reset to resting conformation when membrane reaches normal resting potential (-70 mV). K+ channels begin to close (delayed closing) when membrane reaches normal resting potential (-70 mV). |
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Generation of Action Potentials: Summary
Step 4: Hyperpolarization |
K+ channels finish closing after membrane is hyperpolarized to -80mV and returns back to resting; while almost all Na+ channels are reset to resting conformation.
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Absolute refractory period
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Interval during which NO stimulus can elicit an
action potential. Most voltage-gated Na+ channels are inactivated. |
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Relative refractory period
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Interval when a SUPRANORMAL stimulus is
required to elicit an action potential. Due to elevated gK coupled with the residual inactivation of voltage-gated Na+ channels. |
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Negative feedback system
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-Primary type of homeostatic control
-Maintains stability by defending set points -Opposes initial change -Compnents: Sensor- Monitors magnitude of a control variable Integrator- (Control center) Compares sensor's input with a set point Effector- Makes a response to produce a desire effect e.g. thermastat |
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Positive feedback system
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-Do not occur as often as negative feedback system
-Drives physiological values away from set point; destabilizing -Amplifies initial change e.g. Uterine contractions become increasingly stronger until birth of baby due to positive feed back increasing oxytocin secretion positive feedback cycle for opening of Na+ gated channels |
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Homeostasis
Redundancy: Hierarchy and Competition: Adaptability: |
Redundancy: The more vital the parameter is, the more systems the body mobilizes to regulate it.
Hierarchy and Competition: Feedback loops may have opposite effects. The body places a priority ranking among feedback loops. Adaptability: Flexibility of feedback loops allows for many forms of physiological adaptation or acclimatization (e.g. response to altitude). |
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Integral Proteins
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Proteins that are embedded in, and anchored to, the cell membrane
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Peripheral proteins
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Proteins that are loosely attached (not embedded) to either the intracellular or the
extracellular side of the cell membrane |
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Functions of membrane proteins
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Channels
Transporters or carriers Pumps Receptors Adhesion molecules (CAMs) Ability to recognize "self" |
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aquaporins
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proteins formed channels specific for passage of water
allow flow of 1 million water molecules per second |
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Fick's law
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Simple diffusion
a steady state balance will occur with equal concentrations and volumes on each side |
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osmotic pressure
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results from the difference in water concentration
Can be estimated from Van't Hoff equation |
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Hydrostaic pressure
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results from gravitational force on a column of fluid
Since plasma membranes deform easily, the hydrostatic pressure difference is usually zero and does not provide a significant driving force for water transport |
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Van't Hoff equation
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Used to determine osmotic pressure
Osmotic pressure = g C @ RT g= # of particles per mole C= concentration (mmol/L) @= reflection coeffiecient (varies from 0-1) R= Gas constant (0.082L-atm/mol-K) T= absolute temp (K) |
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Isoosmolar
Hyperosmolar Hypoosmolar effective osmolarity |
having the same osmolarity as normal extracellular fluid (approximately 290 mOsm); includes both permeant and impermeant particles
having a greater osmolarity than normal extracellular fluid Refers to the osmolarity of non-permeable particles in solution having a lower osmolarity than normal extracellular fluid |
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Response to Cell Swelling
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Most commonly the Cl-and K+ channels are activated
Resultant net efflux of Cl-and K+ decreases osmolarity and water diffuses out of the cell Cell volume is restore to normal |
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Response to Cell Shrinkage
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Cell shrinking activates solute uptake mechanism
Most commonly the Na+/H+ exchanger is activated (Na+ in /H+ out) H+ extrusion alkalinizes the cell and activates the Cl-/HCO3- exchanger Resultant net increase in intracellular Na+ and Cl- draws water into the cell Cell volume is restored to normal |
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Flux:
Efflux: Influx: Net Flux: |
Flux = Rate of diffusion
Eflux= diffusion out of cell Influx= diffusion into cell Net flux = difference between influx and eflux |
