Ch 8 neurons 9 11

© 2013 Pearson Education, Inc.

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


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


Resting Membrane Potential


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)


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


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


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


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


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


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


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


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


Cell-to-Cell: Neurocrines

• Seven classes by structure– Acetylcholine (choline and acetyl coenzyme A)– Amines– Amino acids– Peptides– Purines– Gases– Lipids


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)


Amines

• Derived from single amino acid• Tyrosine

– Dopamine– Norepinephrine is secreted by noradrenergic neurons– Epinephrine

• Tryptophan– Serotonin (5-Hydroxytryptamine or 5-HT)

• Histadine– Histamine


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+)


Other Neurotransmitters

• Peptides– Substance P and opioid peptides

• Purines – AMP and ATP

• Gases – NO, CO, and H2S

• Lipids – Eicosanoids– cannnabinoid receptors


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


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


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.


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.


Slide 2

How Synapses Work


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


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


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


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.


Slide 6

Documents

Ch 8 neurons 9 11