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BIO 203 > Quiz 2 > Flashcards

Quiz 2 Flashcards

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1
Q

there are 2 aqueous compartments with different concentrations of NaCl and separated by a membrane equally permeable to Na and Cl

  1. what will happen to the concentration of Na and Cl in each compartment
  2. will there be a difference in the electrical potential between the 2 compartments (membrane potential)
A
  1. Na and Cl moves towards the compartment with lower concentration until they are equal
  2. After diffusion the compartment that was originally lower in concentration will be more negative and the other more positive (diffusion potential), this is because Cl diffuses through water faster -> electrical potential will cause the ions to move
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2
Q

diffusion potential

A
  • stabilizes when potential difference balances the greater mobility of Cl-Na & Cl cross membrane at same rate
  • the diffusion creates the potential, the potential influences the diffusion
  • dependent upon the concentration gradient
  • will continue as long as there is a concentration gradient between compartments
  • eventually it will equilibriate and stop
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3
Q

equilibrium potential* ex

A
  • Cl travels down its concentration gradient
  • Na cannot cross
  • Diffusion of Cl creates a neg charge which will cause the opposition of Cl diffusion
  • Diffusion moves Cl from 1->2
  • Electropotential moves Cl from 2->1
  • electropotential prevents Cl from moving down is gradient
  • equilibrium is achieved when electropotential is exactly sufficient to balance the force of diffusion and there is NO NET FLUX of Cl across membrane
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4
Q

nernst equation

A
  • each permeant ion has a unique equilibrium potential that is primarily due to the concentration gradient of that ion across the membrane
  • E=RT/zF ln(ion1/ion2)
  • R=gas constant
  • T= absolute temp (K)
  • F=Faradays constant
  • z=valence electrons
  • assuming T is 20C…E= 58/z log(ion1/ion2)mV
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5
Q

effect of electric potential

A
  • electric potential is zero- Cl moves high to low
  • electric potential is exactly the same as the force of diffusion -> equilibrium
  • electric potential is greater than equilibrium potential it offsets diffusion- Cl moves away from neg charge
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6
Q

steady state

A
  • since the permeability is greater for one ion than the other, the membrane potential is close to the equilibrium potential for the dominant ion
  • resting membrane potential
  • sum of all ionic currents is equal to zero in steady state
  • no net current (sodium leaving is equal to potassium coming in -> sum of ionic currents is zero)
  • permeability ratio is .02
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7
Q

equiliirum

A

-achieved when electrical potential is exactly sufficient to balance the force of diffusion and there is no net flux of Cl across the membrane

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8
Q

membrane potential in most cells

A
  • 70mV
  • Em
  • this is only one membrane potential but can be multiple equilibrium potential
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9
Q

membrane potential is determine by

A
  1. the intracellular and extracellular concentrartion of the permeant ions
    - determines equilibrium potential for each ion
  2. the permeability (P) of the membrane for each ion
    - determines relative influence of each ion on E
    - in cells in the resting state P potassium > P sodium
    - therefore, K is the dominant ion and the membrane potential is close to E
    - if the membrane is permeable to an ion and Eion is not equal to Emembrane then the ion will cross the membrane pulling E membrane towards E ion
    - there is only one membrane potential
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10
Q

goldman equation

A
  • Em= 58 log (concen of potassium out +b(Sodium out)/(potassium in +b(sodium in)))
  • where b=Pna/Pk
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11
Q

Typically at rest, K permeability is 50 times greater than Na permeability (.02) and Em=-70

if b suddenly becomes equal to 20, what happens to Em

A
  • when b becomes much bigger Na concentration becomes more relevant than K
  • Em becomes +50mv because its closer to Na Em
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12
Q

membrane potential becomes less neg

A

depolarize

-less polarized

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13
Q

cell membrane potential becomes more negative

A

hyperpolarize

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14
Q

cell membrane returns to normal

A

repolarization

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15
Q

equilibrium potential

A
  • the membrane potential that exactly balances the force of diffusion for some ion crossing the membrane (no net flux)
  • unique potential for each ion
  • tries to stay constant
  • based on log of ratio of concentration
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16
Q

20 or 37

A

58 and 61

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17
Q

electrical current and movement of ions across membrane

A
  • the amount of current carried by an ion through a membrane (Iion) is equal to ease of movement through the ion channels multiplied by the driving force for diffusion for the ion (Em-Eion)
  • I(ion)=g(ion) (Em-Eion)
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18
Q

membrane potential

A

Em

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19
Q

equilibrium potential

A

Eion

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20
Q

membrane permeability

A
  • determined by the properties of the aqueous ion channels in the plasma membrane
  • can change easily
    1. ion selectivity of channel
    2. channel conductance (gs)- index of ion flux through the membrane (opposite of resistance)
    3. the average proportion of the time individual channels are open (Po)
    4. channel number (N) or density (number per area)- functional density vs. anatomical density
  • determined by the density and conductance of the channels in the membrane that are selective for that ion
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21
Q

cell signaling with membrane potential

A

cell tries to maintain a constant equilibrium potential for the ions and relative permeability can change quickly

