|


 

| 
 



How Neurons Send and
Receive Signals

This multimedia product and its contents are

protected under copyright law. The following are
prohibited by law:
‡ any public performance or display, including
transmission of any image over a network;
‡ preparation of any derivative work, including the
extraction, in whole or in part, of any images;
‡ any rental, lease, or lending of the program.
á



 






4 0nside of the neuron is negative with

respect to the outside
4 Resting membrane potential is about
-70mV
4 Membrane is polarized, it carries a
charge
4 Why?
0
 





4 0ons, charged particles, are unevenly

distributed
4 Factors influencing ion distribution
‡ Homogenizing
‡ Factors contributing to uneven distribution
0
 




4 Homogenizing
‡ Random motion ± particles tend to move down
their concentration gradient
‡ Electrostatic pressure ± like repels like, opposites
attract
4 Factors contributing to uneven distribution
‡ Membrane is selectively permeable
‡ Sodium-potassium pumps
0| 





4 Sodium (Na+)
4 Chloride (Cl-)
4 Potassium (K+)
4 Negatively charged proteins (A-)
‡ synthesized within the neuron
‡ found primarily within the neuron
á




4 0ons move in and out through ion-
specific channels
4 K+ and Cl- pass readily
4 Little movement of Na+
4 A- don¶t move at all, trapped inside
-  


4 The potential at which there is no net
movement of an ion ± the potential it will move
to achieve when allowed to move freely
4 Na+ = 120mV
4 K+ = -90mV
4 Cl- = -70mV (same as resting potential)
á




4 Na+ is u


electrostatic forces
and its concentration gradient
4 K+ is u

 by electrostatic forces u
by its concentration gradient
4 Cl- is at equilibrium
4 Sodium-potassium pump ± active force that
exchanges 3 Na+ inside for 2 K+ outside
`
  

4 What would happen if the
membrane¶s permeability to Na+
were increased?
4 What would happen if the
membrane¶s permeability to K+ were
increased?
†



| 



`
4 Neurotransmitters bind at postsynaptic
receptors
4 These chemical messengers bind and cause
electrical changes
‡ Depolarizations (making the membrane potential less
negative)
‡ Hyperpolarizations (making the membrane potential
more negative)
†



| 



`
4 Postsynaptic depolarizations = Excitatory
PSPs (EPSPs)
4 Postsynaptic hyperpolarizations = 0nhibitory
PSPs (0PSPs)
4 EPSPs make it more likely a neuron will fire,
0PSPs make it less likely
4 PSPs are graded potentials ± their size varies
-`
0`
4 Travel passively from their site of origination
4 Decremental ± they get smaller as they travel
4 1 EPSP typically will not suffice to cause a
neuron to ³fire´ and release neurotransmitter ±
summation is needed
0

 `
†



 



4 0n order to generate an AP (or ³fire´), the

threshold of activation must be reached
at the axon hillock
4 0ntegration of 0PSPs and EPSPs must
result in a potential of about -65mV in
order to generate an AP
0


4 Adding or combining a number of
individual signals into one overall signal
4 Temporal summation ± integration of
events happening at different times
4 Spatial - integration of events happening
at different places
º

 




4 ne neuron fires rapidly?

4 Multiple neurons fire at the same time?
4 Several neurons fire repeatedly?
4 Both temporal and spatial summation
occur simultaneously
á



4 All-or-none, when threshold is reached
the neuron ³fires´ and the action
potential either occurs or it does not.
4 When threshold is reached, voltage-
activated ion channels are opened.
á
0
 


4 When summation at the axon hillock results in
the threshold of excitation (-65mV) being
reached, voltage-activated Na+ channels open
and sodium rushes in.
4 Remember, all forces were acting to move Na+
into the cell.
4 Membrane potential moves from -70 to
+50mV.
á
0
 


4 O

 Na+ moves membrane potential from -70
to +50mV.
4 -


 After about 1 millisec, Na+
channels close.
4 Change in membrane potential opens voltage-activated
K+ channels.
4 O   Concentration gradient and change in
charge leads to efflux of K+.
4
    Channels close slowly - K+ efflux
leads to membrane potential <-70mV.




