Transcript Ch 4: Synaptic Transmission


This chapter is about introducing the function
of neurons
◦ How they conduct & transmit electrochemical
signals through the nervous system
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Function of neurons centers around the
membrane potential
◦ The difference in electrical charge between the
inside & outside of the cell

Can measure membrane potential using a
microelectrode
◦ Measure the charge inside the cell & the charge
outside.
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A neuron’s resting potential is -70mV
◦ Meaning, the charge inside the cell is 70mV less
than the charge outside
◦ Inside < Outside
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Because this value is beyond 0, it is said to be
polarized
So at rest, neurons are polarized.
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It is polarized due to the arrangement of ions
◦ The salts in neural tissues separate into + and –
charged particles called ions
4 main ions are responsible:
1. K+
(potassium)
2. Na+
(sodium)
3. Cl(chloride)
4. - charged proteins
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The ratio of – to + ions is greater inside a
neuron than out, so you have a more – charge
inside
◦ Again, why the neuron’s resting potential is
polarized
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2 things cause this imbalance & 2 things try
to equalize (homogenize)
Equalizers (homogenizers)
1. Random motion
2. Electrostatic pressure
 Cause imbalance
1. Passive flow
2. Active transport
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Random Motion
Ions are in constant random motion
Tend to be evenly distributed because they
move down their concentration gradient
1.
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2.
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Move from areas of higher concentration to lower
concentration
Electrostatic Pressure
Ions with the same charge will repel each
other
Opposite charges attract
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Concentrations of Na+ and Cl- are greater
outside the neuron (extracellularly)
K+ concentration is greater inside the cell
(intracellularly)
Negatively charged proteins generally stay
inside the neuron
Passive Flow
1.
Does not require energy
The membrane is selectively permeable to the
different ions
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K+ and Cl- ions easily pass through the membrane
Na+ ions have difficulty passing through
Ions passively flow across the membrane via ion
channels
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Special pores in the membrane
Active transport
2.
◦
Needs energy to power the pumps
Active transport
2.
Requires energy to power the pumps that
transport the ions
Discovered by Hodgkin & Huxley
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Nobel prize winning research
Why is there high Na+ and Cl- outside and high K+
inside? Why are they not passively flowing down their
concentration gradients & reaching equilibrium?
Calculated the electrostatic pressure (mV) that would
be necessary to counteract the passive flow down the
concentration gradient (aka keep the concentrations
uneven across the membrane) & how this differed
from the actual resting potential
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Discovered that there are active pumps that
counteract the passive flow of ions in & out of
the cell (specifically for Na+ and K+)
Sodium-potassium pumps
◦ Actively (using energy) pumps Na+ out & K+ in
◦ 3 Na+ ions out for every 2 K+ ions pumped in

Other types of active transporters also exist
*Summary Table 4.1 (pg. 79)*
Remember: At a synapse, the presynaptic neuron
releases NT that bind with receptors on the
postsynaptic neuron, to transmit the signal from
one neuron to the next
 When the NT bind with the postsynaptic neuron,
they have either of 2 effects
1. Depolarize the membrane
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2.
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Decrease the resting potential
**this means become less negative, aka approach
zero**
Hyperpolarize the membrane
Increase the resting potential
** make it more negative; further from zero**
hyperpolarize
depolarize
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Postsynaptic depolarizations:
◦ Excitatory postsynaptic potentials
◦ EPSPs
◦ Increase the likelihood that the neuron will fire
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Postsynaptic hyperpolarizations:
◦ Inhibitory postsynaptic potentials
◦ IPSPs
◦ Decrease the likelihood that the neuron will fire
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Graded responses
◦ Weak signals cause small PSPs; strong signals cause
large PSPs
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Travel passively
◦ Very rapid (practically instantaneous)
 Like a cable
◦ Deteriorate over distance
 Lose amplitude as they go along
 Fade out
 Like sound
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Individual PSPs have almost no effect on
getting a neuron to fire
However, neurons can have thousands of
synapses on them & combining the PSPs from
all of those can initiate firing
◦ Called integration
◦ Add all the EPSPs + IPSPs
◦ Remember:
 PSPs are graded & have different strengths
 ExcitatoryPSPs increase the likelihood of firing &
InhibitoryPSPs decrease the likelihood
Neurons integrates PSPs in 2 ways
1. Over space: spatial summation
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EPSP + EPSP = big EPSP
EPSP + IPSP = 0 (cancel each other
out; assuming of equal strength)
IPSP + IPSP = big IPSP
Over time: temporal summation
2.
◦
2 PSPs in rapid succession coming
from the same synapse can produce
a larger PSP

If the sum of the PSPs reaching the axon
hillock area at any one time is enough to
reach the threshold of excitation, an action
potential is generated
◦ The threshold is -65mV
 So the resting membrane potential must be
depolarized 5mV for the neuron to fire

Action potential
◦ Massive, 1ms reversal of the membrane potential
 -70 to +50mV
◦ Not graded; they are all-or-nothing responses
 Either fire at full force or don’t fire at all
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APs are generated & conducted via voltageactivated ion channels
When the threshold of excitation is hit, the
voltage-activated Na+ channels open & Na+
rushes in
The Na+ influx causes the membrane
potential to spike to +50mV
This triggers the voltage-gated K+ channels
to open & K+ flows out
After 1ms, Na+ channels close
End of rising phase

