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Membrane Potential
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Membrane Potential
Is difference in charge across membranes
Results in part from presence of large anions being trapped inside cell Diffusable cations
such as K+ are attracted into cell by anions
Na+ is not permeable and is actively transported out
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Equilibrium Potential Describes voltage across cell membrane if only 1 ion could
diffuse If membrane permeable only
to K+, it would diffuse until it reaches its equilibrium potential (Ek) K+ is attracted inside by
trapped anions but also driven out by its concentration gradient
At K+ equilibrium, electrical and diffusion forces are = and opposite
Inside of cell has a negative charge of about -90mV
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Resting Membrane Potential (RMP)
Is membrane voltage of cell not producing impulses RMP of most cells is –65 to –85 mV RMP depends on concentrations of ions inside and out
And on permeability of each ionAffected most by K+ because it is most permeable
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Some Na+ diffuses in so RMP is less negative than EK+
Resting Membrane Potential (RMP) continued
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Summary of Processes that Affect the Resting Membrane Potential
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Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Chapter 7LectureOutline
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Electrical Activity in Axons
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Resting Membrane Potential (RMP)
At rest, all cells have a negative internal charge and unequal distribution of ions: Results from:
Large cations being trapped inside cellNa+/K+ pump and limited permeability keep Na+
high outside cellK+ is very permeable and is high inside cell
Attracted by negative charges inside
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Excitability
Excitable cells can discharge their RMP quickly By rapid changes in permeability to ions Neurons and muscles do this to generate and
conduct impulses
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Membrane Potential (MP) Changes
Measured by placing 1 electrode inside cell and 1 outside
Depolarization occurs when MP becomes more positive
Hyperpolarization: MP becomes more negative than RMP
Repolarization: MP returns to RMP
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Membrane Ion Channels
MP changes occur by ion flow through membrane channels Some channels are normally open; some closed
K+ leakage channels are always open Closed channels have molecular gates that can be
openedVoltage-gated (VG) channels are opened by
depolarization VG K+ channels are closed in resting cellsNa+ channels are VG; closed in resting cells
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Model of a Voltage-gated Ion Channel)
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Action Potential
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The Action Potential (AP)
Is a wave of MP change that sweeps along the axon from soma to synapse
Wave is formed by rapid depolarization of the membrane by Na+
influx; followed by rapid repolarization by K+
efflux
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Mechanism of Action Potential Depolarization:
At threshold, VG Na+ channels open Na+ driven inward by its electrochemical gradient This adds to depolarization, opens more channels
Termed a positive feedback loop Causes a rapid change in MP from –70 to +30 mV
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Mechanism of Action Potential continued
Repolarization: VG Na+ channels close; VG K+ channels open Electrochemical gradient drives K+ outward Repolarizes axon back to RMP
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Depolarization and repolarization occur via diffusion Do not require active transport After an AP, Na+/K+ pump extrudes Na+, recovers K+
Mechanism of Action Potential continued
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Mechanism of Action Potential continued
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When MP reaches threshold an AP is irreversibly fired Because positive
feedback opens more and more Na+
channels Shortly after
opening, Na+ channels closeand become
inactivated until repolarization
APs Are All-or-None
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Increased stimulus intensity causes more APs to be fired Size of APs remains constant
How Stimulus Intensity is Coded
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Refractory Periods
Absolute refractory period: Membrane cannot
produce another AP because Na+ channels are inactivated
Relative refractory period occurs when VG K+ channels are open, making it harder to depolarize to threshold
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Axonal Conduction
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Cable Properties
Refer to how axon’s properties affect its ability to conduct current
Includes high resistance of cytoplasm Resistance
decreases as axon diameter increases
Current leaks out through ion channels
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Conduction in an Unmyelinated Axon After axon hillock reaches
threshold and fires AP, its Na+ influx depolarizes adjacent regions to threshold Generating a new AP
Process repeats all along axon
So AP amplitude is always same
Conduction is slow
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Conduction in Myelinated Axon
Ions can't flow across myelinated membrane Thus no APs
occur under myelin
and no current leaksThis increases
current spread
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Conduction in Myelinated Axon continued
Gaps in myelin are called Nodes of Ranvier APs occur only at nodes
VG Na+ channels are present only at nodes
Current from AP at 1 node can depolarize next node to threshold Fast because APs
skip from node to node
Called saltatory conduction
