Post on 26-May-2015
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Neurons: Cellular and Network Properties
Chapter 8
Figure 8.2-2 ESSENTIALS – Neuron Anatomy
Parts of a Neuron
Nucleus
Dendrites
Inputsignal
Cellbody
Integration Output signal
Axonhillock
Axon (initialsegment)
Myelin sheath Postsynapticneuron
Presynapticaxon terminal
Synapticcleft
Postsynapticdendrite
Synapse: Theregion where anaxon terminalcommunicateswith itspostsynaptictarget cell
– Cell Body=Soma– Dendrites: receive incoming signals– Axons: carry outgoing signals
The Organization of the Nervous System
• 2 Parts: CNS and PNS• Stimulus-sensor-input
signal-integrating center-output signal-target-response
• PNS: Efferent and Sensory (Afferent)
• Efferent divides into Autonomic and Somatic
• Autonomic: Sympathetic and Parasympathetic
Neuron Anatomy• Classified either structural or functional• Structural: # of axons from cell body• Function: sensory (afferent), interneurons,
efferent• Afferent nerves=sensory nerves• Efferent nerves=motor nerves• Both=mixed nerves• Dendritic spines
https://www.ipmc.cnrs.fr/~duprat/neurophysiology/video.htm
http://www.youtube.com/watch?v=s9-fNLs-arc
Functional Categories
Structural Categories
Sensory Neurons
Pseudounipolar Bipolar
Somatic senses
Dendrites
Neurons forsmell and vision
Axon
Schwanncell
Pseudounipolarneurons have asingle processcalled the axon.During development,the dendrite fusedwith the axon.
Bipolar neuronshave tworelatively equalfibers extendingoff the centralcell body.
Figure 8.2e ESSENTIALS – Neuron Anatomy
Cells of Nervous System (NS): Axons Transport
• Slow axonal transport– Moves material by axoplasmic (cytoplasmic) flow at 0.2–
2.5 mm/day
• Fast axonal transport– Moves organelles at rates of up to 400 mm/day (~15 in)– Forward (or anterograde) transport: from cell body to axon
terminal – Backward (or retrograde) transport: from axon terminal to
cell body
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GLIAL CELLS
Peripheral Nervous System
are found in
contains
form
secrete
Schwann cells Satellitecells
Myelin sheaths
Neurotrophicfactors
Supportcell bodies
Glial Cells PNS
• Glial cells of the PNS• Schwann Cells• Satellite Cells:
non-myelinating Schwann cells, supportive cells around ganglia (group of cell bodies in PNS).
• group of cell bodies in CNS =nucleus
Glial Cells: CNS
GLIAL CELLS
Central Nervous System
Astrocytes
are found in
contains
act as form
create take up secrete help form provide
Ependymalcells
Microglia (modifiedimmune cells)
Oligodendrocytes
Barriersbetween
compartments
Source ofneural
stem cells
K+, water,neurotransmitters
Neurotrophicfactors
Blood-brain
barrier
Substratesfor ATP
production
Scavengers Myelin sheaths
Figure 8.5b ESSENTIALS – Glial Cells
Glial Cells of the Central Nervous System
Section of spinal cord
Interneurons Ependymalcell
Microglia
Astrocyte
CapillaryOligodendrocyteMyelin (cut)Node
Axon
Figure 8.5c ESSENTIALS – Glial Cells
Each Schwann Cell Forms Myelin Arounda Small Segment of One Axon.
Cell body
1–1.5 mm
Schwann cell
Node of Ranvier is a section ofunmyelinated axon membranebetween two Schwann cells.
Myelin consistsof multiple layersof cell membrane.Axon
Figure 8.6
PERIPHERAL NEURON INJURY
When an axon is cut, thesection attached to thecell body continues to live.
The section of the axon distal to the cut begins to disintegrate.