Beginning of repolarizing phase
◦ K+ continues to flow out until the cell has been
repolarized; then the K+ channels close

Cell returns to baseline resting membrane
potential

For about 1-2ms after the AP, it is impossible
to fire another one
◦ Absolute refractory period
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Followed by a period during which another AP
can be fired, but it requires higher than
normal levels of stimulation
◦ Relative refractory period
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Afterwards, the neuron returns to baseline &
another AP can be fired as usual
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Ions can pass through the membrane at the
nodes of Ranvier between myelin segments
APs move instantly through myelinated
segments to the next node, where
concentrated Na+ channels allow the signal
to be “recharged” and sent to the next
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Overall, this allows APs to be conducted much
faster than in unmyelinated axons, because the AP
“jumps” from node to node and effectively “skips”
the lengths covered in myelin (saltatory conduction)
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Speed of conduction is faster with myelin
Faster in thicker axons
Ex: mammalian motor neurons are thick &
myelinated & can conduct signals at around
224 mph!!
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Different types of synapses based on the
location of the connection on each neuron
◦ Axodendritic
 “Normal” synapses
 Terminal button of axon on Neuron1
to dendritic spine of Neuron2
◦ Axosomatic
 Axon of N1 to soma of N2
◦ Dendrodendritic
◦ Axoaxonic
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2 categories of NTs
◦ Large:
 Neuropeptides
◦ Small:
 Made in terminal buttons & stored in vesicles
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NTs are released via exocytosis
At rest, NTs are in vesicles near membrane of
presynaptic neurons
When an AP reaches the terminal button,
voltage-activated Ca2+ channels open & Ca2+
rushes in
◦ Ca2+ causes the vesicles to fuse with the membrane
& release contents into the synaptic cleft
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NTs released from the presynaptic neuron
cross the cleft & bind to receptors on the
postsynaptic neuron
Receptors contain binding sites for only
certain NTs
Any molecule that binds is a ligand
There are often multiple receptors that allow
one kind of NT to bind: receptor subtypes
◦ Different subtypes can cause different reactions
There are 2 general types of receptors
1. Ionotropic
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NT binds & ion channel opens & ions flow through
Immediate reaction
Metabotropic
2.
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NT binds & initiates a G-protein to trigger a
second messenger, which moves within the cell to
create a reaction
Slow, longer lasting effects
More abundant
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A special type of metabotropic receptor
Located on the presynaptic neuron & bind
with NTs from its own neuron
Function to monitor the # of NTs in the
synapse
◦ If too few, signal to release more
◦ Too many, signal to slow/stop
release
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In order to allow the synapses to be available to
signal again, the extra NT in the synaptic cleft
need to be “cleaned up” by:
Reuptake
◦ Most of the extra NT are quickly taken back into the
presynaptic neuron by transporters to be repackaged in
vesicles for future release
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Enzymatic degradation
◦ NTs in the cleft are broken down by enzymes
◦ Ex: acetylcholine broken down by acetylcholinesterase
◦ Even these pieces are taken back into the neuron &
recycled
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Unique signal transmission alternative to
traditional synapses
Called electrical synapses
Narrow gaps between neurons connected by
fine tubes called connexins that let electrical
signals pass
Very fast & allow communication in both
directions
Not yet fully understood in mammalian systems
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Amino Acid NTs
Monoamine NTs
Acetylecholine
Unconventional/Misc. NTs
Neuropeptides
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AAs are the building blocks of proteins
Glutamate
◦ Most common excitatory NT in the CNS
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Aspartate
Glycine
GABA
◦ Most common inhibitory NT
2 groups with a total of 4 NTs in this class
 Catecholamines:
1. Dopamine (DA)
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Made from tyrosine/L-Dopa
Norepinephrine (NE)
2.
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Made from dopamine
Epinephrine
3.
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Made from NE
Indolamines:
Serotonin (5-HT)
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4.
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Made from tryptophan
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Functions at neuromuscular junctions, in ANS
& CNS
Extra is mostly broken down in the synapse;
by acetylcholinesterase
Receptors for Ach are said to be cholinergic
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Act differently than traditional NTs
Nitric oxide & carbon monoxide
◦ Gases that diffuse across the membrane, across the
extracellular fluid & across the membrane of the
next neuron
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Endocannabinoids
◦ Essentially, the brain’s natural version of THC (main
active chemical in marijuana)
◦ Ex: annandimide
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Don’t worry about the specific types
Just know that they are another type of NT
Generally large NTs
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Pharmaceutical drugs generally affect
synaptic in 2 ways
◦ Agonists facilitate the effects of a NT
 Can bind to a receptor & activate it like the NT would
◦ Antagonists inhibit
 Can bind to a receptor & block it so NTs cannot bind
Acetylcholine has 2 types of receptors
1. Nicotinic
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2.
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Many in the PNS between motor neurons & muscle
fibers
Ionotropic
Nicotine: agonist
Curare: antagonist (causes paralysis)
Botox: antagonist
Muscarinic
Many located in the ANS
Metabotropic
Atropine: antagonist, receptor blocker
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Endogenous
◦ Compounds naturally made within the body
◦ Ex: enkephalins & endorphins
 The body’s endogenous opioids
 An exogenous opioid is morphine
 Opioids are analgesics (pain relievers)