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How does the impulse travel from one neuron to another ?
How does an impulse travel from a neuron to a muscle or gland
(effector)?
How can they do this when they are not physically
connected (there‟s a GAP)?
•When an impulse arrives at the end of an
axon, it must make a connection to the next
nerve cell, or to the muscle or gland.
•BUT neurons do NOT directly contact each
other
•There is a small space, termed the
SYNAPTIC GAP / CLEFT, which the impulse
must cross.
How does this work?
Synaptic Cleft
Presynaptic
membrane
Postsynaptic
membrane
PRESYNAPTIC
MEMBRANE
Encloses synaptic vesicles
filled with neurotransmitters
(n.t.) = a chemical message
manufactured by the axon
POSTSYNAPTIC
MEMBRANE
Contains protein receptor
sites within the membrane to
recognize specific n.t..
STEP 1:
When an impulse arrives at the end of an axon, the sodium
gates open and sodium floods into the axon bulb / terminal.
STEP 2:
At the same time, the CALCIUM GATES OPEN and calcium
(Ca2+) also moves into the axon bulb / terminal of the
presynaptic neuron
Calcium ions
Calcium channel with a
calcium ion
STEP 3: The calcium binds with CONTRACTILE PROTEINS
(microfilaments) attached to the vesicles and this causes them
to contract, thus pulling the vesicles towards the presynaptic membrane.
Requires
ATP
STEP 4: EXOCYTOSIS occurs as the vesicles release
neurotransmitters into the synaptic gap. The n.t. diffuses
across the gap.
STEP 5: Neurotransmitters bond with the receptor
sites on the postsynaptic membrane.
STEP 6: When an excitatory n.t. attaches to the receptors,
the voltage of the post-synaptic membrane changes to
cause the sodium gates to open.
o This depolarizes the membrane.
Sodium & potassium
ions (sodium moves in
and potassium moves out)
Neurotransmitter
If an inhibitory neurotransmitter is released and attaches
to the receptors, the post-synaptic membrane will be
hyperpolarized
Sodium & potssium ions
(sodium moves in and
potassium moves out)
Neurotransmitter
“Hyperpolarization” makes it more difficult for the
threshold to be reached
less likely an action potential will occur
Chemical Synapse
Animation Ch 17
http://highered.mcgrawhill.com/classware/ala.do?alaid
=ala_1039849
STEP 7: If the synapse is between an axon and dendrite,
then the Action Potential will continue down the next neuron.
If the synapse is between an axon and a muscle cell, then
the muscle will contract.
If the synapse is between an axon and a gland, then the
gland will release a hormone.
STEP 8: The synaptic gap contains enzymes that will
destroy the neurotransmitters, thus returning the synapse
to its original condition prior to the arrival of the impulse.
ENZYME THAT DESTROYS
NEUROTRANSMITTER
Causes the sodium gate to close
STEP 9: The calcium ions are returned to the synaptic gap
by active transport.
Because only the axon bulb
has the neurotransmitters,
and only the dendrite has
the receptors, synaptic
transmission may only occur
in one direction.
The energy for this entire process comes from the
mitochon/dria that can be found in abundance in the
synaptic/axon knob
EXCELLENT SYNAPSE ANIMATION:
http://faculty.plattsburgh.edu/donald.slish/NMJ.htm
DO NOT WRITE THIS DOWN:
Acetylcholine is involved in arousal, attention, memory, motivation,
and movement. Involved in muscle action. Degeneration of neurons
that produce ACh have been linked to Alzheimer‟s disease. Too
much can lead to spasms and tremors; too little, to paralysis or torpor.
Dopamine is involved in many behaviors and emotions, including
pleasure. It has been implicated in schizophrenia and Parkinson‟s
disease.
Serotonin is involved in the regulation of sleep, dreaming, mood,
eating, pain, and aggressive behavior. Implicated in depression.
Noradrenalin affects arousal, wakefulness, learning, memory, and
mood.
DO NOT WRITE THIS DOWN:
Endorphins are involved in the inhibition of pain. Released during
strenuous exercise. May be responsible for “runner‟s high.”
Glutamate is involved in long-term memory and the perception of
pain.
GABA is a largely inhibitory neurotransmitter distributed widely
throughout the CNS. Implicated in sleep and eating disorders. Low
levels of GABA have also been linked to extreme anxiety.
Glycene is mainly responsible for inhibition in the spinal cord and
lower brain centers.
The 2 neurotransmitters you need to know!
1) Acetylcholine: *
•This is responsible for promoting all responses in a relaxed
state
•Also involved in controlling skeletal muscles.
*it is destroyed by the enzyme acetylcholinesterase
2) Noradrenalin:
•This is the excitatory transmitter (also known as
norepinephrine).
•It almost always increases the activity of the receiving
cell/tissue/organ.
•It is involved in „fight or flight‟ situations (stress).
*it is destroyed by the enzyme monoamine oxidase
Drugs have different ways of acting on the synaptic transmission
system:
1. Some drugs hold the receptors open for a longer time.
 Alcohol causes the GABA neurotransmitters to work
for a longer amount of time, thus quieting the brain
ALCOHOL:
more than normal.
2. Some drugs block the enzymes from destroying the
neurotransmitters.
 When you are depressed, your serotonin is usually
reabsorbed before it can do its job.
 Prozac stops this from happening.
http://www.p
bs.org/wnet/
closetohome
/animation/g
aba-animmain.html
3. Some drugs cause increased secretions of n.t..
• Cocaine increases dopamine secretion and causes
pleasure sensations
• Ecstasy increases serotonin secretion and produces a
sense of intimacy with others and diminished feelings of
fear and anxiety.
4. Some drugs imitate or mimic the neurotransmitters and
take their place on the receptors.
• Morphine binds to the receptors that endorphins
naturally would and cause a sense of well being (like
you normally get after exercise).
• Nicotine binds to the receptors for acetylcholine and
cause arousal and reward sensations.
• Caffeine counters inhibitory neurons to increase
alertness
5. Some drugs stop the neurotransmitters from joining the
receptors.
 Pain killers occupy the receptor sites so that the
sensation of pain cannot be transmitted between the nerve
cells.
Drug Addiction (ex. Cocaine)
 Normally at a synapse, the neurotransmitter is
broken down and recycled so receptors do not
continually fire.
 Some drugs, like cocaine, bind to “recyclers” so
the neurotransmitter cannot be removed from the
synapse which causes neurons to increase their
rate of depolarization
 To compensate, the postsynaptic membrane
can decrease the number of protein
receptors
 If you remove the drug, the level of
neurotransmitter returns to normal BUT
with fewer receptors
 Result with usage? Decreased number of
receptors will make it difficult to depolarize
the neurons which makes the “high” more
difficult to get
 You crave the drug! And can experience
withdrawal symptoms without it
Complete Synaptic Transmission WS