membrane potentials that act as signals two types of signals graded potentials oincoming...
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Membrane Potentials That Act as Signals Two types of signals
• Graded potentials
o Incoming short-distance signals
o Short-lived, localized changes in membrane potential
o Depolarizations or hyperpolarizations
o Graded potential spreads as local currents change the membrane potential of adjacent regions
• Action potentials
o Long-distance signals of axons
Graded potentials
Figure 11.9a
Depolarizing stimulus
Time (ms)
Insidepositive
Insidenegative
Restingpotential
Depolarization
(a) Depolarization: The membrane potentialmoves toward 0 mV, the inside becoming less negative (more positive). Increases the probability of producing a nerve impulse.
Graded Potential: Depolarization
Stimulus causes gated ion channels to open
• E.g., receptor potentials, generator potentials, postsynaptic potentials
Magnitude varies directly (graded) with stimulus strength
Decrease in magnitude with distance as ions flow and diffuse through leakage channels
Figure 11.9b
Hyperpolarizing stimulus
Time (ms)
Restingpotential
Hyper-polarization
(b) Hyperpolarization: The membranepotential increases, the inside becomingmore negative. Decreases the probability of producing a nerve impulse.
Graded Potential: Hyperpolarization
Figure 11.10c
Distance (a few mm)
–70Resting potential
Active area(site of initialdepolarization)
(c) Decay of membrane potential with distance: Because current is lost through the “leaky” plasma membrane, the voltage declines with distance from the stimulus (the voltage is decremental ). Consequently, graded potentials are short-distance signals.
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Membrane Potentials That Act as Signals Two types of signals
• Graded potentials
o Incoming short-distance signals
o Short-lived, localized changes in membrane potential
o Depolarizations or hyperpolarizations
o Graded potential spreads as local currents change the membrane potential of adjacent regions
• Action potentials
o Long-distance signals of axons
Action Potential (AP) Brief reversal of membrane potential with a
total amplitude of ~100 mV
Occurs in muscle cells and axons of neurons
Does not decrease in magnitude over distance
Principal means of long-distance neural communication
Actionpotential
1 2 3
4
Resting state Depolarization Repolarization
Hyperpolarization
1 1
2
3
4
Time (ms)
ThresholdMem
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Figure 11.11 (1 of 5)
• Only leakage channels for Na+ and K+ are open
• All gated Na+ and K+ channels are closed
Depolarizing local currents open voltage-gated Na+ channels
Na+ influx causes more depolarization
•Na+ channel slow inactivation gates close
•Membrane permeability to Na+ declines to resting levels
•Slow voltage-sensitive K+ gates open
•K+ exits the cell and internal negativity is restored
•Some K+ channels remain open, allowing excessive K+ efflux
•This causes after-hyperpolarization of the membrane (undershoot)
Anatomy of an Action Potential
Actionpotential
1
2
3
4
Na+ permeability
K+ permeability
Rela
tive m
em
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erm
eab
ility
Channel gating (online animation)
Figure 11.12a
Voltageat 0 ms
Recordingelectrode
(a) Time = 0 ms. Action potential has not yet reached the recording electrode.
Resting potential
Peak of action potential
Hyperpolarization
Voltage Change at Point in Neuron as Action Potential Passes By
Figure 11.12b
Voltageat 2 ms
(b) Time = 2 ms. Action potential peak is at the recording electrode.
Voltage Change at Point in Neuron as Action Potential Passes By
Figure 11.12c
Voltageat 4 ms
(c) Time = 4 ms. Action potential peak is past the recording electrode. Membrane at the recording electrode is still hyperpolarized.
Voltage Change at Point in Neuron as Action Potential Passes By
Action potential online
Threshold Stimulus
Subthreshold stimulus—weak local depolarization that does not reach threshold
Threshold stimulus—strong enough to push the membrane potential toward and beyond threshold (Membrane is depolarized by 15 to 20 mV)
AP is an all-or-none phenomenon—action potentials either happen completely, or not at all
All action potentials are alike and are independent of stimulus intensity
Figure 11.13
Threshold
Actionpotentials
Stimulus
Time (ms)
Stimulus
Absolute refractoryperiod
Relative refractoryperiod
Time (ms)
Depolarization(Na+ enters)
Repolarization(K+ leaves)
After-hyperpolarization
ARP
Time from the opening of the Na+ channels until the resetting of the channels
Ensures that each AP is an all-or-none event
Enforces one-way transmission of nerve impulses
RRP
•Most Na+ channels have returned to their resting state
•Some K+ channels are still open
•Repolarization is occurring
Threshold for AP generation is elevated
Exceptionally strong stimulus may generate an AP
Figure 11.14
Refractory Periods
Figure 11.15
Size of voltage
Voltage-gatedion channel
Stimulus
Myelinsheath
Stimulus
Stimulus
Node of Ranvier
Myelin sheath
(a) In a bare plasma membrane (without voltage-gatedchannels), as on a dendrite, voltage decays becausecurrent leaks across the membrane.