  • use this to signal in a cell
  • changing membrane potentials signal to the cell
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22
Q

membrane potential becomes positive

A

overshoot

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23
Q

graded potentials

A
  • increase in amplitude with increase in stimulus strength (amplitude is graded)
  • membrane potential is changing due to change in permeability in channels in the membrane
  • can be hyperpolarizing or depolarizing
  • localized bc its not regenerative
  • spatially and temporally summate- two graded potentials come together and make a larger one or smaller one (if opposing)
  • spreads passively to neighboring membranes, NOT regenerative- the potential doesnt regenerate -> it gets weaker by distance
  • decrease in amplitude as a function of distance traveled along the membrane in an excitable tissue
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24
Q

ex. of graded potential

A

BETA CELL AT REST
-creates insulin in response to a increase in glucose (transported into the cell through facilitated diffusion carrier protein)
-low glucose -> low metabolism -> low ATP
-transmembrane integral protein (potassium channel) senses the ATP (ligand gated channel)-> ATP bound- close, ATP not bound- open
-relative permeability of K is high when ATP is low -> membrane potential is negative from K leaving
BETA CELL SECRETES INSULIN
-high glucose in plasma -> high metabolism -> high ATP
-K gated channel closes
-decrease in permeability to K -> membrane potential increases (depolarizes)
-voltage gated calcium channel opens due to depolarization -> calcium enters -> exocytosis of cell -> releases insulin into blood stream

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25
Q

excitable cells

A

a cell that has voltage gated channels

-cells are excitable when gates are closed (at rest) (not inactivated)

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26
Q

neuron

A
  • cell body and dendrites- receives information and integrate it through temporal and spatial summation of graded potentials
  • decides to fire a action potential
  • conduction of action potential travels down the axon and causes the release of neurotransmitters -> stimulates next cell
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27
Q

action potential

A
  • if you depolarize an excitable cell it will give a graded depolarizing potential
  • depolarizes until it reaches threshold potential- cell generations all or none action potential
  • large, short (varies) change in membrane potential
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28
Q

characteristics of an action potential

A
  • triggered by depolarization
  • threshold depolarization is required
  • all or none events
  • at peak the membrane potential reverses sign- cell becomes inside positive (overshoot)
  • at the end the membrane potential is transiently more negative (undershoot)
  • after a neuron fires an action potential, it cannot generate another one for a brief period (absolute refractory period)
  • propagate along axon without decrement
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29
Q

action potentials are dependent on

A
  • voltage gated channels, specially voltage gated sodium channels
  • depolarization begins to open voltage gated sodium channels
  • sodium rushes in and membrane potential changes rapidly
  • equilibrium potential is similar to sodium and b=20
  • sodium permeability decreases at peak while potassium increases
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30
Q

depolarization triggers 3 things

A
  • activates voltage gated sodium channels- fast
  • inactivates voltage gated sodium channels- causes them to close but slow* (at peak)
  • activates voltage gated potassium channels- open and close slow (at peak)
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31
Q

depolarization cycle

A

hodgken cycle

  • depolarization causes the opening of voltage gated sodium channels
  • this causes more sodium to enter which causes depolarization
  • this causes more gates to open
  • positive feedback
  • stops at threshold
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32
Q

activating and deactivating gates

A
  • at rest the activation sodium channel is closed, the inactivation is open, and K gate is closed
  • activation gate opens in response to depolarization
  • potassium gates havnt opened yet bc slow
  • inactivation gates havnt closed yet bc slow
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33
Q

undershoot

A
  • hyperpolarization
  • sodium channels are inactivated (slow to close)
  • potassium channels are still open (bc slow to close)
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34
Q

absolute refractory period

A
  • even if the cell were to depolarize the gates are inactivated (bc they are slow to close)
  • arnt enough closed gates to respond
  • dependent only upon sodium channels
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35
Q

difference between inactivated and closed

A
  • both wont let sodium through

- closed will respond to depolarization but inactive wont (until it open)

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36
Q

relative refractory period

A
  • only a larger than normal stimulus can initiate a new action potential
  • dependent upon both the number of sodium channels that have closed and the number of potassium channels that are still open
  • once the cell repolarizes the sodium gates will begin to close (but not completely at rest)
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37
Q

regenerable

A
  • action potentials are regenerable because of positive feedback
  • neighboring gates are reaching threshold- all or none
  • each patch of the membrane is firing its own action potential as it goes down
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38
Q

myelinated axon

A
  • insulates to prevent current ion from leaving the cell
  • shwan cells- produces myelin
  • node of ranvier- gaps
  • blocks the flow of ions into and out of the axons- the only place the current can flow is in the nodes of ranvier
  • action potential skips from node to node- saltatory conduction
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39
Q

how do cells pick up information from the environment and respond appropriately

A
  • fundamental problem for all life
  • cells need to translate an external signal into an internal change
  • cells can use electrical or chemical signals to relay messages, sometimes over long distances
  • similar messages used in all forms of multicellular life
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40
Q

cells communicate over short distances- local

A
  • gap junctions
  • contact dependent signals
  • paracrine signals
  • autocrine signal (same cell)
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41
Q

gap junctions

A
  • form direct cytoplasmic connections between adjacent cells
  • electrical communication
  • localized
  • express proteins in their cells called connexins- form channels (pores) between the two cells -> allow for diffusion between the cells
  • *electrical synapse
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42
Q

