Exam 3 Flashcards
Luigi Galvani
father of electrophysiology, connected lightning rod to the sciatic nerve of the leg of a frog, when lightning struck the rod the electrical current passed through the wire which caused the frog leg to contract
Bioelectricity
ability to pass an electrical current
How do like charges behave with each other?
repel
How do opposite charges behave with each other?
attract
What does the plasma membrane do and how does it do it?
regulates movements of ions with integral membrane proteins like transporters and channels
How is the membrane like a battery?
each type of battery has a different voltage just like excitable cells have different voltages from each other
How do we measure membrane potential?
voltmeter with recording lead and reference lead
Recording lead
is placed directly into the cell to measure the charge in that environment in the intracellular fluid at the inside face of the membrane
Reference lead
is placed in the surrounding interstitial fluid that measures the charge of the environment there
Voltmeter
calculates the difference in charge between two environments and that allows it to calculate the voltage
Voltage
is the potential inside the cell relative to the potential outside
What is the only way to maintain a concentration gradient?
ions are not distributed equally across the cell membrane
K+
higher concentration inside the cell
Na+
higher concentration outside the cell
Cl-
higher concentration outside the cell
Anions
higher concentration inside the cell
Ca2+
higher concentration outside the cell
How are membranes permeable to various ions?
they are permeable unequally, the membrane K+ is more permeable than Na+ at rest
What is the relationship between concentration gradients and electrostatic potentials?
Ions do follow a concentration gradient from higher to lower but this is only if the integral protein selects for that charge
Equilibrium potential
membrane potential at which the concentration gradient and electrical potential forces are equal and opposite
Equilibrium potential for K
no net flux of ion K across the membrane
Common misconception of membrane potential
small movements produce big changes in Vm (this is only true for the one part of the plasma membrane not the entire cell)
Nernst Equation
is used to calculate membrane potential if the cell is permeable to a single ion and is completely permeable
What does the Z in the nernst equation stand for?
For potassium and sodium, Z would be 1 since it is positive. For chloride, Z would be -1 since it is negative.
What does Z in the nernst equation tell us?
Z tell us that equilibrium potential is affected by charge, charge interactions
What does it mean if the equation is log(1)?
There are equal concentrations on both the inside and outside
What is potassium’s equilibrium potential?
-75mV, most negative
What is Na+ equilibrium potential?
58mV, most positive
What is Cl- equilibrium potential?
-59mV
Do equilibrium potentials change?
No except in labs or states of disease. This is because the charge cannot be changed without a nuclear reaction and homeostasis prevents major shifts in ion concentrations
What is the problem with the nernst equation?
cells are rarely permeable to just a single ion because one ion does not set the membrane potential
Steady state
this is NOT a movement of no ions instead it is a condition where all the ions moving have equal and opposite movements to each other
Membrane potential
the voltage that develops across the membrane from the movement of all permeable ions, is a steady state but not one that the net flux equals 0
Relationship between equilibrium potential and membrane potential
equilibrium potentials help create membrane potential (weighted average and the weight is the permeability of each ion)
Which ion have the highest permeability at rest? Lowest?
The highest is K+ while the lowest is Cl-
Can membrane potential be more positive than the most positive ion? Can it be more negative than the most negative ion?
no (cause of tug of war) because it has to fell between the floor and ceiling
Resting membrane potential
-70mV
Why is the resting membrane potential so close to potassium’s?
this is because the cell is more permeable to K+
GHK equation
is used to calculate the membrane potential and takes into account concentration gradients like nernst equation but also takes into account the permeability for each ion
If the permeability is set to 0 for all ions except one, what does that mean?
this means the cell is only permeable to 1 ion which brings us to the nernst equation so membrane potential and equilibrium potential would be the same
What can be done to change the membrane potential?
changing concentration (hard), changing permeability (easy)
Relationship between active and passive transport
concentration gradient disappears if the ions are continuously going from high to low so active transport is needed to maintain the gradient and membrane potential does not become 0
Na/K/ATPase
pump 3 sodium ions out of the cell while 2 potassium ions get pumped into the cell against their concentration gradient
Neurons
the basic unit of the nervous system, their job is to propagate signals
What does the nervous system depend on to function?
concentration gradients
Why is a neuron the longest living cell in the body?
It does not go through mitosis
How does a neuron regenerated itself when damaged?
stem cell differentiation process
How has much progress not been made with respect to neurons-degenerative diseases?