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Carrier-mediated transpo
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Accomplished by membrane carrier flipping its shape
Can be passive or active |
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The Na+-K+ ATPase (Na+-K+ pump)
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Electrogenic (imparts an electrical imbalance between the ECF and ICF)
Maintains gradients of Na+ and K+ pumps 3 Na+ out and 2 K+ in Utilizes ATP Inhibited by: -cardiac glycosides -ouabain -inhibit the Na+-K+ ATPase by binding to the E2~P conformation form near the K+-binding site on the extracellular side, thereby preventing the conversion of E2~P back to E1. By disrupting the cycle of phosphorylation-dephosphorylation, these drugs disrupt the entire enzyme cycle and its transport functions. |
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2 types of 2ndry Active transport
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Cotransport: occurs when uphill solute moves in same direction as Na+
Countertransport: occurse when uphill solute moves in the opposite direction of Na+ |
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Total Body Water
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TBW = ICF + ECF
ICF = 2/3 of TBW ECF = 1/3 of TBW Interstitial fluid (3/4 ECF) Plasma (1/4 ECF) Water accounts for 50-70% of body weight TBW=.7LBM + .1AT |
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Body Water Compartments: Daily Intake/Daily losses
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Ingested: liquids or foods = 2100 ml/day
Produced from the oxidation of carbohydrates = 200 ml/day Loss that is not precisely regulated and not aware of -Evaporation from lungs: 350 ml/day -Diffusion through skin: 350 ml/day Fluid loss in sweat = 100 ml/day H2O loss in feces = 100 ml/day H2O loss by kidney as formation of urine = 1400 ml/day |
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Plasma osmolarity
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Plasma Osmolarity = 2Na + Glucose/18 + BUN/2.8
At equilibrium all compartments have the same osmolarity; estimated from plasma osmolarity |
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Gain of Isotonic Fluid:
Isosmotic volume expansion what effect would this have? |
IncreaseinECFvolume
No change in ICF volume IncreaseinTBW No change in ECF or ICF osmolarity No shift in H2O between ICF and ECF Decrease plasma protein concentration and hematocrit (diluted because of increase in ECF volume) e.g. salin infusion |
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Loss of Isotonic Fluid:
Isosmotic volume contraction what effect would this have? |
Decrease in ECF volume
No change in ICF volume Decrease on TBW No change in ECF or ICF osmolarity No shift in H2O between ICF and ECF Increaseplasmaproteinconcentrationand hematocrit (concentrated because of loss in ECF volume) e.g. diarrhea |
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Gain of Hypotonic Solution:
Hypoosmotic volume expansion what effect would this have? |
Increase in ECF volume
Decrease in ECF osmolarity Shift in H2O from ECF to ICF Increase in ICF volume Decrease in ICF osmolarity Increase in TBW Decrease plasma protein concentration (by dilution) No change in hematocrit (no net change): -RBC volume increases because of water shift into RBCs, but concentration of RBCs decreases by dilution. e.g. drinking pure water, syndrome of inappropriate antidiuretic hormone secretion SIADH |
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Gain of Sodium
what effect on water balance would this have? |
Increase in ECF osmolarity
Shift in H2O from ICF to ECF Decrease in ICF volume Increase in ECF volume Increase in ICF osmolarity No change in TBW Decrease plasma protein concentration (by dilution) Decrease hematocrit -RBC concentration decreased by dilution and also because of water shift out of RBCs decreasing cell volume. e.g. high salt intake |
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Loss of sodium
what effect on water balance would this have? |
Decrease in osmolarity
Shift in H2O from ECF to ICF Increase in ICF volume Decrease in ECF volume Decrease in ICF osmolarity No change in TBW Increase plasma protein concentration (by fluid loss) Increase hematocrit -RBC concentration increased by ECF fluid loss and also because of shift of H2O into RBCs, increasing cell volume. e.g. aldosterone insuficiency (aldosterone promotes Na reabsorbtion & prevents loss in urine) |
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Loss of Hypotonic Solution:
Hyperosmotic volume contraction what effect would this have |
Decrease in ECF volume
Increase in ECF osmolarity Shift in H2O from ICF to ECF Decrease in ICF volume Increase in ICF osmolarity Decrease in TBW Increased plasma protein concentration (by fluid loss) No change in hematocrit (no net change): -RBC volume decreases because of water shift out of RBCs e.g water depravation, sweating but concentration of RBCs increases with fluid loss. |
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Isotonic Glucose Infusion
effect on water balance? |
Increase in ECF volume with no initial changes in osmolarity (isotonic solution)
Glucose is metabolized into CO2 and H2O Increase in ICF volume Decrease in ICF osmolarity Shift in H2O from ICF to ECF Further increase in ECF volume (addition of hypotonic solution, e.g. water) Decrease in ECF osmolarity Increase in TBW Decrease plasma protein concentration and hematocrit (by dilution due to increase in ECF volume) |
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Magnitude of Membrane Potential
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The magnitude of the potential depends on the number of opposite charges separated.