contact-dependent signals

A
  • signal transduction proteins
  • require interaction between membrane molecules on two cells
  • matches up and starts intercellular messaging
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43
Q

autocrine signals

A
  • act on the same cell that secreted them
  • release signals that bind to receptors on the outside of the same cell
  • signal being transfer via extracellular fluid
  • local
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44
Q

paracrine signals

A
  • are secreted by one cell and diffuse to adjacent cells
  • local
  • signal being transfer via extracellular fluid
  • doesnt go into the circulatory system
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45
Q

hormonal signaling

A
  • signal being transferred through the plasma
  • goes through the circulatory system
  • long distances
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46
Q

endocrine cells

A
  • release chemicals into the blood stream
  • goes to every other cell in the body (only cells with the specific receptor respond)
  • long distance
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47
Q

electrical communication

A
  • Withing a cell
  • action potentials
  • graded potentials
  • Between cells
  • electrical synaptic transmission
  • gap junction
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48
Q

chemical communication

A
  • Within a cell
  • cell signaling (intracellular signaling molecules and pathways)
  • Between cells
  • chemical synaptic transmission
  • endocrine system
  • specialized paracrine
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49
Q

electrical synaptic transmission

A

electrical signals move between cells through gap junctions

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50
Q

chemical synaptic transmission

A
  • the electrical signal from the action potential in the presynaptic neuron axon is converted into a chemical signal at the synapse
  • involves 2 cells (sometimes more)
  • requires a receptor and ligand (first messenger)
  • chemical message is relayed within the cell and translated into a cellular change using signal amplification
  • specialized paracrine
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51
Q

presynaptic cell

A

always a neuron

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52
Q

postsynaptic cell

A
  • neuron
  • muscle cell
  • cardiac conducting system cell
  • endocrine cell
  • target cell
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53
Q

synaptic terminal bouton

A
  • the end of the presynaptic cell
  • does not contain voltage gated Na or K channels
  • region that releases neurotransmitters
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54
Q

neurotransmitter release

A
  • action potential depolarizes the axon terminal
  • graded depolarization opens Ca channels and Ca enters cell
  • Ca binds to snare proteins (synaptotagmin)
  • synaptic vesicles release neurotransmitters into the synaptic cleft- exocytosis (slowest step)
  • neurotransmitters binds to ligand gated receptors on the postsynaptic cell -> cellular response
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55
Q

excitation of the synaptic terminal

A
  • the action potential coming down is stopped by the Na and K gates
  • excitation in the synaptic terminal itself is a graded depolarization that spread from the axon into the terminal
  • > activates Ca channels
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56
Q

three ways to stop an action potential

A
  1. some mechanism that transmits the neurotransmitters back up into the cell- can be done by a support cell or cells in the synaptic terminal
  2. enzymes preset to breakdown the neurotransmitter- (AChE breaks down ACh) -> recycles the ACh to be used again
  3. neurotransmitters diffuse away from the synaptic cleft (slow)
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57
Q

saltatory conduction of graded potentials occurs more rapidly in myelinated axons compared to unmyelinated axons

A
  • false
  • there are no saltatory conductions of graded potentials
  • there are no saltatory conduction in an unmyelinated axon!
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58
Q

in neurons, activation of ligand-gated channels that generate hyperpolarizing graded potentials will inhibit the formation of an action potential

A
  • true
  • getting farther away from threshold
  • inhibits
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59
Q

the extracellular and intracellular compartments are in osmotic equilibrium, but chemical and electrical disequilibrium

A
  • true
  • cell are in osmotic equilibrium (or else they would be changing sizes)
  • cells are in chemical and electrical equilibrium in order to cell signal
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60
Q

receptor signaling

A
  • chemical
  • endogenous and exogenous ligands can activate receptors
  • **cellular response depends on the receptor not the ligand
  • chemical message is relayed within the cell and translated into a cellular change using signal amplification
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61
Q

second messengers

A
  • the first messenger (ligand) binds and initiates an amplification process that produces other chemicals inside the cell
  • the other chemicals that are signaling molecules are second messengers
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62
Q

4 types of Receptors

A
  • receptor-channel
  • G protein-coupled receptor
  • receptor enzyme
  • integrin receptor
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63
Q

receptor-channel

A
  • ligand binding opens or closes the channel
  • ligand gated channel
  • ex. ATP gated potassium channel in the beta cell
  • *the channel is the receptor
  • fast!!
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64
Q

G protein-coupled receptor

A
  • ligand binding opens an ion channel or alters enzyme activity
  • membrane proteins that interact with GPCR’s
  • ligand binding causes a conformational change
  • contains 3 subunits that dissociate upon activation- alpha, beta gamma
  • alpha subunit drops GDP and picks up GTP
  • GDP goes around the cell and activates things
  • different subunits are active in different signaling pathways
  • diverse, common
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65
Q

receptor-enzyme

A

-ligand binding activates an intracellular enzyme

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66
Q

integrin receptor

A
  • ligand binding alters enzymes or the cytoskeleton
  • integrated into the cytoskeleton of the cell
  • causes changes in the structure of the cell
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67
Q