When neurons undergo stem cell differentiation, the neurons might not differentiate in the right spot or make the same connections with other cell types
4 major parts of neuron
dendrites, cell body (soma), axon, axon terminal
Dendrites
place of signal input, contain high densities of receptors since they are constantly receiving signals from external and internal environments
How do the dendrites look?
they are highly branched and highly overlapping
Multipolar neurons
many dendritic processes that are coming off of the cell body
Variations in dendrites
some have hundreds, some have 1 or 2, some have none at all
Cell body
also known as soma, contains organelles, nucleus, mitochondria, contains missile bodies
Missile bodies
have large amounts of ribosomes and they account for the large amount of protein synthesis that neurons have to do (protein synthesis happens anywhere, not only in soma)
Axon hillock
initial segment of axon that connects to the cell body
Axon
can be very short or long, some do not have axons at all, action potentials are sent through the axon
Axon terminal
important for forming synapses with other cell types (connections)
Axodendritic synapse
axon terminal connects to dendrites of another neuron, most common
Axo-axonic synapse
dendrite synapses with axon of another neuron
Passive Electrical Signals
a transient change in membrane potential that dissipates as it propagates in space and time
ex: graded/synaptic potential
Active electrical signals
a change in membrane potential that is maintained over a long distance
ex: action potential
Depolarization
positive change in membrane potential
Repolarization
returns to the resting membrane potential
Hyperpolarization
a membrane at rest which experiences a negative membrane potential
What do dendrites do?
the signal of input to the neuron
What does the soma do?
the place where signals are integrated
What does the axon hillock do?
this is where the action potential is generated
What does the axon do?
has the action potential being spread over large distances into the axon terminal
What does the axon terminal do?
this is where the synapses occurs and the signal gets relayed to the next cell which could be a neuron or some other cell type
What type of message does synapses send out?
chemical
What does the post-synaptic neuron need to receive the chemical message?
ligand-gated ion channels on its dendrites
What is the response to the neurotransmitters binding?
ion channels will open or close
Synaptic potential
the change in membrane potential due to the synapses, are also applied examples of GHK equation
Excitatory Postsynaptic potential (EPSP)
depolarization, could be produced by opening a sodium channel
Inhibitory Postsynaptic potential (IPSP)
hyperpolarization, could be produced by opening up a potassium channel
What are synaptic potentials?
graded and detrimental (they decrease their intensity over time and over distance from their starting point)
Graded potentials
refers to the fact that these changes in membrane potential can have a variable amplitude, can be very weak or very strong
Why are synaptic potentials detrimental?
when a neurotransmitter binds to a channel on the dendrites, ions are moving into or out of the channel through diffusion but only from that spot
Why does the change in membrane potential from an ion get weaker as it diffuses through the cell?
membrane potential is a very localized effect so graded potentials decrease in strength as they spread out in all directions from the point of origin
Why is the job of the soma so important?
they receive many EPSPs and IPSPs at once, and must try to make sense of these signals
How does a neuron undergo depolarization?
through summation of EPSPs, then an action potential can be produced
Summation
the process of adding up all of the graded or synaptic potentials
Why is summation needed?
a single membrane potential will not be the cause of an action potential because of limitations of diffusion
Threshold potential
the EPSPs needed to generate an action potential (-55mV)
Spatial summation
can occur due to the fact that channels that are close together can be activated at the exact same time
Temporal summation
channels open at the exact same time if they are simulated with high frequency
EPSP-IPSP cancellation
cancel each other out by working in opposite directions
Function of IPSPs
serve as a breaking mechanism for action potential and make sure action potentials only get produced when it is necessary
Action potential
a burst of electrical activity that rapidly propagates through the cell, it is not detrimental, cyclical events
Initiation of action potential
occurs at axon hillock because there is a high density of voltage-gated sodium channels in this region
What happens when the channel in a close state?
sodium ions close so sodium ion cannot enter the cell
What happens in an active state?
sodium ions can enter the cell
What happens in an inactive state?
sodium ion channels are closed on one side but open on other side so sodium ions cannot go through since no pore has been created
How does the Na+ ion channel a feedback loop?
depolarization opens a channel which causes more depolarization and that opens nearby voltage-gated channels bringing them to threshold and allows more sodium ions to come into the cell
What serves as the outside factor to turn the system off?