Site of injury
Connective tissue Myelin
Proximal axonDisintegrating
distal axon
Under some circumstances,the proximal axon mayregrow through the existingsheath of Schwann cellsand reform a synapse withthe proper target.
• Describes the membrane potential that a single ion would produce if the membrane were permeable to only that ion
• Membrane potential is influenced by– Concentration gradient of ions– Membrane permeability to those ions
– GHK: Predicts membrane potential that results from the contribution of all ions that can cross the membrane
• Resting membrane potential is determined by the combined contribution of the concentration gradient X membrane permeability for each ion
Electrical Signals: Nernst Equation and GHK
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Resting Membrane Potential
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A&P FlixTM: Resting Membrane Potential
Electrical Signals: Ion Movement
• Resting membrane potential determined primarily by– K+ concentration gradient– Cell’s resting permeability to K+, Na+, and Cl–
• 4 major types of channels in most neurons: Na+ channels, K+ channels, Ca2+ channels, and Cl- channels
• conductance: the ease at which the ion flows through a channel• Gated channels control ion permeability
– Mechanically gated– Chemically gated– Voltage-gated
• Threshold voltage varies from one channel type to another (Ex. Voltage gated channels that we think of as “leak” channel)
© 2013 Pearson Education, Inc.
Unfigure 8.3 page 250
Time (msec)
Resting membranepotential difference (Vm)
Vm
depolarizes Vm
hyperpolarizes
Mem
bra
ne p
ote
nti
al (m
V)
−20
+20
−60
−100
0
16
– Voltage changes across the membrane can be classified as either graded potentials or action potentials
– Graded potentials :– vary in their strength– local or travel over very short distances,– lose their strength as they travel– if they are strong enough they can initiate an action
potential– Action Potential:
– very brief large depolarizations– travel a long distance thru the neuron without losing
strength– function is to signal rapidly over long distances
Graded Potential and Action Potential
Figure 8.7a ESSENTIALS – Graded Potentials
Graded Potentials Reflect Stimulus Strength
• Local current flow is a wave of depolarization that moves through the cell
• Graded potentials lose strength as they move through the cell due to– Current leak: membrane has open leak channels that allow positive
charges to leak out– Cytoplasmic resistance: cytoplasm provides resistance to the flow of
electricity
• If strong enough, graded potentials reach the trigger zone• efferent and interneurons it is in the axon hillock and initial
segment• sensory neurons it is near the receptor where dendrites join axon
• Excitatory (graded potential) versus inhibitory (hyperpolarization)• Threshold usually around -55 mV
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Figure 8.7b ESSENTIALS – Graded Potentials
Time
−70mV
−70mV
−70mV
−55
−55
−55
−40
−40
−40
Time
Time
Stimulus
Graded potentialbelow threshold
Stimulus
Triggerzone
No actionpotential
Synapticterminal
Cellbody
Axon
Subthreshold Graded Potential
A graded potential starts above threshold (T) at its initiation point butdecreases in strength as it travels through the cell body. At the trigger zone,it is below threshold and therefore does not initiate an action potential.
Action Potentials Travel Long Distances
• Conduction is the high-speed movement of a action potential along an axon
• All-or-none
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Figure 8.7c ESSENTIALS – Graded Potentials
Time
−70mV
−70mV
−70mV
−55
−55
−55
−40
−40
−40
Time
Time
Stimulus
Graded potentialabove threshold
T
T
T
Triggerzone
Stimulus
Actionpotential
Suprathreshold Graded Potential
A stronger stimulus at the same point on the cell body creates agraded potential that is still above threshold by the time it reachesthe trigger zone, so an action potential results.
Figure 8.8
CONDUCTION OF AN ACTION POTENTIAL
The conduction of an action potential down an axon is similar to energy passed alonga series of falling dominos. In this snapshot, each domino is in a different phase of falling. In the axon,each section of membrane is in a different phase of the action potential.
A wave of electrical current passes down the axon.