Nicotinic acetylcholine receptor (nAChR)

A
  • receptor-channel ex.
  • monovalent
  • when ACh binds the channel opens and ion can flow
  • change in permeability in the membrane to Na and K -> depolarization graded potential -> electrical signal -> voltage gated channels are signaled
  • Na driving force > K driving force- Na will have a stronger electrochemical gradient
  • skeletal muscles cells -> muscle contraction
  • non selective (monovalent) cation-specific ion channel
  • depolarizing graded potential
  • nicotine is an exogenous agonist to this receptor
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68
Q

antagonist

A

-blocks receptor activity

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69
Q

agonist

A

-activates the receptor

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70
Q

Muscarinic (mAChR)

A
  • G protein coupled receptor ex.
  • Ach binds to receptor and activates it releasing the g protein (betta and gamma)
  • Subunits activate ligand gated potassium channels
  • permeability to potassium increases -> change in membrane potential -> inhibitory response due to hyperpolarizing graded potential
  • muscerin is the exogenous agonist
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71
Q

Alpha and beta Adrenergic receptors

A
  • g protein coupled receptors ex.
  • epinephrine
  • both bind epinephrine
  • alpha- found on blood vessel in the intestine -> constricts in response (arteriolar smooth muscle)
  • beta- found on blood vessels in the airway -> dilates in response (bronchiolar smooth muscle)
72
Q

Signal amplification

A
  • G protein coupled receptors are usually amplified
  • signal produces a cascade of active signaling molecules inside the cell
  • everytime a signaling molecule becomes activated there is opportunity for amplification of the signal
  • secondary messengers
  • allows small signal to have a large effect
  • one ligand is amplified into many intracellular molecules
  • slower bc there are multiple steps and long lasting
73
Q

G protein coupled receptor using cAMP: beta adrenergic receptors

A
  • ligand binds to beta adrenergic receptor
  • g coupled proteins dissociate
  • alpha and beta subunit
  • alpha unit finds an enzyme in the membrane, adenylyl cyclase, and binds
  • response catalyzes the reaction of ATP into cAMP
  • cAMP- a second messenger that activates protein kinase A (PKA) that phosphorylate other proteins which activates them -> large cellular response
74
Q

G protein coupled receptor using IP3: alpha adrenergic receptor

A
  • ligand binds to alpha adrenergic receptor
  • g coupled proteins dissociate
  • alpha subunit activates a membrane protein, phospholipase C (PLC)
  • PLC activates messengers from the membrane, diacylglycerol (DAG) and IP3, which active protein kinases
  • IP3 diffuses into the cell and binds to receptors in the ER causing the release of Ca
  • Ca triggers vasoconstriction
75
Q

receptor enzyme

A
  • receptor itself is an enzyme that catalyzes changes inside the cell
  • ex. insulin receptor
  • when insulin binds the receptor is activates a receptor enzyme that causes change in metabolism
  • enzyme phosphylates proteins which changes the behavior of the proteins making them more active
  • the receptor itself is a tyrosine kinase
  • when insulin binds it dimerizes -> protein self phosphorylates -> activation -> allows the enzyme to phosphylate other proteins inside the cell
76
Q

which of the following is true for both graded potentials and action potentials in a neuron

A
  • incorrect- depends on activation of voltage gated channels- graded potential doesnt need to be voltage gated (can be ligand gated)
  • correct- may produce and action potential in a neighboring path of membrane
77
Q

during the repolarization phase of the action potential, the activation gates in the voltage gated sodium channels are closed

A
  • activated and inactivated

- both need to be opened for Na to go through

78
Q

channel configuration

A
  • closed- activation closed and inactivation is open (when the membrane is at rest)
  • open- activation and inactivation are open (during depolarization)
  • inactivated- activation is open and inactivated is open (during repolarization)
  • at peak sodium channel becomes inactivated
  • when the cell becomes more negative the inactivated gates close
79
Q

3 types of muscle

A
  • skeletal
  • cardiac
  • smooth
80
Q

skeletal muscle

A
  • attaches to our bones
  • striated
  • voluntary- somatic
  • large, multinucleated- muscle fibers fuse together
  • internal organs that use skeletal muscle- diaphragm, sphincters (bowels and urine), eyes
  • one neuron connect to many muscle fibers and depolarizes them all (motor unit)
  • actin & myosin
81
Q

cardiac muscle

A
  • striated
  • involuntary- autonomic
  • cells are fused together, branched fibers but have one nucleus
  • gap junctions
  • generate heart contraction
  • actin & myosin
  • depolarization
82
Q

smooth muscle

A
  • internal organs
  • involuntary- autonomic
  • one nucleus, small
  • some gap junctions and motor units
  • actin & myosin
  • depolarization
83
Q

which of the following muscle cells contain electrical synapses

A
  • cardiac and smooth
  • gap junctions
  • skeletal muscle has chemical synapses
84
Q

antagonist

A
  • on the opposite side of the bone
  • relaxes
  • moves bones in opposite direction
  • ex. when curling arm triceps are antagonist, when straightening arm contract triceps (agonist) and relax bicep (antagonist)
85
Q

agonist

A
  • muscle you contract in order to produce movement

- ex. when curling arm bicep is agonist, when straightening arm contract triceps (agonist) and relax bicep (antagonist)