inactivation gate
Voltage-gated potassium channels
open more slowly than voltage-gated sodium channels and achieve their peak permeability during repolarization phases of the action potential
Leaky potassium channels
open all the time
Congenital Insensitivity to Pain (CIP)
unable to feel physical pain but still feel emotional pain, voltage-gated sodium channels are dysfunctional so pain neurons are not able to fire action potentials
Extreme pain disorders
slight touch causes pain, voltage-gated sodium channels cause action potentials to fire more rapidly
Lidocaine
inhibitors of voltage-gated sodium channels but are reversible
Refractory period
channels that are in the inactive state, prevents actions potentials from moving backward
Absolute refractory period
all of the voltage-gated sodium channels are inactivated so action potential cannot be continued
Relative refractory period
some of the voltage-gated sodium channels are inactivated but some are still open so action potential can still occur
Myelination
increases the speed of conduction by up to 100, contains fewer ion channels that require to move the action potential through the axon
Internodes
myelinated parts of the axon
Node of Ranvier
unmyelinated parts of the axon
What happens in a myelinated axon?
current is spread rapidly at internodes then pause to recharge before spreading rapidly again in the next internode,
Saltatory conduction
action potential appears to jump from node to node, do not like this term cause it is jumping over something which does not happen
Biggest problem with demyelinating diseases
neurons do not have enough channels to propagate the action potential through the internodes when the myelin is gone so the conduction efficiency starts to break down
Calcium
allows the vesicles to move to the presynaptic membrane and attach to snares
Snares
a family of proteins at the membrane
What happens to the neurotransmitters?
They are exocytosed into the synapse and ligand-gated channels on the post-synaptic dendrites can start the entire process over again
Relationship between calcium and action potential
as the sodium voltage-gated ion channels depolarize, it brings the calcium voltage-gated ion channels to threshold causing them to open and bringing calcium into the cell and have the vesicle dock and release the neurotransmitters
Tetrodotoxin
inhibits sodium voltage-gated ions channels
General properties of muscles
excitability, contractility (what action potential is used for), elasticity (does not lose membrane integrity), extensibility (shorten and extends)
Functions of muscles tissue
heat (as byproduct and maintaining thermal homeostasis), movement, posture
Myocyte Development
myosatellite cells go to myoblasts go to muscle fibers
Myosatellite cells
differentiation multipotent stem cell within muscle tissue
Myoblasts
immature muscle precursor
Muscle fibers
myoblasts that line up next to each other and form a tube-like structure, as known as myocytes
Skeletal muscle tissue
only multi-nucleated tissue (3 or more nuclei per cell), cylindrical shape, striations, densely packed tissue
Organization of muscles
comprised of a network of bundled fascicles
Fascicles
tube-like structures and is bundle of muscle fibers that is held together by connective tissue wrapper
Myofibrils
created from the arrangement of the contractile proteins inside the cell, contains many sarcomeres
Myogoblin
oxygen binding protein
Type 1 fibers
darkest red, have most myoglobin so can trap oxygen easier, produce more ATP and stay contracted for longer periods of time, slow twitch fibers
Type 2b fibers
lightest in color, have least amount of myoglobin, rely on anaerobic respiration and less efficient at producing ATP, fast fibers are used for short bursts of activity
Type 2a fibers
intermediate, have some myoglobin, have the ability to do limited amount of aerobic respiration
Myocytes
tend to be larger and thicker and more cylindrical (not like most cells), tend to cram as many myofibrils as possible into the cell, little cytoplasmic space, organelles are pushed into the sides of cell
Sarcoplasm
cytoplasm in muscle
Sarcolemma
plasma membrane in muscle
Sarcoplasmic Reticulum (SR)
endoplasmic reticulum (ER)
What makes up the sarcomere?
thick filament = myosin
thin filament = actin
elastic protein = titan
Sliding filament theory
actin slide across myosin towards the center of the sarcomere (oscillatory contraction), results in shortening of the H zone & I zone but the A-band does not change so the Z-lines move closer together
Proteins of the sarcomere
troponin and tropomyosin (regulatory), myosin and actin (contractile)
What is actin as a monomer?
G actin (standing for globular)
What is actin as a long chain?
F actin (standing for filamentous)
Tropomyosin
filamentous rope-like protein which blocks the myosin binding site on actin
Troponin
made up of 3 subunits (TnT, TnI, TnC), important for muscle contraction regulation
What happens at rest with the calcium?
with low calcium levels, tropomyosin blocks the myosin binding site on actin, which prevents binding
What happens when the calcium concentration inside the cell increases?
calcium binds to troponin and troponin allows the tropomyosin to be moved out of the binding site which makes it physically possible to cross bridges to form
What does all muscle cells need for muscle contraction?