Trigger zone
Direction of conduction
Action potential
Electrodes have beenplaced along the axon.
Membrane potentialsrecorded simultaneouslyfrom each electrode.
Time
Simultaneous recordings show that each section ofaxon is experiencing a different phase of the action potential.
Mem
bra
ne p
ote
nti
al (m
V)
Table 8.3 Comparison of Graded Potential and Action Potential in Neurons
Threshold
Mem
bra
ne p
ote
nti
al (m
V)
PNa
PNa
PK
PK
+30
−10
+10
0
−30
−50
−70
−90
0 1 2 3 4
Depolarizing stimulus
Membrane depolarizes to threshold.Voltage-gated Na+ and K+
channels begin to open.
Rapid Na+ entry depolarizes cell.
Na+ channels close and slowerK+ channels open.
K+ moves from cell to extracellularfluid.
K+ channels remain open andadditional K+ leaves cell, hyperpolarizing it.
Voltage-gated K+ channels close,less K+ leaks out of the cell.
Cell returns to resting ion permeabilityand resting membrane potential.
2
3
4
5
6
7
8
9
Resting membrane potential1
– Conduction of action potential requires, voltage gated Na+ channels and voltage gated K+ channels, and leak channels to restore resting membrane potential
– Action Potential (3 Phases): rising phase (Na+ channels, Na +equilib of +30mv=peak, falling phase (K+ channels open, slow), and after-hyperpolarization phase
– Action Potential= Na+ (enters cell) K+ (leaves cell)
– Does not change relative conc. of Na+ or K+, only 1 in every 100,000 K+ leaves the cell
Action Potential: Flow of Na+ and K+
Figure 8.9-2 ESSENTIALS – The Action Potential
K+
Na+
Time (msec)
Ion p
erm
eabili
ty
0 1 2 3 4
Voltage
Resting Rising Falling After-hyperpolarization Resting
A&P FlixTM: Generation of an Action Potential
Figure 8.10a (1 of 5)
−55−70
+30
0mV
Na+
ICF
ECF
Inactivationgate
Activationgate
At the resting membrane potential, the activation gatecloses the channel.
Figure 8.10b (2 of 5)
−55−70
+30
0mV
Na+
Depolarizing stimulus arrives at the channel. Activation gate opens.
Figure 8.10c (3 of 5)
−55−70
+30
0mV
Na+
With activation gate open, Na+ enters the cell.
Figure 8.10d (4 of 5)
−55−70
+30
0mV
Na+
Inactivation gate closes and Na+ entry stops.
Figure 8.10e (5 of 5)
−55−70
+30
0mV
Na+
During repolarization caused by K+ leaving the cell, the twogates reset to their original positions.
Refractory Period
0 1 2 3 4Time (msec)
REFRACTORY PERIODS FOLLOWING AN ACTION POTENTIAL
A single channel shown during a phase means that the majority ofchannels are in this state.
Where more than one channel of aparticular type is shown, thepopulation is split between the states.
Bothchannels
closedNa+ channels reset to original position
while K+ channels remain openNa+ channels close and
K+ channels open
Na+
channelsopen
Bothchannels
closed
Na+ and K+ channels
K+ K+ K+
+30
0
−55
−70
High High
Increasing
Zero
Absolute refractory period Relative refractory periodDuring the absolute refractory period, nostimulus can trigger another action potential.
During the relative refractory period, only a larger-than- normal stimulus can initiate a new action potential.
Action potential
Na+
K+
High
Low
Ion
perm
eab
ility
Mem
bra
ne p
ote
nti
al (m
V)
Exc
itab
ility
– Action potential cannot be triggered no matter how large the stimulus in absolute refractory period, a second action potential cannot occur until the first is finished (action potentials cannot overlap or travel backwards)
– relative refractory period follows the absolute refractory period, in which some Na+ channels gates have reset and K+ channels are still open. It would require a large stimulus for another action potential
Figure 8.13
LOW CURRENT FLOW
When a section of axon depolarizes, positive chargesmove by local current flow into adjacent sections of thecytoplasm. On the extracellular surface, current flowstoward the depolarized region.
