Exam 2 ZOOL 4380
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This 13 page Study Guide was uploaded by Tiffany Schweda on Saturday March 12, 2016. The Study Guide belongs to ZOOL 4380 at University of Texas at El Paso taught by DR. ZAINEB AL-DAHWI in Spring 2016. Since its upload, it has received 135 views. For similar materials see Vertebrate Physiology in Animal Science and Zoology at University of Texas at El Paso.
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Date Created: 03/12/16
Exam 2 Study Aid 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 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 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 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 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) 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 Ca - binding family During excitation SR releases Ca2+ stores through Ca2+ channel called ryanodine receptor (RyR) 2+ Cardiac muscle uses a process called Ca -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
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