×
Log in to StudySoup
Get Full Access to UTEP - ZOOL 4380 - Study Guide
Join StudySoup for FREE
Get Full Access to UTEP - ZOOL 4380 - Study Guide

Already have an account? Login here
×
Reset your password

UTEP / Animal Science / ANSC 4380 / Can myofibers facilitate action potential conductance throughout the

Can myofibers facilitate action potential conductance throughout the

Can myofibers facilitate action potential conductance throughout the

Description

Exam 2 Study Aid


Myofibers can facilitate action potential conductance throughout the?



Electrical Signals in Neurons

∙ Property of excitability that gives neurons the ability to store, recall and distribute information ∙ During depolarization charge difference between the inside and outside of the cell membrane  decreases, membrane potential becomes less negative

∙ Either positively charged ions entering the cell or negatively charged ions moving out of the cell  can make the inside of the cell membrane less negatively charged causing depolarization ∙ During hyperpolarization membrane potential becomes more negative

∙ Either negatively charged ions entering the cell or positively charged ions moving out of the cell  can make the inside of the cell membrane more negative causing hyperpolarization ∙ During repolarization cell membrane returns to the resting membrane potential Signals in the Dendrites and Cell Body


Motor neuron axon termini are located in a?



∙ Binding of neurotransmitter to a specific ligand-gated receptor causes ion channels in membrane  to open or close, changing permeability of membrane

∙ Permeability alters the membrane potential and causes and electrical signal ∙ In dendrites and cell bodies of neurons the electrical signals are called graded potentials Graded potentials vary in magnitude

∙ Graded potentials vary in magnitude depending on strength of stimulus

∙ The amplitude of the graded potential directly reflects strength of the incoming stimulus ∙ Graded potentials can either hyperpolarize or depolarize cell, depending on type of ion channel  that’s opened/closed

∙ Opening Na+ or Ca2+ channels will depolarize a neuron


Removal of neurotransmitter depends on what proccesses?



Don't forget about the age old question of What is the most common type of lava?

∙ Opening K+ or Cl- channels will hyperpolarize a neuron

Graded potentials are short-distance signals

∙ When neurotransmitter binds to a ligand-gated Na+ channel, the channel open and Na+ ions  move into the cell

∙ Na+ entry causes a local depolarization in a small area of the membrane surrounding the opened  channel

∙ Positive charge then spreads along the inside of the membrane causing depolarization ∙ Called electrotonic current spread

∙ Extent of this depolarization decreases as it moves farther and farther from the opened channels ∙ Action potentials are used to transmit information across distances of more than a few  millimeters If you want to learn more check out When was jacopo tintoretto painted stealing the body?

∙ Action potentials are triggered by the net graded potential at the membrane of the axon hillock ∙ Graded potential causes the membrane potential at the axon hillock to depolarize beyond the  threshold potential, the axon will “fire” an action potential

∙ If the membrane potential at the axon hillock does not reach the threshold potential the axon will  not initiate an action potential

Figure 4.7: Subthreshold and suprathreshold potentials: the resting potential of most neurons is around -70mV and  the threshold potential is -55mV. A: Subthreshold graded potentials (less than +15mV) don’t trigger an action potential. B: graded potentials that are at or above the threshold potential (greater than +15mV) trigger an action  potential We also discuss several other topics like How government raises revenue?

∙ Depolarizing graded potential is called an excitatory potential because it makes an action potential  more likely to occur by bringing the membrane potential closer to threshold potential ∙ Hyperpolarizing graded potential makes an action potential less likely to occur, which is an  inhibitory potential

Graded potentials are integrated to trigger action potentials

∙ Graded potentials from different sites can interact with each other to influence the net change in  membrane potential at the axon hillock (spatial summation)If you want to learn more check out What are the nonvolatile nonelectrolyte solutions?

Don't forget about the age old question of What is the best definition of elasticity?
We also discuss several other topics like What is the mean reaction time?