86
Q

muscle contractions

A
  • can pull on a bone but cannot push a bone away

- during contraction muscles shorten -> pull

87
Q

lengthening contractions

A
  • control the rate of a movement

- the antagonist muscle is creating more force

88
Q

skeletal muscle

A
  • nerve and blood vessels move through it
  • bundles of muscle fibers connected by connective tissue- fascicles
  • within the fascicles are individual muscle fibers (cell)
  • a lot of mitochondria
  • inside the muscle fiber there is a myofibril- made up of thick and thin filament
89
Q

myofibril

A
  • contractile element
  • in the muscle fiber
  • made up of thick and thin filament
  • myosin- thick filament
  • actin- thin filament
  • accessory proteins- troponin and tropomyosin
90
Q

muscle fibers

A
  • muscle cells
  • fused cells with many nuclei
  • cells bundled into fascicles surrounded by connective tissue
91
Q

sarcolemma

A

cell membrane

92
Q

sarcoplasm

A

-cytoplasm

93
Q

sarcoplasmic reticulum

A

endoplasmic reticulum

-specialized to store calcium

94
Q

network of transverse tubules

A

-T-tubules connected with the sarcolemma

95
Q

T-tubules

A
  • holes poked through the internal structure of the muscle fiber
  • continuous with the extracellular fluid and interstitial fluid
  • extension of the cell membrane that associate with the ends (terminal cisternae) of the sarcoplasmic reticulum
  • action potential follows down the t-tubules into the interior of the muscle fiber (terminal cisternae) which activates voltage gated channels -> Ca release
96
Q

myosin

A
  • thick filaments (heavy)
  • two myosin heads on each myosin molecule
  • golf club
  • line up on the M line
97
Q

actin

A
  • thin filaments (light)
  • globular actin molecules
  • chain like
  • toponin and tropomyosin are here
98
Q

titin and nebulin

A
  • skeleton of the cell
  • connective tissue
  • hold everything in place
99
Q

terminal cisternae

A
  • ends of the sarcoplasmic reticulum
  • 2 terminal cisteraes and a t-tubule make up a triad (triads decrease with age -> less Ca -> fewer crossbridges -> less tension)
  • the action potential in the t-tublues triggers the release of Ca in the terminal cisternae through voltage gated channels
100
Q

sarcomere: contractile unit

A
  • functional unit of contraction
  • light and dark bands seen under light microscopy
  • light regions are only one type of filament (these shorten)
  • one sarcomere between two z disks
  • I Band- made of thin filaments only
  • A band- made of darker regions where both thin and thick filaments overlap
  • H zone- a clear band in the middle of the A band, thick (heavy) filaments only
  • M line- represents the proteins to which heavy filaments attach
101
Q

sliding filament theory

A
  • actin and myosin filaments slide when contracting
  • do not shorten
  • power stroke cycle- myosin crossbridges move actin filament
    1. Calcium release from SE
    2. Ca binds troponin
    3. troponin pulls tropomyosin from myosin-binding site on actin
    4. myosin binds tightly to and moves actin (power stroke) and releases ADP + phosphate (low energy conformation)
    5. ATP binds to myosin, myosin hydrolyses ATP to ADP + phosphate
    6. energy releases the actin-myosin bind and rotates the myosin head that then binds weakly to actin down the molecule
    7. head of myosin is cocked ready for the next power stroke
102
Q

I band

A
  • actin only, no myosin
  • only thin
  • shortens
103
Q

A band

A
  • made of darker regions where both thin and thick filaments overlap
  • does not change in length
  • myosin does not change in length
  • measure the length of A band to get the length of the myosin fibers
104
Q

H zone

A

a clear band in the middle of the A band, thick (heavy) filaments only
-shortens

105
Q

Z line - Z line

A
  • one sarcomere
  • both actin and myosin
  • shortens
106
Q

Z line - M line

A
  • both actin and myosin
  • shortens
  • one half of a sarcomere
107
Q

M line

A

-represents the proteins to which heavy filaments attach

108
Q

excitation

A
  • synaptic transmission at the neuromuscular junction & sarcolemma depolarization
  • initial phase of depolarization of the sarcolemma membrane
109
Q

coupling

A
  • release of intracellular calcium

- link between electrical stimulus (action potential) and mechanical events of the muscle contraction

110
Q

contraction

A

-sliding filament theory

111
Q

Steps of excitation

A

Step 1- Action potential travels down the motor neuron to the axon terminal (graded potential forms at motor endplate and propagates to adjacent areas to generate action potential)
Step 2- voltage gated calcium channels open and Ca diffuse into the terminal
Step 3- Calcium causes synaptic vesicles to release ACh via exocytosis
Step 4- Ach diffuses across the synaptic cleft and binds to receptors on the motor end plate (on muscle fiber) which contain ligand gated monovalent cation channels
Step 5- Ligand gated monovalent cation channels open
Step 6- net sodium ions ENTER the muscle fiber and potassium ions EXIT -> greater sodium influx causes membrane potential to become less neg
Step 7- membrane potential reaches threshold and action potential propagates along the sarcolemma