(b) In an unmyelinated axon, voltage-gated Na+ and K+
channels regenerate the action potential at each pointalong the axon, so voltage does not decay. Conduction is slow because movements of ions and of the gatesof channel proteins take time and must occur beforevoltage regeneration occurs.
(c) In a myelinated axon, myelin keeps current in axons(voltage doesn’t decay much). APs are generated onlyin the nodes of Ranvier and appear to jump rapidlyfrom node to node, about 30 times faster than a bare axon.
1 mm
AP Velocity a Function of Axon Diameter and Myelination
Saltatoryconduction
Continuous conduction
Multiple Sclerosis (MS) Nature
• An autoimmune disease that mainly affects young adults
• Symptoms: visual disturbances, weakness, loss of muscular control, speech disturbances, and urinary incontinence
• Myelin sheaths in the CNS become nonfunctional scleroses
• Shunting and short-circuiting of nerve impulses occurs
• Impulse conduction slows and eventually ceases
Treatment
• Some immune system–modifying drugs, including interferons and Copazone:
o Hold symptoms at bay
o Reduce complications
o Reduce disability
Nervous Tissue and Function Function of the Nervous System
Organization (Structural and Functional)
Supporting Cells of the Nervous System
Anatomy of a Neuron
Classification of Neurons by Function
Graded and Action Potentials
Myleination and MS
Reflexes
Synapses
EPSPs and IPSPs
Neurotransmitters
The Reflex Arc
Types of Reflexes and Regulation Autonomic reflexes
• Smooth muscle regulation
• Heart and blood pressure regulation
• Regulation of glands
• Digestive system regulation
Somatic reflexes
• Activation of skeletal muscles
Nervous Tissue and Function Function of the Nervous System
Organization (Structural and Functional)
Supporting Cells of the Nervous System
Anatomy of a Neuron
Classification of Neurons by Function
Graded and Action Potentials
Myleination and MS
Reflexes
Synapses
EPSPs and IPSPs
Neurotransmitters
Two Kinds of Synapses
Electrical Synapses
• Less common than chemical synapses
• Neurons are electrically coupled (joined by gap junctions)
• Communication is very rapid, and may be unidirectional or bidirectional
• Are important in:
o Embryonic nervous tissue
o Some brain regions
Chemical Synapses
• Specialized for the release and reception of neurotransmitters
• Typically composed of two parts
o Axon terminal of the presynaptic neuron, which contains synaptic vesicles
o Receptor region on the postsynaptic neuron
How Neurons Communicate at Synapses
Irritability – ability to respond to stimuli
Conductivity – ability to transmit an impulse`
SodiumPotassium pump (online animation)
Events at the Synapse (online animation)
Narrated synapse (online)
Figure 11.17, step 1
Action potentialarrives at axon terminal.
Chemical synapsestransmit signals fromone neuron to anotherusing neurotransmitters.
Ca2+
Synapticvesicles
Axonterminal
Mitochondrion
Postsynapticneuron
Presynapticneuron
Presynapticneuron
Synapticcleft
Ca2+
Ca2+
Ca2+
Postsynapticneuron
1
Figure 11.17, step 2
Action potentialarrives at axon terminal.
Voltage-gated Ca2+
channels open and Ca2+
enters the axon terminal.
Chemical synapsestransmit signals fromone neuron to anotherusing neurotransmitters.
Ca2+
Synapticvesicles
Axonterminal
Mitochondrion
Postsynapticneuron
Presynapticneuron
Presynapticneuron
Synapticcleft
Ca2+
Ca2+
Ca2+
Postsynapticneuron
1
2
Figure 11.17, step 3
Action potentialarrives at axon terminal.
Voltage-gated Ca2+
channels open and Ca2+
enters the axon terminal.
Ca2+ entry causesneurotransmitter-containing synapticvesicles to release theircontents by exocytosis.
Chemical synapsestransmit signals fromone neuron to anotherusing neurotransmitters.
Ca2+
Synapticvesicles
Axonterminal
Mitochondrion
Postsynapticneuron
Presynapticneuron
Presynapticneuron
Synapticcleft
Ca2+
Ca2+
Ca2+
Postsynapticneuron
1
2
3
Figure 11.17, step 4
Action potentialarrives at axon terminal.
Voltage-gated Ca2+
channels open and Ca2+
enters the axon terminal.
Ca2+ entry causesneurotransmitter-containing synapticvesicles to release theircontents by exocytosis.
Chemical synapsestransmit signals fromone neuron to anotherusing neurotransmitters.
Ca2+
Synapticvesicles
Axonterminal
Mitochondrion
Postsynapticneuron
Presynapticneuron
Presynapticneuron
Synapticcleft
Ca2+
Ca2+
Ca2+
Neurotransmitterdiffuses across the synapticcleft and binds to specificreceptors on thepostsynaptic membrane.