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Synaptic Transmission
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Synapse
Is a functional connection between a neuron (presynaptic) and another cell (postsynaptic)
There are chemical and electrical synapses Synaptic transmission at chemical synapses is via
neurotransmitters (NT) Electrical synapses are rare in NS
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Electrical Synapse Depolarization flows from
presynaptic into postsynaptic cell through channels called gap junctions Formed by connexin
proteins Found in smooth and
cardiac muscles, brain, and glial cells
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Chemical Synapse
Synaptic cleft separates terminal bouton of presynaptic from postsynaptic cell
NTs are in synaptic vesicles
Vesicles fuse with bouton membrane; release NT by exocytosis
Amount of NT released depends upon frequency of APs
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Synaptic Transmission
APs travel down axon to depolarize bouton Open VG Ca2+ channels in bouton Ca2+ is driven in by electrochemical gradient
Triggers exocytosis of vesicles; release of NTs
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Neurotransmitter Release
Action potentials reach the axon terminal Ca2+ enters axon terminal via voltage gated channels Ca2+ binds to sensor protein in cytoplasm Ca2+ -protein complex stimulates fusion and exocytosis
of neurotransmitterNeurotransmitter is released from the vesicles
into synapse
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Synaptic Transmission continued
Neurotranmitter diffuses across cleft Binds to receptor proteins on postsynaptic
membraneOpening chemically-regulated ion channels
Depolarizing channels cause EPSPs (excitatory postsynaptic potentials)
Hyperpolarizing channels cause IPSPs (inhibitory postsynaptic potentials)
These affect VG channels in postsynaptic cell
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Synaptic Transmission continued
EPSPs and IPSPs summate
If MP in postsynaptic cell reaches threshold at the axon hillock, a new AP is generated axon hillock has
many VG channels and is site where APs are normally initiated
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Synaptic Transmission continued
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Acetylcholine (ACh)
Most widely used NT Used in brain and ANS; used at all neuromuscular
junctions Has nicotinic and muscarinic receptor subtypes
These can be excitatory or inhibitory
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Ligand-Gated Channels
Contain both a NT receptor site and an ion channel Open when ligand (NT) binds
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Nicotinic ACh Channel
Formed by 5 polypeptide subunits
2 subunits contain ACh binding sites Opens when 2 AChs
bind Permits diffusion of
Na+ into and K+ out of postsynaptic cell
Inward flow of Na+ dominates
Produces EPSPs
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G Protein-Coupled Channels
NT receptor is not part of the ion channel Is a 1 subunit membrane polypeptide Activates ion channel indirectly through G-proteins
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Muscarinic ACh Channel
Binding of 1 ACh activates G-protein cascade which affects gated K+ channels Opens some, causing hyperpolarization Closes others, causing depolarization
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Acetylcholinesterase (AChE)
Inactivates ACh, terminating its action; located in cleft
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Neurotransmitters
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Acetylcholine in the PNS
Cholinergic neurons use acetylcholine as NT The large synapses on skeletal muscle are termed end
plates or neuromuscular junctions (NMJ) Produce large EPSPs called end-plate potentials
Open VG channels beneath end plateCause muscle contraction
Curare blocks ACh action at Neuromuscular Junction
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Monoamine NTs
Primarily active in the CNS Include serotonin, norepinephrine and dopamine Serotonin is derived from tryptophan Norepinephrine and dopamine are derived from
tyrosine Called catecholamines
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Serotonin
Involved in regulation of mood, behavior, appetite and cerebral circulation
LSD is structurally similar SSRIs (serotonin-specific reuptake inhibitors) are
antidepressants e.g., Prozac, Zoloft, Paxil, Luvox Block reuptake of serotonin, prolonging its action
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Dopamine
There are 2 major dopamine systems in brain Nigrostriatal dopamine system originates in the
substantia nigra and is involved in motor controlDegeneration of this system causes Parkinson's
disease Mesolimbic dopamine system is involved in behavior
and emotional rewardMost addictions activate this systemOveractivity contributes to schizophrenia
Which is treated by anti-dopamine drugs
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Norepinephrine (NE)
Used in PNS and CNS In PNS is a sympathetic NT In CNS affects general level of arousal
Amphetamines stimulate NE pathways
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Amino Acids NTs
Glutamic acid and aspartic acid are major CNS excitatory NTs
Glycine is an inhibitory NT Opens Cl- channels which hyperpolarize Strychnine blocks glycine receptors
Causes spastic paralysis GABA (gamma-aminobutyric acid) is most common NT
in brain Inhibitory, opens Cl- channels These degenerate in Huntington’s disease (see Ch
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Polypeptide NTs (neuropeptides)
Cause wide range of effects Many are neuromodulators
Involved in learning and neural plasticity Most neurons release a classical and polypeptide NT
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Gaseous NTs
NO and CO are gaseous NTs Act through cGMP second messenger system NO causes smooth muscle relaxation
Viagra increases NO In some cases it may act as a retrograde NT
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