Depolarized sectionof axon
Electrical Signals: Trigger Zone
• Graded potential enters trigger zone• Voltage-gated Na+ channels open, and Na+ enters
axon• Positive charge spreads along adjacent sections of
axon by local current flow• Local current flow causes new section of the
membrane to depolarize• Loss of K+ repolarizes the membrane• The refractory period prevents backward
conduction
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Figure 8.14
CONDUCTION OF ACTION POTENTIALS
Trigger zone
AxonA graded potential abovethreshold reaches thetrigger zone.
Voltage-gated Na+ channelsopen, and Na + enters the axon.
Na+
Positive charge flows into adjacentsections of the axon by local current flow.
Na+
Local current flow from theactive region causes new sectionsof the membrane to depolarize.
K+
Refractoryregion
Active region Inactive region
The refractory period prevents backwardconduction. Loss of K+ from thecytoplasm repolarizes the membrane.
FIGURE QUESTION
Match the segments of theneuron in the bottom frame withthe corresponding phrase(s):
(a) proximal axon (blue)(b) absolute refractory period (pink)(c) active region (yellow)(d) relative refractory period (purple)(e) distal inactive region (blue)
1. rising phase of action potential2. falling phase of action potential3. after-hyperpolarization4. resting potential
Electrical Signals: Speed of Action Potential
• Speed of action potential in neuron influenced by1. Diameter of axon :Larger axons are faster
2. Resistance of axon membrane to ion leakage out of the cellMyelinated axons are faster
Saltatory conduction between nodes of Ranvier, voltage gated Na+ channels
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Figure 8.15
LARGE AXONS OFFER LESS RESISTANCE.
FIGURE QUESTIONA squid giant axon is 0.8 mm in diameter. Amyelinated mammalian axon is 0.002 mmin diameter. What would be the diameter of amammalian nerve if it contained 100 axons thatwere each the size of a squid giant axon?(Hint: The area of a circle is π × radius2, andπ = 3.1459.)
Smallerunmyelinatedaxons
Squid giantaxon
One giant axon froma squid is 0.8 mm in
diameter
Figure 8.16a (1 of 2)
Action potentials appear to jump from one node of Ranvier to the next. Only the nodes have voltage-gated Na+ channels.
Node Node
Na+
Node of Ranvier Myelin sheath
Depolarization
Figure 8.16b (2 of 2)
Na+
Degeneratedmyelin sheath
Current leakslows conduction
In demyelinating diseases, conduction slows when current leaks out of the previously insulated regions between the nodes.
A&P FlixTM: Propagation of an Action Potential
Blood Potassium Levels
Normal plasma [K+] is 3.5 – 5 mM.
Threshold
Stimulus
Time
Mem
bra
ne p
ote
nti
al (m
V)
When blood K+ is in thenormal range (normokalemia),a subthreshold gradedpotential does not firean action potential.
−55
−70
0
Figure 8.17b (2 of 4)
Threshold
StimulusMem
bra
ne p
ote
nti
al (m
V)
−55
−70
0
Normal plasma [K+] is 3.5 – 5 mM.
In normokalemia, asuprathreshold (above-threshold) stimulus willfire an action potential.
Figure 8.17c (3 of 4)
Threshold
Stimulus
−55
−70
0
Hyperkalemia depolarizes cells.
Hyperkalemia, increasedblood K+ concentration,brings the membrane closerto the threshold. Now astimulus that would normallybe subthreshold cantrigger an action potential.
Threshold
Stimulus
−55
−70
0
Hypokalemia hyperpolarizes cells.