112
Q

motor neuron

A

-neuron that synapses muscles

113
Q

monovalent

A
  • one charge

- sodium and potassium

114
Q

What causes a large depolarization of skeletal muscle

A
  • Na driving force > K driving force
  • Electropotential of sodium is 58 while the resting membrane potential of a cell is around -70
  • This large driving force causes sodium to rush in creating a large depolarization
115
Q

neuromusclular junction

A
  • where the motor neuron attaches
  • motor neuron ALWAYS depolarize skeletal muscle fibers (always reach threshold)
  • there are NO voltage-gated channels in the motor endplate, (only AChR)
  • voltage gated Na channels are adjacent to the motor endplate- action potentials can be generated at these regions -> graded potential at the motor end plate that propagates to the area adjacent that has voltage gated channels (always large enough)
116
Q

can action potentials be generated at the motor end plate

A
  • no

- there are not voltage gated channels (only ligand)

117
Q

motor end plate

A
  • the part of the sarcolemma that is closes associated with the neuron
  • no voltage gated channels here (only ligand)
  • cannot have action potential here
  • graded potentials here that propagate to areas adjacent which has voltage gated channels (always large enough)
  • terminal bouton
118
Q

high safety factor

A
  • one action potential in a motor neuron ALWAYS generates an action potential in a skeletal muscle fiber
  • not always true for neuron -> do not always reach threshold
119
Q

action potential in skeletal muscle

A
  • membrane potential- -70-80
  • *Net Na entry through ACh-operated channels
  • rising phase- Na entry
  • repolarization- rapid, caused by K efflux
  • hyperpolarization- excessive K efflux at high K permeability, when K channels close, leak of K and Na restores potential to resting
  • duration- 1-2 ms
  • refractory period- generally brief
120
Q

difference between events leading up to threshold potential in neuron and skeletal muscle

A
  • skeletal- Net Na entry through ACh operated channel, always leads to action potential
  • neuron- can be hyperpolarizing or depolarizing graded potentials, do not always reach threshold
121
Q

excitation-contraction coupling

A
  • Ca links excitation to contraction
  • Action potential travels down the t-tubules and encounters DHP receptors
  • DHP- voltage gated receptor
  • action potential causes a conformational change
  • DHP is mechanically linked to ryanodine (RYR) (mechanically gated) receptor channel which opens and releases Ca
  • Ca enters the cell
  • Ca binds to troponin and allows for actin myosin binding
122
Q

DHP rectopor

A
  • voltage gated receptor
  • action potential causes conformational change
  • mechanically linked to the ryanodine receptor channel (RyR) on the sarcoplasmic reticulum
123
Q

Calcium

A
  • links excitation with coupling

- Ca binds to troponin allowing actin-myosin binding

124
Q

steps in cross bridge cycle

A

Step 1- cross bridge formation- activated myosin head binds to actin forming a cross bridge
Step 2- power stroke- ADP and phosphate is released and the activated myosin head pivots, sliding the thin myofilament towards the center of the sarcomere (low energy conformation)
Step 3- cross bridge detachments- when another ATP binds to the myosin head, the link between myosin head and actin weaken, myosin head detaches
Step 4- reactivation of the myosin head- ATP is hydrolyzed to ADP and phosphate, energy released during hydrolysis reactivates the myosin head, returning it to cocked position (weakly bonded to actin here)

125
Q

Contraction

A
  • Ca binds to troponin
  • troponin goes through conformational change which pulls tropomyosin away from binding site
  • Myosin and actin bind
  • power stroke- pulls actin towards the middle of sarcomere
  • sarcomere shortens
126
Q

Relaxation

A
  • Ca is *actively pumped away by sarcoplasmic Ca -ATPase pumps into the sarcoplasmic reticulum
  • decrease in Ca causes the Ca to unbind to troponin
  • tropomyosin covers the actin myosin binding site
127
Q

Rigor state

A
  • tight binding
  • Stiff
  • these bonds are weakened by binding of ATP
128
Q

ATP

A
  • needed to actively pump Ca out into the SE during relaxation
  • needed to bind to detach strong bonds in the rigor state
  • if you run out of ATP your muscles will stay contracted (rigor mortis)
  • allows myosin heads to swivel in order to adopt the high energy conformation
  • powers the sodium potassium ATPase- asymmetries
129
Q

cocked position

A
  • high energy position

- when ATP is hydrolyzed into ADP and phosphate and they are still attached

130
Q

Low energy position

A

after the power stroke

131
Q

what factors affect the tension generated by a muscle

A
  • sarcomere length within a muscle fiber
  • summation of twitches within a muscle fiber
  • recruitment of additional motor units
  • the properties of recruited motor units (type2b)
132
Q

which sarcomere length (before contraction begins) would produce maximum tension in a muscle fiber

