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Membrane Potentials
the potential current flow across the cell if barrier of membrane is removed
present in all cells
Nernst equation
predicts equilibium potential
when chemical and electrical gradients are opposite and equal→ no net mvmt
for each ion
Goldman Equation
calculates voltage of membrane potential
only looks at 1 ion at equilibrium unlike the nerst
Why are membrane potentials reversal (Why does the electrical charge change?)
sodium ions follow electrochemical gradient in
potassium ions follow chemical gradient out
How can membrane potential change if only positive ions move past each other?
each ion has its own gate
the gates don’t open or close at the same time
Glial Cells a.k.a Neuroglia
regulating extracellular fluid
preventing potassium accumulation
sodium depletion
support and maintain nervous cells
prevent crosstalk btwn adjacent fibers
make up majority of of brain tx
Eukaryotic Potassium Channel
open due to electrical voltage changes
large and complex
Bacterial Potassium Channel
open in response to pH changes or chemical binds
small and minimalist
Selectivity Filter in Potassium Channels
in humans and bacteria
potassium ions are wrapped in water molecules
to enter gate, potassium must take of water coat
oxygen fits right on top of potassium now, so potassium can go through
sodium is too small and cant reach oxygen because its too much energy
Domain I Sodium Channels
6 segments
when an electrical trigger happens, the sensor pulls the tunnel open so sodium can rush into the cell
Domain II Sodium Channels
6 segments
when an electrical trigger happens, the sensor pulls the tunnel open so sodium can rush into the cell
Domain III Sodium Channels
6 segments
when an electrical trigger happens, the sensor pulls the tunnel open so sodium can rush into the cell
Domain IV Sodium Channels
6 segments
triggers the inactivation gate to shut down channel
Resting Potential
-70mV
sodium and potassium gates shut
Depolarization
positive feedback
depolarization causes a few sodium gates to open so sodium can enter, causing more depolarization, so more gates open
potassium gates are opening much more slowly
All or none Response
if enough sodium gates opened, all sodium and potassium gates are opened
all APs on axon are identical and show same wave form
if too few sodium gates open, then not enough sodium before gates shut and no AP
gates like springs
How are the first Na+ gates opened?
the soma collects incoming signals
signals travel to axon hillock (base of axon)
electrical signal opens up sodium gates
positive sodium charges rush into first tiny part of axon membrane, then next part of axon membrane
Hyperpolarization
end of AP
prevents depolarization from acheiveing threshold
What direction do action potentials travel in?
one direction
Velocity of AP
more resistance less of it
increase diameter of fiber for axon → reduce resistance
decrease diameter of fiber for axon → increase resistance
How do you keep action potentials moving fast?
gaps btwn Schwann cells, known as nodes of Ranvier allow action potentials to skip from point to point
Saltatory Conduction
schwann cells wrap around axon to form myelin sheath
the sheath acts as an electrical insulator, preventing ions from leaking
the nodes of Ranvier have lots of sodium gates
electrical current flows quickly through axon and regenerates action potentials only in nodes
Dietary fatty acids
n-6 and n-3 fatty acids are good for neural development
human breast milk is 40-55% fat in first 6 months of feeding
Synapse
fluid-filled gap btwn two cells
Pre-synaptic Cell
the action potential travels down axon of this neuron
releases neurotransmitters to chemical synapse or ions through gap junction
Cleft
physical space between pre and post synaptic cells
Post-synaptic Cell
neurotransmitters land on specific receptor proteins in chemical synapse
binding opens ion channels in chemical synapse
receive ions from presynaptic cell
Gap Junction- Typse of Synpase
direct transmission of AP
no neurotransmitters or cleft
ions just flow into postsynaptic cell
tight junction or electrical junctions
smooth, cardiac muscle, retina, CNS
Chemical Synapse- Type of Synpase
action potential arrives at pre-neuron ending
depolarization opens Ca++ gates on pre-
Ca++ activates kinase
release of neurotransmitter into cleft
common
Kinase
causes vesicles containing neurotransmitter to fuse with pre-membrane, emptying contents into cleft in chemical synapse
What happens after neurotransmitters are released into cleft?
NT diffuse across cleft
NT binds to receptors sites on post-membrane
binding causes ion gates to open
post- is depolarized or hyperpolarized
enzymes on post-break down NT, so gates close
Excitatory Post-Synaptic Potential (EPSP)
if depolarized
only in chemical synapse
Inhibitory Post-Synaptic Potential (IPSP)
if hyperpolarized
only in chemical synapse
Fast Chemical Transmission
miliseconds
neurotransmitters opens a gate directly
briefly changes the cell’s electrical charge to spark or stop an action
controls rapid actions like reflexes, movement, and quick thoughts
Slow Chemical Transmission
seconds to minutes
neurotransmitter starts a chain reaction
alters the cell’s internal chemistry
regulates longer-lasting states like mood, sleep, hunger, and focus
Different categories of neurotransmitters
amines
catecholmines
amino acids
polypeptides
hormones
Types of amine neurotransmitters
acetylcholine
serotonin
Types of catecholamines
nor-epinephrine
dopamine
Cholinergic Fibers
releases acetylcholine (Ach) as its chemical messenger
can be excitatory or inhibitory
same NT but different gates on post-
Two Types of cholinergic fibers
nicotinic
muscarinic
Nicotinic
ACh binds to non-specific ion gate
only open and close with presence or absence of Ach
2 AcH required to open, and when open is unstable
more sodium enters than potassium leaves
excitatory
fast chemical synapse
Muscarinic
Excitatory Effect
ACh binds to G-protein complex, which subunit closes some potassium channels so potassium can’t leak
cell keeps becoming positive because Na-K pump still pumping potassium and sodium inside
causes slow depolarization (makes it so that when a neurotransmitter or ions come by, it triggers a very fast action potential)
makes cell more sensitive
Inhibitory Effect
ACh binds to other G-protein complex, which subunit of it opens the potassium channels or stay open longer
the potassium leaves cell, making cell more negative
hyperpolarization happening
Acetylcholine esterase or AChe
breaks ACh down into acetate and choline
acetate and choline is taken up by pre-fiber and recycled into ACh
found in cleft
Anti-cholinesterases
causes continual depolarization
blocks synaptic transmittion
Adrenergic synpases
use nor-epinephrine as NT
can cause EPSP or IPSP
What are 4 types of adrenergic synapses?
a1
a2
B1
B2