Figure 4.8: Spatial Summation

∙ Depolarization that occur at two slightly different times can also combine to determine the net  change in membrane potential at the axon hillock (temporal summation)

Figure 4.9: Temporal Summation

Signals in the Axon

∙ Action potentials can be transmitted across long distances without degrading and differ from  graded potentials in many respects

∙ Action potentials typically have three phases

∙ Depolarization phase

o Triggered when the membrane potential at the axon hillock reaches threshold o Once reaches threshold, the adjacent axonal membrane quickly depolarizes ∙ Repolarization phase

o Membrane potential rapidly returns to the resting membrane potential

o Following repolarization membrane potential becomes even more negative  than the resting membrane potential

o May approach the K+ equilibrium potential

∙ After-hyperpolarization phase

o Typically lasts between 2-15 msec

o Membrane returns to the resting membrane potential

Voltage-gated channels shape action potential

∙ Opening and closing of voltage-gated ion channels cause the characteristic phases of the action  potential

∙ Changes in membrane potential change the shape of voltage-gated ion channels, allowing ions to  move across the membrane

∙ When membrane potential at axon hillock approaches the threshold potential voltage-gated Na+  channels in the axon hillock begin to open, changing the permeability of the membrane to Na+  ions, allowing Na+ ions to move across the membrane

∙ Probability of a given voltage-gated Na+ channel being open depends on the size of the graded  potential

∙ Excitatory graded potential that depolarizes the membrane toward the threshold potential  increases the probability that a voltage-gated Na+ channel will be open

∙ At the threshold potential more voltage-gated Na+ channels will be open tan when the axon  hillock is at the resting membrane potential increasing permeability of the membrane to Na+ ∙ Na+ influx from the first voltage-gated channels to open in response to the graded potential  further depolarizes the local region of the membrane

∙ further increasing the probability that voltage-gated Na+ channels will open o causing even more voltage-gated Na+ channels to open

o further increasing the permeability of the membrane allowing even more Na+  ions to enter the cell

∙ Action potentials generally occur in the axon not in the cell body or dendrites of a neuron ∙ Voltage-gated Na+ channels close, terminating the depolarization phase of the action potential ∙ Threshold depolarization of the membrane at the axon hillock increases probability that voltage gated K+ channels will open

∙ When voltage-gated K+ channels open the permeability of the membrane to K+ ions increases ∙ K+ ions leave the cell in response to their electrochemical driving force  

∙ Making the intracellular side of the membrane more negative

∙ Causes repolarization phase of the action potential

Voltage-gated Na+ channels have two gates

∙ To open, Na+ channel undergoes a conformation change that opens an activation gate allowing  Na+ ions to move across the membrane

∙ Opening of activation gate increases permeability of the membrane to Na+ ∙ As Na+ enters the cell more and more voltage-gated Na+ channels open and axonal membrane  potential rapidly becomes less negative, depolarizing cell toward equilibrium potential for Na+ ∙ As membrane potential approaches the equilibrium potential for Na+ the electrochemical  gradient that acts as a driving force for Na+ movement decreases and Na+ entry slows

∙ Meanwhile time-dependent conformational change occurs in the channel, closing the inactivation  gate

∙ With the inactivation gate closed, no more Na+ can enter the cell, terminating the depolarization  phase of the action potential

∙ In response to changes in the membrane potential caused by the actions of the voltage-gated K+  channels, the inactivation gate resets and the channel returns to its initial conformation ready to  initiate another action potential

Action potentials transmit signals across long distances

∙ Action potentials are often described as all or nothing phenomena because once an action  potential has been initiated it always proceeds to conclusion

∙ Action potential in one part of the axon triggers other action potentials in other action potentials  in adjacent areas of the axonal membrane

∙ In neurons the first action potential at the axon hillock causes another action potential farther  down the axon and so on down to the axon terminal

∙ The last axon potential at the axon terminal is identical to the first action potential at the axon  hillock

