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Microsoft word - psyc101_notes.doc

Neuron cell structure
Dendrites: Contain neuroreceptors that respond when exposed to
neurotransmitters.
Soma: Body of neuron cell. DNA in the nucleus in the soma code for all
the proteins of the neuron.
Axon hillock: Contains a high concentration of voltage dependent
sodium channels and considered the spike initiation zone for action
potentials.
Axon: Electrical pathway from the soma to the axon terminal. The axon
hillock is the transition from soma to axon. The part of the axon beneath the
myelin covering is the axon core.
Myelin sheath: This is an insulating covering formed by multiple
Schwann cells, each about 100uM long. Schwann cells are glial (“Glue”)
cells, cells that are needed to support nerve cells.
Nodes of Ranvier: These are gaps of about 1um width between
adjacent myelin sections that act as mini-axon-hillocks to regenerate action
potentials periodically from the voltage impulses traveling under the myelin
coating and serve to increase the propagation of axon signaling versus an
unmyelinated axon.
Axon terminal / Terminal buttons: When triggered by an action
potential from the soma, the terminal buttons release stored
neurotransmitters which are then received by nearby dendrites of other
neurons.
Terminal
NEURON WITH
Dendrites
MYELINATED AXON
Terminal
Myelin sheath
Synapse and neuron signaling
Action potential: This is an electrical signal from the soma that travels
down the axon to the terminal buttons at the terminal end of the axon. This
releases the neurotransmitter (NT) molecules stored in the terminal buttons
into the synapse, the gap between the terminal buttons of one neuron and
the dendrites of the next. Some of these neurotransmitters land on the
nearby dendrites of a neuron at receptor (R) sites that cover both the soma
and dendrites (dendrites are essentially fingerlike extensions of the soma).
As neurons become more and more closely associated with other neurons
through long term potentiation, the distance of the synaptic gap approaches
zero and the number of dendrites of one neuron that are associated with the
terminal buttons of another neuron may be increased.
Neuron #1
Neuron #2
Terminal
Dendrites
Synapse and neuron signaling.
NT dependent ion channels: When a neurotransmitter from a terminal
button or other source hits a receptor on a dendrite, an ion channel specific
to that receptor is opened.
Excitatory postsynaptic channel: A sodium channel is opened
which pulls in positive ions thus increasing the internal cell potential.
Inhibitory postsynaptic channel: A potassium channel is opened
which allows positive potassium ions to leave the cell thus lowering the
cell potential.
Voltage dependent ion channels: In the soma, in response to
activation of receptors by released neurotransmitters on the dendrites and
soma body that change the resting potential inside the cell, ion channels that
open at one voltage and close at another cause the neuron to fire in an “All
or nothing” manner therefore Increased neurotransmitter exposure does not
change the level at which neurons fire but instead the number of times the
neurons will fire per unit time.
Neurotransmitters
Seratonin (5-Ht; Hydro-triptomine): Controlled by pre-frontal lobe and
is used for self-control, mood, sleep, appetite, sensory perception, arousal,
temperature regulation and pain suppression.
Acetylcholine (Ach): Used for muscle action, learning memory, REM
sleep and emotion. Lactic acid in muscles breaks down Ach, so stretching
after exercise releases the lactic acid so it can’t eat all of your Ach reserves.
Dopamine (DA): Used for muscle control for movement, attention,
learning and emotion. Too little and you can’t move, too little and you’re
schizophrenic!
Norepinephrine (NE) or NoradrenalineTM: Used in the central nervous
system for mental energy and wakefulness.
Epinephrine or AdrenalineTM: Used by the peripheral nervous system
for physical energy.
Gamma Aminobutyric Acid (GABA): Inhibitory neurotransmitter that
always is used to compete with Norepinephrine to put you to sleep.
Endorphins: The brains naturally produced morphine that binds to
opiate receptors to suppress pain, control appetite etc.
Neuron polarization
0. –70mV / Fully polarized: When the neuron is at rest, the anion
content of the neuron gives the inside of the neuron a net negative potential
of –70mV with respect to the exterior of the cell that is surrounded by the
saline solution of the brain fluid.
0. -70mV / Neuron at rest
Na+ Sodium Ion
Cl- Chlorine Ion
Terminal
Dendrite
K+ Potassium Ion
NT NeuroTransmitter
Anion Na+ K+
1. –70mV / Depolarization begins: Neurotransmitters activate
receptors on the dendrites. If the neuron does not reach the threshold of
–55mV due to the insufficient stimulus of failed initiations, it will return to the
fully polarized –70mV resting potential.
1. NT dependent ion channels open
Terminal
Dendrite
2. –55mV / Depolarization accelerates: At about –55mV the voltage
dependent sodium channels open which draw more sodium ions from the
outside of the neuron, which further increases the depolarization of the
neuron and drives it to full depolarization without and/or regardless of
further external neurotransmitter stimulus.
2. -55mV / Sodium channels open
Terminal
Dendrite
3. 0mV / Depolarization continues: When the neuron potential reaches
0mV, the voltage dependent potassium channels open which allow positively
charge potassium ions already in the neuron to be pushed out through
electrostatic repulsion to the incoming sodium ions. The neuron potential
will continue to climb as more sodium ions enter than potassium ions leave.
3. 0mV / Potassium channels open
Terminal
Dendrite
4. 40mV / Fully depolarized “Action potential”: When the neuron
potential reaches about 40mV, the voltage dependent sodium channels
close and prevent any more sodium ions from entering. Potassium ions
continue to exit the neuron causing its potential to begin to fall back toward
the rest state.
4. 40mV / Sodium channels close
Terminal
Dendrite
5. -70mV / Fully repolarized: Between stage 3 and 4 as potassium ions
continue to exit, the neuron potential falls until it reaches the -70mV rest
state at which time the voltage dependent potassium channels close. At this
point, sodium ions have replaced the potassium ions of the rest state so the
neuron is not yet able to re-fire. (When the action potential propagates to
the axon terminal, neurotransmitters are released.)
5. -70mV / Potassium channels close
Terminal
Dendrite
5/6. < -70mV / Hyper polarization and rest state restoration: Hyper
polarization occurs as the neuron potential goes more negative than the rest
state because so many potassium channels were opened between stages 3
and 5 and they don’t all close at once. The period between stages 5 and 6
is also called undershoot.
Absolute refractory period: After an action potential, the sodium
channels can’t be re-opened for this period due to entering into a
temporary inactivated state, thus preventing re-firing regardless of the
level of stimulus.
Relative refractory period: Sodium ions are pumped out and
potassium ions are pumped into the neuron to return it to its original
resting potential. During this time, some few potassium channels
remain open so that although the neuron may re-fire at this time, it
takes a higher than normal stimulus that during the resting state. The
ion pumping requires expenditure of energy by the cell that consumes
ATP.
potential
Absolute
Relative
Refractory
Refractory
initiations
p rizedlaHyPo
Myelinated axons: In a myelinated axon, action potentials travel
between the Nodes of Ranvier electrically, and then are regenerated
chemically at the nodes. The nodes are typically 1um wide and the
distance between nodes is typically 100um which results in a majority of
electrical impulse conduction that is faster than chemical conduction.
Unmyelinated axons: In an unmyelinated axon, the action potential is
propagated in a purely chemical fashion as sodium channels ahead of the
action potential are activated while sodium channels behind are inactivated
during their absolute refractory period leading to the unidirectional
propagation from the soma to the terminal.

Source: http://www.tayloredge.com/reference/Science/Neuron101.pdf

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