Hypokalemia, decreasedblood K+ concentration,hyperpolarizes the membraneand makes the neuron lesslikely to fire an actionpotential in response to astimulus that would normallybe above the threshold.
The EK of −90 mV is based on ECF [K+] = 5 mM and ICF [K+] = 150 mM.Use the Nernst equation to calculate EK when ECF [K+] is (a) 2.5 mM and (b) 6 mM.
Figure 8.17d (4 of 4)
FIGURE QUESTION
Cell-to-Cell: Neurons Communicate at Synapses
• Electrical synapses pass electrical signals through gap junctions (CNS, glial, cardiac muscle, smooth muscle, pancreatic beta cells)
• Chemical synapses use neurotransmitters that cross synaptic clefts (most nervous system), electrical signal is converted to a chemical signal that crosses the synaptic cleft
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Cell-to-Cell: Neurocrine Receptors
• Ionotropic receptors– Receptor-channels– Mediate rapid responses– Alter ion flow across membranes
• Metabotropic receptors– G protein–mediated receptors– Mediate slower responses– Some open or close ion channels
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Cell-to-Cell: Neurocrines
• Seven classes by structure– Acetylcholine (choline and acetyl coenzyme A)– Amines– Amino acids– Peptides– Purines– Gases– Lipids
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Receptors
• Cholinergic receptors– Nicotinic on skeletal muscle, in PNS and CNS
– Monovalent cation channels → Na+ and K+
– Muscarinic in CNS and PNS – G protein–coupled receptors
• Adrenergic Receptors– Alpha and Beta– G protein–coupled receptors (different secondary messenger
systems)
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Amines
• Derived from single amino acid• Tyrosine
– Dopamine– Norepinephrine is secreted by noradrenergic neurons– Epinephrine
• Tryptophan– Serotonin (5-Hydroxytryptamine or 5-HT)
• Histadine– Histamine
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Amino Acids
• Glutamate: Excitatory - CNS• Aspartate: Excitatory- brain• GABA: Inhibitory-brain• Glycine
– Inhibitory - spinal cord, opens Cl- channels allowing Cl- to enter the cell
– May also be excitatory– AMPA receptors: ligand-gated monovalent cation channels, bind
glutamate and channel opens– NMDA receptors: bind glutamate and change in membrane
potential causes open channel (non-selective for K+, Na+, and Ca2+)
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Other Neurotransmitters
• Peptides– Substance P and opioid peptides
• Purines – AMP and ATP
• Gases – NO, CO, and H2S
• Lipids – Eicosanoids– cannnabinoid receptors
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Table 8.4 Major Neurocrines
Figure 8.18 A chemical synapse
Schwann cell
Axon terminal
Mitochondrion
Synaptic cleftMuscle fiber
Vesicles with neurotransmitter
Cell-to-Cell: Events at the Synapse
• Neurotransmitter synthesis, storage, release, and termination of action• Synthesis occurs at soma and axon terminal• Storage occurs at axon terminals and released via exocytosis • Release: when depolarization reaches axon terminal, voltage gated
Ca2+channels open, allowing Ca2+ into the cell, Ca2+ binds to proteins that cause exocytosis
• Termination: rapid removal or inactivation of NT from cleft• diffusion• inactivation due to enzymes (acetylcholinesterase)• transport (dopamine aromatic transporter)
• Kiss-and-run pathway
– Vesicles fuse with membrane at the fusion pore
– Neurotransmitters pass through a channel
– Vesicles pull back from fusion pore
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Figure 8.19a ESSENTIALS – Synaptic Communication
Neurotransmitter Release
Docking protein
Action potentialarrives at
axon terminal
Postsynaptic cell
Synaptic vesiclewith neurotransmittermolecules
Synapticcleft
ReceptorVoltage-gatedCa2+ channel Cell
response
Ca2+
An action potential depolarizesthe axon terminal.
The depolarization opens voltage-gated Ca2+ channels, and Ca2+
enters the cell.