A
  • C
  • the actin and myosin are overlapping completely (more cross bridges) and there is also space for it to move (sarcomere to shorten)
  • actin filaments can be pulled towards the M line
133
Q

resting fiber length affects tension

A
  • sarcomeres contract with optimum force if its at optimum length (neither too long nor too short) before the contraction begins
  • tension generated proportional to number of cross bridges
  • too short- it can not be shortened much -> less tension
  • too long- reduce the amount of cross bridges you are able to form -> less tension
134
Q

summation affects tension

A
  • neuromuscular junction has a high safety factor
  • each action potential in the motor neuron produces a twitch contraction in all of the muscle fibers innervated by that motor neuron
  • contractions can sum if multiple action potentials are exciting that fiber
  • action potentials do not summate
135
Q

motor neuron -> muscle fiber -> tension

A
  • action potential of muscle fiber takes 1-2 ms after action potential of motor neuron
  • tension takes about 10-100ms after
136
Q

latent period

A
  • short delay between muscle action potential and start of contraction
  • this is due to the time it takes for intracellular Ca to increase
  • everything between an action potential and muscle contraction is happening in this period
137
Q

couples excitation to contraction

A

calcium

  • time is required for this
  • latent period
138
Q

twitch

A

-response to a single action potential

139
Q

summation

A

-second action potential causes more Ca to be released increases the cross bridges increases muscle contraction

140
Q

unfused tetanus

A
  • tiny relaxation periods between stimuli
  • stimuli are far enough apart
  • maximum tension
141
Q

complete tetanus

A
  • muscle reaches steady tension
  • if muscle fatigues tension decreases rapidly (even if stimulation continues)
  • maximum tension
142
Q

more motor units can be recruited to increase muscle tension

A
  • when a motor neuron generates an action potential all of the muscle fibers it innervates will generate action potentials and contract
  • motor unit
  • each muscle fiber is innervated by only one motor neuron, but one motor neuron can innervate many muscle fibers
  • all of the muscle fibers within a motor unit have the same properties
  • different motor units within the same muscle may have different properties
  • whole motor unit belongs to one of the three twitch fiber groups
143
Q

motor unit

A

1 motor neuron and all of the muscle fibers it innervates

144
Q

slow twitch (ST, type 1)

A
  • rely primarily on oxidative phosphorylation
  • slow relatively weak contractions (myosin ATPase activity)
  • fatigue resistant
  • darker, smaller
  • large amounts of red myoglobin, numerous mitochondria, extensive capillary* blood supply compared to fast twitch
  • ex. slow walking, diaphragm, posture muscles
145
Q

fast twitch fibers

A
  • develop tension faster
  • split ATP more rapidly
  • pump Ca into sarcoplasmic reticulum more rapidly
  • develop tension faster
  • relax faster
  • 2 types: fast twitch oxidative glycolytic fiber (FOG, type2A), and fast twitch glycolytic fibers (FG, type 2/X)
146
Q

Fast twitch oxidative glycolytic fiber (FOG, type2A)

A
  • use oxidative glycolytic metabolism
  • fast, strong contractions
  • intermediate mitochondria and myoglobin content
  • medium size
  • can be more glycolytic or more oxidative (endurance) depending on training
  • fatigue resistant
  • ex. routine movements, walking
147
Q

fast twitch glycolytic fibers (FG or type 2B/X)

A
  • rely primarily on anaerobic glycolysis (few capillaries)
  • fast, very strong contractions
  • rapidly fatiguing
  • maximum force
  • larger (muscles look big)
  • paler
  • ex. sprinting, high jumping
148
Q

muscle fatigue

A
  • inability to maintain tension during periods of sustained, repetitive activation
  • occurs in fibers that use glycolytic metabolism to produce ATP
  • correlated with lactic acid production
149
Q

in motor unit, the motor neuron (not the muscle fiber) determines the timing and strength of a single twitch contraction

A

false

-the length of the sarcomere before contraction does determine strength of contraction

150
Q

proprioception

A
  • the sense of your bodys position, movement and effort
  • provided by proprioceptors
  • ex. muscle spindles (in skeletal muscles), golgi tendon organs (in tendons), joint receptors (in joint ligamets and capsules)
151
Q

muscle spindles

A
  • proprioception
  • in skeletal muscle
  • sense position
  • provide information about the length of the muscle and change in length
  • active all the time
  • small bundles of muscle fibers (intrafusal fibers), sensory receptors, sensory neurons and motor neurons that lie in parallel with the rest of the muscle (extrafusal fibers)
  • intrafusal muscle fibers maintain the sensitivity of the muscle spindle to stretch (not for tension)
  • fusiform- meaning they are tapered at both ends (football)
  • increase firing rate with lengthening in the muscle
152
Q

golgi tendon organs

A
  • proprioception
  • in tendons
  • sense load
  • sensory neuron
  • founds at the end of muscles (between muscle and tendon)
  • woven within the collagen fibers)
  • as load increases golgi tendon shortens
  • collagen pulls tight and squeezes the golgi -> fires action potential
  • give an idea how much muscle is contracting and how much tension
  • walking, chewing, writing, talking affect GTO impairment
  • specifically calibrates the amount of force you need (cant break teeth while eating)
153
Q

joint receptors

A
  • proprioception

- in joint and ligaments and capsules

154
Q

sensory neuron

A
  • senses stimulation
  • afferent- arrive
  • bring information to the spinal cord
155
Q

motor neurons

A
  • efferent- exits

- information exits the spinal cord

156
Q

proprioceptors

A
  • muscle spindles and golgi tendon organs are sensory receptors in muscle
  • sensory receptors in the muscle
157
Q