The greater the number of charges separated the greater the potential. |
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Driving forces for Diffusion of Ions through an Open Channel
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Chemical driving force = concentration gradient
Electrical driving force = electrical gradient (negative ions attract positive ions) Electrochemical gradient = the 2 combined to act in the same or opposite directions |
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Diffusion Potential:
-definition -4 types |
potential difference generated across the membrane when there is an unequal diffusion of positive and negative ions.
Equilibrium potential -Chemical & electrical forces are equal & opposite Resting membrane potential -difference that exists across the membrane of excitable cells at steady-state. (-70mV) Graded potential Action potential |
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Typical Values for Equilibrium Potential for Common Ions
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E Na+ = +65 mV
EK+ =-90mV ECl- =-50mV E Ca2+ = +120 mV |
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The Nernst Equation
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Used to colculate equilibrium potential for an ion at a given concentration across the membrane
Eion = (60/z) log ( [ion]out / [ion]in) E ion = equilibrium potential for ion (mV) z = ionic valence of ion (charge +/-) [ion]out = extracellular concentration for ion (mmol/L) [ion]in = intracellular concentration for ion (mmol/L) |
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Ionic Ohm's Law
(chord conductance equation) and Resting Membrane potential equation |
Estimates membrane potential knowing equilibrium potentials and conductances for each ionic species in question
The ion with the higher conductance will have a greater effect on RMP Since the resting membrane potential is determined almost entirely by Na+ and K+ concentrations and permeabilities, we can simplify the equation to include the equilibrium potentials and the relative conductance of Na+ and K+ only. Em = (gK EK + gNa ENa) \ (gK + gNa) |
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Conductance (g)
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Conductance = permeability
g = NPoY where N = the number of channels Po = the probability that a channel is open Y = The conductance of a single open channel |
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The process of chemical transmission can be summarized by the following series of 7 steps:
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Step 1: Neurotransmitter molecules are packaged into synaptic vesicles. Specific transport proteins in the vesicle membrane use the energy of an H+ gradient to energize uptake of the neurotransmitter in the vesicle.
Step 2: An action potential, which involves voltage-gated Na+ and K+ channels, arrives at the presynaptic nerve terminal. Step 3: Depolarization opens voltage-gated Ca2+ channels, which allows Ca2+ to enter the presynaptic terminal. Step 4: The increase in intracellular Ca2+ concentration ([Ca2+]i) triggers the fusion of synaptic vesicles with the presynaptic membrane. As a result, packets (quanta) of transmitter molecules are released into the synaptic cleft. Step 5: The transmitter molecules diffuse across the synaptic cleft and bind to specific receptors on the membrane of the postsynaptic cell. Step 6: The binding of transmitter activates the receptor, which in turn activates the postsynaptic cell. Step 7: The process is terminated by (1) enzymatic destruction of the transmitter (e.g., hydrolysis of ACh by acetylcholinesterase), (2) uptake of transmitter into the presynaptic nerve terminal or into other cells by Na+- dependent transport systems, or (3) diffusion of the transmitter molecules away from the synapse. |
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10 Common Neurotransmitters
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Acetylcholine
-Neuromuscular junction Glutamate -Major excitatory in CNS Glycine -Ihibitory NT Norepinephrine Epinephrine Dopamine -Tyrosine derivatives Serotonin Histamine y-Aminobutyric acid (GABA) Nitric Oxide (NO) -Gas; Inhibitory in CNS |
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Neuropeptides
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Large molecules consisting of anywhere from 2 to 40 aa.