Calcium entry triggers exocytosisof synaptic vesicle contents.
Neurotransmitter diffuses acrossthe synaptic cleft and binds withreceptors on the postsynaptic cell.
Neurotransmitter binding initiatesa response in the postsynapticcell.
Figure 8.19b ESSENTIALS – Synaptic Communication
Neurotransmitter Termination
Bloodvessel
Enzyme
Postsynaptic cell
Synapticvesicle
Axonterminal of
presynaptic cell
Glialcell
Neurotransmitters can be returnedto axon terminals for reuse ortransported into glial cells.
Enzymes inactivateneurotransmitters.
Neurotransmitters can diffuseout of the synaptic cleft.
Neurotransmitter action terminates when the chemicals are broken down,are taken up into cells, or diffuse away from the synapse.
Figure 8.20
SYNTHESIS AND RECYCLING OF ACETYLCHOLINE
Mitochondrion
Acetyl CoA CoA
Enzyme Acetylcholine
Synapticvesicle
ACh
ACh
ACh
ACh
ChA
Ch
Axonterminal
Na+ Choline Cholinergicreceptor
Postsynapticcell
Acetate Acetylcholinesterase (AChE)
Acetylcholine (ACh) is madefrom choline and acetyl CoA.
In the synaptic cleft ACh is rapidlybroken down by the enzymeacetylcholinesterase.
Choline is transported back intothe axon terminal by cotransportwith Na +.
Recycled choline is used to makemore ACh.
Stronger Stimulus releases more NT
Strong stimulus causes more action potentials and releases more neurotransmitter.
Threshold
20
0
−20−40−60−80M
em
bra
ne p
ote
nti
al
(mV
)
Moreneurotransmitterreleased
Axonterminal
Cell bodyActionpotential
Gradedpotential
Trigger zone
Stimulus Receptor
Afferentneuron
Weak stimulus releases little neurotransmitter.
Threshold
20
0
−20−40−60−80M
em
bra
ne p
ote
nti
al
(mV
)Neurotransmitter
release
57
Communication and Integration of Neural Information
– divergent:branches– convergent:group of presynaptic input neurons to
smaller group of post synaptic neurons– Synaptic plasticity: ability of the nervous system to
change activity at synapse, facilitation or depression
Figure 8.22a ESSENTIALS – Divergence and Convergence
In a divergent pathway, one presynaptic neuron branchesto affect a larger number of postsynaptic neurons.
Figure 8.22b ESSENTIALS – Divergence and Convergence
In a convergent pathway, many presynaptic neurons provideinput to influence a smaller number of postsynaptic neurons.
60
Post-Synaptic Responses– Slow synaptic responses are a result NT bind to GPCR and
secondary messenger systems. This may open or close ion channels. Any change in membrane potential result from these alternation in ion flow are called slow synaptic potentials (bc it is a slower way to open/close ion channels, it often has long lasting effects).
– fast synaptic potentials: always associated with the opening of ion channels, begins quickly and lasts only a few millisec.
– EPSP: synaptic potential is depolarizing it is called excitatory postsynaptic potential, likely to cause action potential
– IPSP: inhibitory postsynaptic potential: hyperpolarization, less likely to fire action potential
– IPSP
Slide 1
Presynaptic axonterminal
Neurocrine
Chemicallygated ion channel
Neurotransmitterscreate rapid, short-actingfast synaptic potentials.
Postsynapticcell
Ion channelsopen
MoreNa+ in
LessNa+ in
More K+
out orCl– in
EPSP =excitatory
depolarization
IPSP =inhibitory
hyper-polarization
Ion channelsclose
Less K+
out
EPSP =excitatory
depolarization
Alters openstate of
ion channels
Inactivepathway
G
R
G protein–coupledreceptor
Neuromodulatorscreate slow synapticpotentials and long-term effects.