intrafusal

A

within the muscle

-maintain the sensitivity of the muscle spindle to stretch

158
Q

extrafusal

A

outside the muscle

159
Q

muscle spindles: length

A
  • provide information about the length of the muscle and change in length
  • some components of the muscle spindle response to actual length while some respond to change
  • change- shows huge increase
  • ex. tripping
160
Q

muscle action is ALWAYS to

A

contract

161
Q

Antagonist pairs

A

-muscles working against each other to move body parts in opposite directions

162
Q

earthworm

A
  • when the earth worm is stretching the circular muscle contracts
  • longitudinal muscle relaxes
  • similar to gut, peristalsis
163
Q

reflexes

A
  • responses to changes in the environment
  • usually serve a protective role (prevent injury)
  • more likely to be evoked with sudden, unexpected changes in the environment than with slow or anticipated changes
  • often result in coordinated movement of a joint (agonist and antagonist muscles are often involved)
  • muscle spindles, golgi tendon organs, and skin receptors (nocieptors) can elicit reflexes IF these receptors detect a sudden, unexpected change (sensory activity does not equal reflex)
  • usually inhibited
  • fewest number of synapses in the classes of movement (least complex)
  • dont require cognitive processing- neural pathways loop through the spinal cord and the brain is not required to generate a motor response
  • functional- restoring balance, pulling away hand from fire, quickly release tension if tension becomes too great
164
Q

monosynaptic relfex pathway

A
  • has a single synapse between the afferent and efferent neurons
  • stimulus -> regulator -> sensory neuron -> synapse with motor neuron -> efferent neuron -> skeletal muscle -> contraction
  • stretch reflex
165
Q

polysynaptic reflex

A
  • have two or more synapses
  • stimulus -> regulator -> sensory neuron -> synapse 1 -> interneuron -> synapse 2 -> efferent neuron -> skeletal muscle -> contraction
166
Q

postural reflex

A

-involve your vestibular system

167
Q

3 general classes of movement

A
  • reflexes
  • rhythmic- chewing
  • voluntary- reaching for something
  • increasing complexity
  • more synapses = more time
168
Q

flexion cross extensor reflex

A
  • removing a limb from painful stimulus
  • remove one leg from painful stimulus while balancing on the other
  • polysynaptic
  • 3 interneurons
    1. painful stimulus activates nocieptor (pain receptor) -> action potentials sent into spinal cord
    2. primary sensory neuron enters spinal cord and diverges
    3. one collateral activates ascending pathways for sensation (pain) and postural adjustment (shift in gravity)
    4. withdrawal reflex pulls foot away from painful stimulus
    5. crossed extensor reflex support body as weight shifts away from painful stimulus
  • excitatory pathways- synapse with hamstring muscles to contract and withdrawal leg -> on the other leg the it synapses with quad to contract to stand straight
  • inhibitory pathways- interneuron inhibits activity in quadriceps muscles to remove leg from stimulus -> on the other leg hamstrings are relaxed in order to stand straight
169
Q

stretch reflex- muscle spindle reflex

A
  • returning a limb to its original position if its unexpectedly moved
  • monosynpatic- fastest
  • muscle spindle reflex
  • entirely within the spinal cord
  • stretch that is sudden enough it may induce a reflex
  • ex. unexpectedly dropping a book into arms -> muscle stretches (arms move down) and biceps contract to catch
  • ex. tendon tap reflex- tricks into thinking the leg moved backward -> quadriceps contract ->leg swings forward (hamstring relax (antagonist))
170
Q

Loading reflex- golgi tendon refelx

A
  • polysynaptic
  • antagonist is not involved
  • prevents agonist from over exerting
  • extreme situation
  • carrying something so heavy
  • golgi tendon organ fires
  • synapses with inhibitory interneuron motor neuron is inhibited
  • muscle relaxes and load is dropped
171
Q

a motor neuron must release ACh into the synapse to depolarize both skeletal and cardiac muscle cells

A
  • this is true for skeletal
  • neurotransmitters are not necessary in electrical synapses (cardiac)
  • cardiac muscle cells have gap junction
  • in fact we dont need a motor neuron at all
172
Q

an action potential in any muscle fiber (skeletal, cardiac, smooth)

A
  • each skeletal muscle must be excited by a motor neuron

- this is only true for cardiac and some smooth

173
Q

one skeletal muscle contains

A

many sarcomeres

174
Q

an action potential in the terminal bouton of a motor neuron causes voltage gated Ca channels to open

A
  • graded potential in the terminal bouton

- propagates action potential

175
Q

stopping the cross bridge cycle in the rigor state

A
  • depletion of ATP (ATP cant bind)

- blocking the release of ADP

176
Q

muscle relaxation happens whenever actin myosin cross bridges break

A
  • false
  • cross bridges break all the time
  • they just dont happen at the same time
177
Q

an increase in action potential frequency in muscle spindles of the biceps (arm muscle) means that

A
  • muscle spindle reflex will occur- false, reflex does not occur unless there is high activity (rapid stretch in muscle)
  • the biceps muscle has lengthened- change in space
  • tension in the biceps muscle has increased- doesnt relate to tension (golgi tendon organ does)
  • gives information about your body in space

BIO 203 (5 decks)

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