∙ Action potentials can be conducted across long distances without decaying

Vertebrate motor neurons are myelinated

∙ Axons of vertebrate motor neurons are wrapped in an insulating layer of myelin ∙ Specialized lipid-rich cells (Schwann cells) form the myelin sheath by wrapping in a spiral pattern  around the axon of the neuron

∙ Several Schwann cells may wrap long axons separated by areas of exposed axonal membrane  called nodes of Ranvier that contain high densities of voltage-gated channels ∙ Myelinated regions of the axons are the internodes

∙ Action potentials only occur in the nodes of Ranvier

∙ Action potential appears to jump from node to node along the axon

∙ Electrotonic currents can travel farther with less degradation trough the internodes than through  an equivalent region of unmyelinated axon

∙ Electrontonic current spread is much faster than generating an action potential

Figure 4.14: Structure of the myelin sheath

Axons conduct action potentials unidirectionally

∙ Action potentials occur only in the downstream direction

∙ Absolute refractory period prevents backward transmission of action potentials ∙ Also prevents summation of action potentials

∙ The absolute and relative refractory periods prevent retrograde transmission of action potentials

Figure 4.10: the phases of a typical action potential. A: changes in membrane potential during an action potential. B:  changes in membrane permeability during and action potential

Action potential frequency carries information

∙ Action potentials carry information by changing frequency rather than amplitude Figure 4.15: Frequency of action potentials

Signals Across the Synapse

∙ Cell that transmits the signal is referred to as the presynaptic cell

∙ Cell receiving the signal is called postsynaptic cell

∙ Space between the presynaptic and postsynaptic cell is referred to as the synaptic cleft

∙ Synapse between a motor neuron and a skeletal muscle cell is termed the neuromuscular junction Intracellular Ca2+ regulates neurotransmitter release

∙ When an action potential reaches membrane of presynaptic axon terminal of neurotransmitter  junction, resulting depolarization triggers opening of voltage-gated Ca2+ channels on cell  membrane of axon terminal

∙ Concentration of Ca2+ inside neuron is much lower than the concentration outside ∙ Both concentration and electrical gradients favor movement of Ca2+ into cell ∙ Resulting increase Ca2+ concentration inside axon terminal acts as signal to neurotransmitter  containing synaptic vesicles

∙ Readily releasable pool of vesicles is located at the active zone of synapse, bound to docking  proteins at synaptic membrane, ready to release contents by exocytosis

∙ Storage pool consists of vesicles bound cytoskeleton and not docked to membrane ∙ Ca2+ signal causes vesicles from readily releasable pool to fuse with plasma membrane and  release contents by regulated exocytosis

∙ Ca2+ signal also causes vesicles from storage pool to move to active zone of plasma membrane  and bind to docking proteins, ready for release following subsequent action potentials ∙ Because each vesicle contains many molecules of neurotransmitter the amount of  neurotransmitter a neuron releases increases in a step fashion, each corresponding to contents of  a vesicle, rather than smoothly graded fashion

∙ Called quantal release of neurotransmitter

Figure 4.16: Events of signal transmission at a chemical synapse

Action potential frequency influences neurotransmitter release

∙ Amount of neurotransmitter released at synapse is related to frequency of action potentials at  axon terminal

∙ Weak signals cause fewer synaptic vesicles to release contents

∙ Strong signals cause more synaptic vesicles to release contents

∙ After arrival of a single action potential at axon terminal, Ca2+ enters cell through activated  voltage-gated Ca2+ channels

∙ Ca2+ is quickly bound up by intracellular buffers or removed from cytoplasm by Ca2+ ATPaes,  keeping intracellular Ca2+ concentration low and limiting release of neurotransmitter ∙ When action potentials arrive at axon terminal at high frequency the processes of removing Ca2+  from cell can’t keep up with the influx of Ca2+ through activated channels, and intracellular Ca2+  concentration increases