4 Absolute ± impossible to initiate another
action potential
4 Relative ± harder to initiate another
action potential
4 Prevent the backwards movement of
APs and limit the rate of firing
á





4 http://intro.bio.umb.edu/111-
112/112s99Lect/neuro_anims/a_p_anim
1/WW1.htm
4 http://bio.winona.msus.edu/berg/AN0MT
NS/actpot.htm
`



4 EPSPs/0PSPs 4 Action Potentials

4 Decremental 4 Nondecremental
4 Fast 4 Conducted more
4 Passive (energy is slowly than PSPs
not used) 4 Passive and active
|



4 Passive movement of AP within myelinated
portions occurs instantly
4 Nodes of Ranvier (unmyelinated)
‡ Where ion channels are found
‡ Where full AP is seen
‡ AP appears to jump from node to node
‡ Saltatory conduction
‡ http://www.brainviews.com/abFiles/AniSalt.htm
`
 `


4 Most common
‡ Axodendritic ± axons on dendrites
‡ Axosomatic ± axons on cell bodies
4 Dendrodendritic ± capable of
transmission in either direction
4 Axoaxonal ± may be involved in
presynaptic inhibition
`



á

 


á

4 NT molecules
‡ Small
‡ Synthesized in the terminal button and packaged in
synaptic vesicles
‡ Large
‡ Assembled in the cell body, packaged in vesicles,
and then transported to the axon terminal




 á


4 Exocytosis ± the process of NT release
4 The arrival of an AP at the terminal opens
voltage-activated Ca++ channels.
4 The entry of Ca++ causes vesicles to fuse with
the terminal membrane and release their
contents
4 http://www.tvdsb.on.ca/westmin/science/
sbioac/homeo/synapse.htm
 
 

 á

4 Released NT produces signals in postsynaptic

neurons by binding to receptors.
4 Receptors are specific for a given NT.
4 Ligand ± a molecule that binds to another.
4 A NT is a ligand of its receptor.



4 There are multiple receptor types for a
given NT.
4 0onotropic receptors ± associated with
ligand-activated ion channels.
4 Metabotropic receptors ± associated with
signal proteins and G proteins.
0


4 NT binds and an associated ion channel
opens or closes, causing a PSP.
4 0f Na+ channels are opened, for example,
an EPSP occurs.
4 0f K+ channels are opened, for example,
an 0PSP occurs.





4 Effects are slower, longer-lasting, more
diffuse, and more varied.
4 NT (1st messenger) binds > G protein
subunit breaks away > ion channel
opened/closed R a 2nd messenger is
synthesized > 2nd messengers may have
a wide variety of effects



-








4 As long as NT is in the synapse, it is

active ± activity must somehow be
turned off.
4 Reuptake ± scoop up and recycle
NT.
4 Enzymatic degradation ± a NT is
broken down by enzymes.
`







4 Amino acids ± the building blocks of

proteins
4 Monoamines ± all synthesized from a
single amino acid
4 Soluble gases
4 Acetylcholine (ACh) ± activity terminated
by enzymatic degradation




4 ±sually found at fast-acting directed synapses
in the CNS
4 Glutamate ± Most prevalent excitatory
neurotransmitter in the CNS
4 GABA ±
‡ synthesized from glutamate
‡ Most prevalent inhibitory NT in the CNS
4 Aspartate and glycine
 


4 Effects tend to be diffuse
4 Catecholamines ± synthesized from tyrosine
‡ Dopamine
‡ Norepinephrine
‡ Epinephrine
4 0ndolamines ± synthesized from tryptophan
‡ Serotonin
` 
†


|
4 Soluble gases ± exist only briefly
‡ Nitric oxide and carbon monoxide
‡ Retrograde transmission ± backwards communication
4 Acetylcholine (Ach)
‡ Acetyl group + choline
‡ Neuromuscular junction
÷



4 Large molecules
4 Example ± endorphins
‡ ³Endogenous opiates´
‡ Produce analgesia (pain suppression)
‡ Receptors were identified before the natural
ligand was


 `

á


4 Many drugs act to alter neurotransmitter

activity
‡ Agonists ± increase or facilitate activity
‡ Antagonists ± decrease or inhibit activity
‡ A drug may act to alter neurotransmitter
activity at any point in its ³life cycle´
! "



4 Cocaine - catecholamine agonist
‡ Blocks reuptake ± preventing the activity of
the neurotransmitter from being ³turned off´
4 Benzodiazepines - GABA agonists
‡ Binds to the GABA molecule and increases
the binding of GABA

! "



4 Atropine ± ACh antagonist
‡ Binds and blocks muscarinic receptors
‡ Many of these metabotropic receptors are in the brain
‡ High doses disrupt memory
4 Curare - ACh antagonist
‡ Bind and blocks nicotinic receptors, the ionotropic
receptors at the neuromuscular junction
‡ Causes paralysis