Synthesized in neuronal cell body and are subsequently moved by axonal transport to the axon terminal. Packaged in large, dense-core vesicles present in axon terminal. Dense-core vesicles undergo Ca2+ - induced exocytosis and release neuropeptides at the same time as neurotransmitters are release from synaptic vesicles. Exhibit a slow, prolonged response by acting on adjacent neurons at lower concentrations than neurotransmitters. Act as neuromodulators = chemical messengers that do not cause the formation of EPSPs or IPSPs, but rather bring subtle long-term changes that modulate (depress or enhance) the action of the synapse. |
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Model of synaptic vesicle fusion and exocytosis: 6 steps
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Initial state
-Vesicles with synaptotagmin & syanptobrevin (a v-SNARE) move to the nerve terminal membrane which contains syntaxin & SNAP-25 (both t-SNAREs) Formation of Ternary Complex of SNAREs - n-sec-1 dissociates from syntaxin, allowing the syntaxin & SNAP-25 to form a complex. The distal end of synaptobrevin begins to wind around the syntaxin/SNAP-25 complex forming a ternary complex Tightening of ternary SNARE complex -the 3 SNAREs, synaptobrevin, syntaxin, & SNAP-25, continue to form a tight bundle of alpha helices, drawing vesicle & presnyaptic membranes into close apposition Fusion & Exocytosis -The entry of Ca and its binding to synaptotagmin triggers fusion Disassembly of ternary SNARE complex -alpha-SNAP and the ATPase NSF bind to the ternary SNARE complex and use the energy of ATP hydrolysis to disassemble the SNAREs Recycling of SNAREs -With the endocytosis of the vesicle, the syaptobrevin is effectively recycled. The syntaxin & SNAP-25 are now free for an additional cycle of vesicle fusion 3. |
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Neurotransmitters Can Activate Ionotropic or Metabotropic Receptors
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Activation of an ionotropic receptor causes rapid opening of ion channels. This channel activation in turn results in depolarization or hyperpolarization of the postsynaptic membrane, the choice depending on the ionic selectivity of the conductance change
Activation of a metabotropic G protein-linked receptor results in the ␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣␣ cellular responses by direct interaction with either ion channel proteins or other second-messenger effector proteins. |
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Presynaptic Facilitation/Inhibition
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Axoaxon?
An excitatory/inhibitory neuron synapse impinging on presynaptic terminal or axon can increase/decrease the amount of NT released from the presynaptic terminal. -only one or the other, one nerve cannot do both |
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DRUG action: Blocks Ach release from presynaptic terminals
Effect? |
Effect: total blockade, paralysis of respiratory muscles & death
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Drug action: Competes with Ach for receptors on motor end plate
Effect? |
Effect: Decreases size of EPP; in maximal doses produces paralysis of respiratory muscles and death
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Drug action: AchE inhibitor
Effect? |
Effect: Prolongs & enhances action of Ach at motor end plate
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Drug action: Blocks reuptake of choline into presynaptic terminal
Effect? |
Effect: Depletes Ach stores from presynaptic terminal
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Clinical Applications:
Lambert Eaton syndrome |
Autoimmune disorder caused by antibodies attacking the presynaptic voltage-gated Ca channels
Most often seen in patients with certain types of cancer such as small cell lung carcinoma |
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3 Exceptions to general rule of dual reciprocal innervation by the two branches of autonomic nervous system
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Most arterioles and veins receive only sympathetic nerve fibers (arteries and capillaries are not innervated)
Most sweat glands are innervated only by sympathetic nerves Salivary glands are innervated by both ANS divisions but activity is not antagonistic both stimulate salivary secretion |
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3 Regions of CNS Involved in Control of Autonomic Activities
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Hypothalamus plays important role in integrating autonomic, somatic, and endocrine responses that automatically accompany various emotional and behavioral states
Medulla within brain stem is region directly responsible for autonomic output Some autonomic reflexes, such as urination, defecation, and erection, are integrated at spinal cord |
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Autonomic Agonists and Antagonists
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Agonists
-Bind to same receptor as neurotransmitter -Elicit an effect that mimics that of neurotransmitter Antagonists -Bind with receptor -Block NT's response |