∙ Increase provides stronger signal for exocytosis

∙ Signal intensity that was coded by action potential frequency is translated into differences in  amount of neurotransmitter released by neuron

Acetylcholine is the primary neurotransmitter at the vertebrate neuromuscular junction ∙ Vertebrate motor neurons release the neurotransmitter acetylcholine into synapse ∙ ACh synthesis occurs in axon terminal in a reaction catalyzed by the enzyme choline acetyl  transferase

Signaling is terminated by acetylcholinesterase

∙ Acetylcholinesterase removes ACh from its receptor, breaking ACh down into choline and acetate ∙ Acetylcholinesterase plays important role in regulating strength of the signal to the postsynaptic  cell by regulating the concentration of neurotransmitter at the synapse

Figure 4.17: Synthesis and recycling of acetylcholine (ACh) at synapse

Postsynaptic cells express specific receptors

∙ Postsynaptic cells detect neurotransmitters using specific cell-surface receptors ∙ When a neurotransmitter binds to its receptor the receptor changes shape ∙ This change in shape of receptor acts as a signal in target cell

∙ Skeletal muscles cells express a class of receptor called nicotinic ACh receptors

∙ Have ability to bind to nicotine

∙ Ligand-gated ion channels

∙ When ACh binds to nicotinic ACh receptor, receptor changes shape opening a pore in middle of  receptor that allows ions to cross membrane

∙ Nicotinic ACh receptors contain a relatively nonselective channel permeable to Na+, K+ and to  lesser extent Ca2+

∙ Graded potentials in postsynaptic cell caused by these channels are Na+ dominated ions due to  high driving force for Na+ influx relative to K+ efflux

∙ ACh binding to nicotinic receptors on skeletal muscle cells always cause rapid excitatory  postsynaptic potential because the resulting influx of Na+ depolarizes the postsynaptic muscle cell Neurotransmitter amount and receptor activity influence signal strength ∙ Both the amount of neurotransmitter present in the synapse and the number of receptors on the  postsynaptic cell influence the strength of signal in target cell

∙ Small amounts of neurotransmitter provoke relatively small responses in postsynaptic cell ∙ As neurotransmitter concentration increases the response of postsynaptic ell increases up to point  that all available receptors are saturated

∙ Concentration of neurotransmitter in synapse is result of balance between rate of  neurotransmitter release from presynaptic cell and removal of neurotransmitter from synapse ∙ Amount of neurotransmitter released from presynaptic cell is largely a function of frequency of  action potentials at presynaptic axon terminal

∙ Removal of neurotransmitter depends on three main processes

∙ Neurotransmitters can simply diffuse passively out of synapse

∙ Surrounding cells can also take up neurotransmitter

∙ Enzymes present in synapse can degrade neurotransmitters

∙ Very low density of receptors on postsynaptic membrane, neurotransmitter weak response ∙ Very high density of receptors on postsynaptic membrane, neurotransmitter larger response Contraction and Relaxation in Vertebrate Striated Muscle

∙ Muscle activity initiated by excitation: Depolarization of muscle plasma membrane (sarcolemma) ∙ Translation of excitatory signal at the sarcolemma into a stimulation is called excitation contraction coupling (EC coupling)

∙ Combination of physical and chemical changes within myocyte that elevate Ca2+  concentration

∙ Increase in intracellular Ca2+ activates the action-myosin machinery to induce contraction Relaxation occurs when the Ca2+ falls to resting levels, which is only possible when sarcolemma  repolarizes

Excitation and EC Coupling in Vertebrate Striated Muscle

∙ Excitation in most striated muscles occurs when depolarization of the sarcolemma induces an  increase in cytosolic Ca2+ to trigger contractions

Muscles are excited by an action potential

∙ Resting membrane potential of sarcolemma is about -70mV

∙ Upon activation muscles experience rapid depolarization followed by repolarization and  hyperpolarization