Postsynapticneuron
1
2
3
4
Figure 11.17, step 5
Ion movement
Graded potential
Binding of neurotransmitteropens ion channels, resulting ingraded potentials.
5
Figure 11.17, step 6
Reuptake
Enzymaticdegradation
Diffusion awayfrom synapse
Neurotransmitter effects are terminatedby reuptake through transport proteins,enzymatic degradation, or diffusion awayfrom the synapse.
6
Figure 11.17
Action potentialarrives at axon terminal.
Voltage-gated Ca2+
channels open and Ca2+
enters the axon terminal.
Ca2+ entry causesneurotransmitter-containing synapticvesicles to release theircontents by exocytosis.
Chemical synapsestransmit signals fromone neuron to anotherusing neurotransmitters.
Ca2+
Synapticvesicles
Axonterminal
Mitochondrion
Postsynapticneuron
Presynapticneuron
Presynapticneuron
Synapticcleft
Ca2+
Ca2+
Ca2+
Neurotransmitterdiffuses across the synapticcleft and binds to specificreceptors on thepostsynaptic membrane.
Binding of neurotransmitteropens ion channels, resulting ingraded potentials.
Neurotransmitter effects areterminated by reuptake throughtransport proteins, enzymaticdegradation, or diffusion awayfrom the synapse.
Ion movement
Graded potentialReuptake
Enzymaticdegradation
Diffusion awayfrom synapse
Postsynapticneuron
1
2
3
4
5
6
SodiumPotassium pump (online animation)
Events at the Synapse (online animation)
Narrated synapse (online)
Nervous Tissue and Function Function of the Nervous System
Organization (Structural and Functional)
Supporting Cells of the Nervous System
Anatomy of a Neuron
Classification of Neurons by Function
Graded and Action Potentials
Myleination and MS
Reflexes
Synapses
EPSPs and IPSPs
Neurotransmitters
Excitatory Synapses and EPSPs Neurotransmitter binds to and opens chemically gated channels that allow simultaneous flow of Na+ and
K+ in opposite directions
Na+ influx is greater that K+ efflux, causing a net depolarization
Excitatory postsynaptic potential (EPSP) helps trigger AP at axon hillock if EPSP is of threshold strength and opens the voltage-gated channels
Figure 11.18a
An EPSP is a localdepolarization of the postsynaptic membranethat brings the neuroncloser to AP threshold. Neurotransmitter binding opens chemically gated ion channels, allowing the simultaneous pas-sage of Na+ and K+.
Time (ms)
Threshold
Stimulus
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Inhibitory Synapses and Inhibitory Postsynaptic Potential (IPSPs)
Neurotransmitter binds to and opens channels for K+ or Cl–
Causes a hyperpolarization (the inner surface of membrane becomes more negative)
Reduces the postsynaptic neuron’s ability to produce an action potential
Figure 11.18b
An IPSP is a localhyperpolarization of the postsynaptic membraneand drives the neuron away from AP threshold. Neurotransmitter binding opens K+ or Cl– channels.
Time (ms)
Threshold
Stimulus
Mem
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V)
Nervous Tissue and Function Function of the Nervous System
Organization (Structural and Functional)
Supporting Cells of the Nervous System
Anatomy of a Neuron
Classification of Neurons by Function
Graded and Action Potentials
Myleination and MS
Reflexes
Synapses
EPSPs and IPSPs
Neurotransmitters
Chemical Classes of Neurotransmitters Acetylcholine (Ach) (Mostly excitory in CNS, PNS if prolonged prod. tetanus (with nerve
gases), receoptors destroyed in myasthenia gravis)
• Released at neuromuscular junctions and some ANS neurons
• Synthesized by enzyme choline acetyltransferase
• Degraded by the enzyme acetylcholinesterase (AChE)
Biogenic amineso Catecholamines
Dopamine (“Feeling good” CNS neurotransmitter, uptake blocked by cocaine, excitory or inhibitory) , norepinephrine (NE), and epinephrine
o Indolamines
Serotonin (Roles in sleep, appetite, nausea, mood; blocked by seritonin-specific reuptake inhibitors (SSRIs) like Prozac and LSD, enhanced by ecstasy (3,4-Methylenedioxymethamphetamine)), histamine
• Broadly distributed in the brain; play roles in emotional behaviors and the biological clock
Amino acids include:
o GABA—Gamma ()-aminobutyric acid (inhibitory brain NT augmented by alcohol, benzodiazepine-valium)
o Glutamate (excitory in CNS, causes stroke when overreleased, overstimulation of neurons) , Glycine, Aspartate
Peptides (neuropeptides) include:
o Substance P, endorphins, somatostatin, cholecystokinin
Purines such as ATP
Gases and lipids
• NO, CO, Endocannabinoids