1/54
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai | Chat |
|---|
No analytics yet
Send a link to your students to track their progress
about how many neurons are in the brain
about 86 billion, each one connecting to about 10,000 others to create a dense, interconnected network
soma (cell body)
contains nucleus
dendrites
receive input from the presynaptic neuron
axon
sends the signal away from the soma to the next neuron
AP is sent down this
myelin sheath
fatty material that insulates the axon for information to pass faster and efficiently
Nodes of Ranvier
breaks in the myelin sheath
exchange of ions along the axon can happen here
axon terminals
where the neuron connects to (with the synapse in between) to another neuron to send the AP
synapse
gap between the first and second neuron
AP must jump across this to pass along
multiple sclerosis (MS)
autoimmune disease where the immune system treats myelin sheaths as foreign substances and attacks them
tends to progress, can be incapacitating
causes demyelination → not many AP correctly fire, signals have a harder time traveling or happening at all
symptoms vary depending on affected regions (difficulty walking, moving, seeing etc.)
glial cells
support neurons structurally and nutritionally
about as many as neurons
specific functions
insulating axons by forming myelin sheaths
providing nutrients and oxygen
cleaning wastes
possibly involved in electrical signal transmission
neuron resting potential
about -70 mV (inside negativity charged relative to outside)
maintained by ion concentrations
Na: outside, positive
Cl: inside, negative
ion channels
open in response to stimulation (gating)
allows Na to rush in and reduce the negative charge
What happens when the voltage potential reaches -55 mV
it hits the threshold, rapid depolarization occurs
Na influx causes internal voltage to increase to +40 mV (peak AP)
action potential
voltage change from -70 mV to +40 mV
driven by ion movement across the membrane
once it peaks, neuron resets to resting potential, ready for another cycle
white matter
consists of myelinated axons that send signals over long distances
gray matter
consists of neural somas and unmyelinated regions doing information processing and local connections
first step of neuron fire
resting potential/state (-70mV)
Na+ ions are outside the neuron
fewer K+ and Cl- are inside the neuron
more negative ions inside the neuron and more positive are outside
makes the inside more negative than the outside
second step of neuron firing
neuron is stimulated by other neurons with neurotransmitters
causes Na+ ions to start slowly going inside the neuron
-70 mV goes up till it hits the -55 mV threshold
threshold
-55mV
catapults the neuron towards the AP at the peak
third step of neuron firing
depolarization - neuron becomes more positive
Na+ rushes into the neuron making it more positive till it reaches +40 mV
action potentials is fired at +40 mV
How do we describe action potentials and why?
“all or nothing”
no such thing as a little excited, think of a light switch
Does a more intense stimulation (from environment stimulus) cause a more intense AP?
no but it does cause:
more frequent AP
AP happening in more neurons
fourth step of neuron firing
hyperpolarization/repolarization
K+ ions flood out because it’s too positive
the neuron kicks out K+ instead of Na+ because it’s faster and Na+ wants to stay inside
makes it more negative inside the neuron
process overshoots the resting state, and the cell will be very negative momentarily (hyperpolarization)
fifth step of neuron firing
back to rest state
what the neuron really wants
Na+/K+ pumps push the K+ back into the neuron and push Na+ out
more Na+ outside the cell making it positive outside the cell
Cl- inside the cell making it more negative than outside
goes back to -70 mV (resting state)
Where does depolarization occur?
at each part of the axon inside the nodes of Ranvier
allows for the exchange of ions at breaks in the myelin sheath
How fast does an AP travel down an axon?
travels at about 50-100 m/s (not the speed of electrical current in wire)
vesicles
located in axonal buttons in presynaptic neuron
contains neurotransmitters
neurotransmitters
the “key”; chemicals that convey electrical signals from one neuron to the next
receptor molecules
the “lock”
located the dendrites of postsynaptic neuron
when NT land on them, Na+ open gates open for Na+ to come into the neuron and start making the neuron more positive
causes process to repeat
What determines if the ion channels opens for Na+ to come in or leave
whether a NT is excitatory or inhibitory
the sequence
vesicles full of NT travel down the presynaptic axon terminals
when they reach the cell membrane (end of the presynaptic), they burst open and attach to cell membrane releasing NT’s inside
NT travel across the synapse
key and lock: NT attach to receptors on postsynaptic with the same shape
ion gates in postsynaptic neuron open
Na+ starts entering neuron, making it more positive in hopes of creating an AP
life cycle of NT
synthesis
storage in vesicles
release
receptor interaction
inactivation
reuptake
degradation
How long does the rise and fall of the action potential take?
one millisecond
sets approximate high firing rate of 1,000 AP per second
Where does the action potential begin?
near the junction of the soma and the axon
local changes in the membrane trigger the next section of axon, propagating the signal along its length
Herman Von Helmholtz
measured nerve conduction 19th century
stimulated frog nerves at different points and timing the resulting muscle response
found that neurons can extend over long distance
found bundles of axons make up nerves
What happens to NT after a certain period of time?
broken down
reuptake
reuptake
NT are taken back into the presynaptic neuron to be used again
serotonin reuptake inhibitors (SSRI)
inhibits the reuptake of serotonin
keeps the serotonin in the synapse to have more to use
less depressed = happier (less serotonin → depression)
“antidepressant”
excitatory postsynaptic potential (EPSP)
more likely to fire an AP in the postsynaptic neuron
NT can open the Na+ channels to start coming to possibly start an AP
makes it more likely to fire bc it starts to get more positive (depolarization)
ex: glutamate
inhibitory postsynaptic potential (IPSP)
less likely to fire an AP in the postsynaptic neuron
NT can open the gates of the K+ ions and have the flood out the neuron
can have Cl- ions come in as well
both makes the neuron less likely to fire because it starts to get more negative (hyperpolarization)
What do neurons weigh the input of? What does this do?
weigh the input from excitatory and inhibitory NT
whichever there are more of wins the battle and the neuron fires or does not fire
clinical significance of EPSP and IPSP
malfunctions in inhibitory NT can lead to epilepsy, mood, and sleep disorders
Charles Sherington
discovered the existence of the synapse
used the dog experiment
Sherrington’s dog experiment
scratch the dog in an area and they’ll itch
eventually they stop scratching, meaning there’s an inhibition in the brain, Sherrington wanted to stop that
he cut the spinal column so there was no inhibition from the brain (disinhibition)
How did Sherrington come the conclusion of the synapse
he stimulated one are over time and it created the reaction to scratch (temporal summation)
he stimulates three areas at just once and together they created the reaction to scratch (spatial summation)
concluded that, therefore, there must be one area where they come together → synapse
inhibition
you stop behave
disinhibition
stops your ability to stop that behavior (ex: snipping spinal column