∙ Depolarization is induced when Na+ channels are opened

∙ Inward rush of Na+ causes rapid reduction in membrane potential

∙ Voltage-sensitive Ca2+ channels open allowing the influx of Ca2+ into cell from extracellular space ∙ After a period, Na+ and Ca2+ channel begin to close and voltage-sensitive K+ channels open  causing cell to repolarize

∙ Striated muscles can’t be depolarized again until the repolarization is nearly complete ∙ The window of insensitivity is called the effective refractory period

∙ Muscle cell can’t be induced to contract again by normal physiological regulators Myogenic muscle cells spontaneously depolarize

∙ Most common examples of myogenic myocytes are from the vertebrate heart ∙ Pacemaker cells transmit their electrical signal throughout the heart and cause other  cardiomyocytes to depolarize and contract

∙ Pacemaker cells are unusual in that they show and unstable resting membrane potential ∙ Once pacemaker cell membrane depolarizes to a critical voltage, voltage-sensitive Ca+ channels  open to initiate the action potential

∙ Action potential of the pacemaker cells induces an action potential in the myocytes to which they  are connected through gap junctions

Neurogenic muscle is excited by neurotransmitters

∙ Most vertebrate skeletal muscles are neurogenic muscles

∙ Receive signals from a motor neuron

∙ Motor neuron axon termini are located in a region of the sarcolemma called motor end plate

Figure 5.25

T-tubules enhance action potential penetration into the myocyte

∙ Myofibers can facilitate action potential conductance throughout the muscle with the help of  extensive sarcolemmal invagination called transverse tubules (T-tubules)

∙ When the sarcolemma depolarizes the action potential follows the T-tubules into the muscle fiber

∙ T-tubule system is extensive in large or quick-contracting muscles

Figure 5.26: T-tubules

Ca2+ for contraction comes from intracellular or extracellular stores

∙ Regulation of Ca2+ transient during muscle contraction involves many transporters and cellular  compartments

∙ L-type Ca2+ channels are open for a Long period with Large conductance

∙ T-type Ca2+ channels are open Transiently with Tiny conductance

∙ L-type Ca2+ channels are also known as dihydropyridine receptors (DHPR) ∙ Muscle endoplasmic reticulum (sarcoplasmic reticulum, SR) has own Ca2+ channel (RyR) and Ca2+  ATPase

∙ Rate of Ca2+ movement into the muscle cell upon depolarization depends on factors related to  structure and activity of DHPR

∙ Structure of DHPR influences electrical properties such as voltage sensitivity and open time, or  alter the sensitivity of the channel to regulatory proteins and ligands

∙ In some situations, Ca2+ delivery through DHPR is sufficient to induce contraction ∙ In most striated muscles the Ca2+ delivery through DHPR is either too slow/minor to achieve the  contraction threshold

∙ DHPR and RyR physically interact with each other to couple sarcolemmal depolarization with SR  Ca2+ release

∙ Upon activation of DHPR, the RyR opens even if no Ca2+ ions move through the DHPR ∙ This pattern of EC coupling: depolarization-induced Ca2+ release

DHPR activation induces Ca2+ release from SR

∙ In striated muscle the SR frequently has enlargements, terminal cisternae, that increase the  capacity for Ca2+ storage and localize it to discrete regions within muscle cell ∙ Terminal cisternae ensure rapid Ca2+ delivery

∙ Muscles are able to accumulate Ca2+ to very high levels within the SR

∙ Most Ca2+ is bound to calsequestrin which is another member of the Ca2+ - binding family ∙ During excitation SR releases Ca2+ stores through Ca2+ channel called ryanodine receptor (RyR) ∙ Cardiac muscle uses a process called Ca2+-induced Ca2+ release to link DHPR and RyR activation ∙ Once DHPR open, extracellular Ca2+ enters cell

∙ Local Ca2+ can increase in the small space between sarcolemma and terminal cisternae

Page Expired
5off
It looks like your free minutes have expired! Lucky for you we have all the content you need, just sign up here