calcium and energy (ATP)
The role of ATP in cross bridge formation
When ATP binds to the head of myosin, the myosin has low affinity for actin and cross bridges cannot form
The role of ADP in cross ridge formation
Myosin head is enzymatic so it can hydrolyze ATP to ADP which stay bound to myosin head. The myosin head then binds to actin since it is in cocked confirmation. Power stroke happens when phosphate is released and moves into low energy state
Cocked confirmation
myosin head twists into a high energy state
Rigor mortis
partially contracting or stiffening of muscles once a person dies, generally lasts between 18-36 hours, ends because of tissue breakdown
What is the cause of rigor mortis?
stops producing ATP after death so cross bridges between myosin and actin cannot be broken, calcium gets released into cytosol and allows new cross bridge to form
Cold shortening of meat
myoctyes contract in response to cold temperature to generate heat for the body, electrocuting at high voltages solved this problem by depleting calcium
How does the cell release calcium?
an action potential needs to be fired
Neuromuscular junction
the synapse between a muscle fiber and a motor neuron
Motor units
a single motor neuron and the muscle fibers it controls
All-or-none principle
a single motor unit controls only a few muscle fibers in a given muscle so most muscles contain multiple motor units
Acetylcholine
a neurotransmitter in NMJ that binds to acetylcholine receptors in the motor end plate and starts the graded potential
Acetylcholine receptor
ligand-gated ion channel and selects for positive charges, allows sodium to come into the cell
End plate potential
diffuses away in both directions from the entry point into different regions of sarcolemma which might make the action potential
Acetylcholine esterase
breaks down acetylcholine so it terminates the signal
Curane
blocks the binding site for acetylcholine which blocks all postsynaptic events in NMJ, induces muscle paralysis
Eserine
inhibits of acetylcholine esterase and can be used to amplify synaptic transmission, used to reverse the effects of sedatives
Succinylcholine
used to paralyze muscle before surgery, binds and activates the acetylcholine receptor, cannot be broken down by acetylcholine esterase
Myasthenia Gravis
autoimmune disorder leading to the destruction of the acetylcholine, might not have enough end plate potential to start an action potential since they do not have enough acetylcholine receptors
Lamber-Eaton Myasthenic Syndrome (LEMS)
mutation in voltage gated calcium channel inside of the axon terminal of the motor neuron which means less calcium enters the cell so less acetylcholine is released
Guillain-Barre Syndrome
autoimmune disorder where the immune system attacks the glial cells that myelinate the internodes and conduction velocity slows down so action potential might not reach the axon terminal, vaccines could cause this by activating the immune system but low
Excitation Contraction Coupling
muscles are excitable cells specialized to transduce electrical energy into a contractile force
Role of T-tubules
allow for rapid ion exchange in isolated regions of myocyte
Triad
membrane of sarcoplasmic reticulum is connected to T-tubules
Steps in excitation contraction coupling
begins with excitation, action potential travels from every membrane segment, it eventually enters the t-tubule and action potential causes DHG to change conformation and RYR allows the calcium to go into the cytosol from SR
How does the calcium return to its resting levels?
active transporter SERCA that uses ATP to move calcium against the gradient and back into the SR
Muscle tension
force created by muscle
Load
weight that opposes contraction
Contraction
creation of tension in the muscle
Relaxation
release of tension in the muscle
Relationship between length and tension
describes the optimal length of sarcomere, stretched sarcomere have difficult time making the cross bridges while shortened sarcomere have no room to slide the filament
Unfused tetanus
tension builds up unevenly
Fused tetanus
when the frequency of stimulation becomes fast enough the graph starts to smooth out and available to get to maximum tension
Fatigue
they become weak and lose their ability to generate tension
Depletion theory
the muscle fiber eventually runs out of the resources it needs to keep the contraction
Creatine
a protein used to store ATP for later use by adding phosphate to make creatine phosphate and later the muscle can remove the phosphate to get the ATP back
What does a weak contraction mean?
small number of motor units
Muscle tone
the continued steady, low level of contraction that stabilizes joints and maintains general muscle health
How to generate more force?
recruitment - motor units stimulated depending on need
Dystonia
a muscle disorder that creates a lack of muscle coordination
Blepharospasm
spasm of the muscle surrounding the tear duct
Parkinson’s disease
severe dystonia that revolves around the brain - muscle contraction where we do not have the intend to and inability to contract muscles that we want to contract, can be able to recruit the intended muscle with the voluntary motor units and overpower the ones that do not work
Botox
blocks release of acetylcholine by inhibiting them from getting released into the synapse
Isotonic contractions
creates movement so force is greater than load, result in a change in muscle size
Isometric contractions
creates tension so load is greater than force