Activated secondmessenger pathway
Modifies existingproteins or
regulates synthesisof new proteins
Coordinatedintracellular
response
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Fast and Slow Postsynaptic Responses
62
Summations
– When 2 or more signals are received by a neuron, the response of the postsynaptic cell is determined by the summed input from the presynaptic neurons
– Two ways:
1. Spatial summation:graded potentials occurred at different locations that overlapped
2. Temporal summation: graded potentials occurred at the same time
– Postsynaptic inhibition: presynaptic neuron releases inhibitory NT on postsynaptic neuron and alters response
SummationSummation of several subthresholdsignals results in an action potential.
Presynapticaxon terminal
Trigger zone
Actionpotential
Three excitatory neurons fire. Theirgraded potentials separately are all below threshold.
Graded potentials arrive at triggerzone together an sum to create asuprathreshold signal.
An action potential is generated.
Figure 8.24c ESSENTIALS – Summation
No summation. Two subthreshold graded potentials willnot initiate an action potential if they are far apart in time.
Threshold
Time (msec)
−55
−70 A1 A2
X1 X2
Mem
bra
ne p
ote
nti
al (m
V)
Stimuli(X1 & X2)
Figure 8.24d ESSENTIALS – Summation
Summation causing action potential. If two subthresholdpotentials arrive at the trigger zone within a short period of time,they may sum and initiate an action potential.
Threshold
X1 X2
A1
A2
Time (msec)
−55
−70
Mem
bra
ne p
ote
nti
al (m
V)
0
+30
Stimuli(X1 & X2)
Inhibition
Trigger zone
Inhibitoryneuron
Noaction
potential
One inhibitory and twoexcitatory neurons fire.
The summed potentialsare below threshold, so noaction potential is generated.
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Slide 2
How Synapses Work
© 2013 Pearson Education, Inc.
BioFlixTM: How Synapses Work
Figure 8.25
A THREE-DIMENSIONAL RECONSTRUCTION OF DENDRITIC SPINES AND THEIR SYNAPSES
Excitatory synapses (red)
Spine head
Spine neck
SpinesInhibitory synapses (blue)
Presynaptic inhibition
In presynaptic inhibition, an inhibitory neuron synapses on one collateral of the presynaptic neuron and selectively inhibits one target.
Excitatoryneuron
An inhibitory neuron fires, blockingneurotransmitter release at one synapse.
An action potentialis generated.
An excitatory neuronfires.
Action potential
Inhibitory neuron
Presynapticaxon terminal
No neurotransmitterrelease
Target cell
No response
Response
Response
Neurotransmitterreleased
Post synaptic inhibition-all targets on postsynaptic neuron equally inhibited
Inhibitory neuron modifies the signal.
Excitatoryneuron
IPSP +
EPSP
One excitatory and oneinhibitory presynapticneuron fire.
Modified signal inpostsynaptic neuronbelow threshold.
No action potentialinitiated at trigger zone.
No response inany target cell.
No response
No response
No response
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Slide 4
Integration: Long-Term Potentiation and Depression
• Activity at a synapse induces sustained changes in quality or quantity of connections
• Glutamate is key element in potentiation• May be related to learning, memory, depression, and
mental illness
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Figure 8.27
Presynapticaxon
Glutamate
AMPAreceptor
Na+
Ca2+
Mg2+
Na+
Ca2+
Paracrinerelease
Postsynapticcell
NMDAreceptor
Secondmessengerpathways
Cell becomesmore sensitiveto glutamate.
Paracrine from postsynapticcell enhances glutamaterelease.
Ca2+ activates secondmessenger pathways.
Ca2+ enters cytoplasm throughNMDA channel.
Depolarization ejects Mg2+
from NMDA receptor-channeland opens channel.
Net Na+ entry through AMPAchannels depolarizes thepostsynaptic cell.
Glutamate binds to AMPA andNMDA channels.
© 2013 Pearson Education, Inc.
Slide 6