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resting membrane potential (RMP)
the electrical charge difference across the cell membrane when the neuron is not sending a signal
outside = positive
inside = negative (-70 mV)
Na+/ K+ pump potential effect
20%
K+ leak channels potential effect
80%
Na+/ K+ pumps
maintenance workers → more positive ions enter than leave; the inside becomes slightly more positive
pumps 3 Na+ out
pumps 2 K+ in
K+ leak channel
channels that are always open/leaking → always wants to leave the cell
K+ concentration high inside - (150 mM)
K+ concentration low outside - (5 mMs)
graded potential
small changes in membrane potential → small push towards an action potential
depolarization → less negative
hyperpolarization → more negative
fatures: variable size, can add together, travel short distances (weaker with distance)
threshold
the membrane potential that must be reached before an action potential begins → (-55 mV)
graded potential depolarizes enough to reach threshold (POINT OF NO RETURN)
1. voltage gated Na+ channels open (axon hillock - initial segment)
2. action potential starts
action potential
a rapid electrical signal that travels down the axon
characteristics:
1. all-or-none
2. same size everytime
3. does not fade away
4. long distance communication
graded potential → knock on action potential → door bursts open
depolarization (phase 1)
voltage-gated Na+ channels open → Na+ rushes INTO the neuron due to high concentration outside + negative inside attracts positive Na+
⭐ Na⁺ enters
peak (phase 2)
maximum positive voltage reached
Na+ channels begin closing/inactivating
K+ channels begin to open
repolarization (phase 3)
voltage gated K+ channels open → K+ leaves the cell
positive charges leaves = making the inside negative again
⭐ K⁺ exits
hyperpolarization (phase 4)
K+ channels remain open for a bit longer (continues to leak out = extra K+ enters)
membrane becomes more negative than resting potential
→ but will eventually return to resting potential
refractory periods
these prevent action potentials from going backwards
absolute refractory period
1. Na+ channels are inactivated
2. no matter how strong the stimulus → another AP cannot occur
(Na+ channels must rest first)
IMPOSSIBLE
relative refractory period
some Na+ channels have reset, but K+ channels are still open
cell is hyperpolarized
another AP is possible (requires a stronger-than-normal stimulus)
POSSIBLE BUT HARDER
propagation of action potentials
how the signal moves down to axon
the depolarized region causes nearby voltage-gated Na+ channels to open
→ signal regenerates itself continuously
contiguous conduction
occurs in unmyelinated axons
action potentials must activate every section of membrane (one section at a time - 0 0 0 0)
→ results: slower + more energy required
saltatory conduction
occurs in unmyelinated axons → (node → node)
myelin acts like insulation
action potentials only occur at Nodes of Ranvier, where voltage-gated channels are concentrated.
→ results: faster + less energy used + more efficient
SKIP AND JUMP CONDUCTION
multiple sclerosis (MS)
an autoimmune disease that destroys myelin
without myelin = conduction slows + signals may fail to reach destination
symptoms:
vision problems, numbness, muscle weakness, poor coordination, paralysis in severe cases
MS = MYELIN STRIPPED AWAY
neurotransmitter release
when the action potential reaches the axon terminal
step 1: action potential arrives
step 2: voltage-gated Ca2+ channels open
step 3: Ca2+ enters the terminal
step 4: Ca2+ causes synaptic vesicles to fuse with the membrane
step 5: neurotransmitter is released into the synaptic celft
AP → Ca2+ in → neurotransmitter out
SNARE proteins
these proteins help vesicles move and fuse with the membrane (hooks for neurotransmitter vesicles)
without SNARE proteins:
vesicles CAN’T fuse + neurotransmitters cannot be released
toxins affecting SNAREs (interfere with neurotransmitter release):
botulinum toxin, tetanus toxin, some venoms
EPSP (excitatory postsynaptic potential)
a graded depolarization that makes the neuron more likely to fire an action potential
positive ions enter: Na+, Ca2+, sometimes Mg2+
result → cell becomes less negative
(excites the neuron → moves toward threshold)
IPSP (inhibitory postsynaptic potential)
a graded hyperpolarization that makes the neuron less likely to fire an action potential
Cl- enters OR K+ leaves
result → cell becomes more positive
(inhibits the neuron → moves away from threshold)
the Nernst equation
tells you the electrical voltage needed to perfectly balance the concentration gradients of one ion
(if one side has a higher concentration, it would want to go to the other side → charge resistance)
Ion + nernest potential:
1. K+ ~ -90 mV
2. Na+ ~ +60 mV
3. Cl- ~ -70 mV
cerebral hemispheres
responsible for thinking, learning, memory, language, and conscious decisions (“thinking brain”)
Everything that makes you, YOU
cerebellum
coordinate movements without thinking about them (“autopilot”)
help with balance, coordination (motor signals, visual stimuli, and equilibrium), smooth voluntary movement, posture (ex: walking and texting)
medulla oblongata
controls vital functions (“life support center”)
heart rate, blood pressure, breathing
coughing, sneezing, swallowing, vomiting
stops working = survival threatened
brain stem
connects the brain to the spinal cord (“connection highway”) + carries signals between the brain and body
reflex center:
visual reflexes
startle reflexes
spinal cord
links transmission of information to and from the brain and integrates many reflexes ('“telephone line”)
functions:
send signals between the brain and body
control reflexes
contains autonomic nervous system pathways
glial cells
keep everything running as neurons do the talking (“support cell”)
90% of cells in the CNS are neuroglia → 10% actual neurons
Astrocytes
the nurses and janitors of the CNS (“caretakers”)
functions:
hold neurons in place
help form blood-brain barrier
clean up neurotransmitters
form scar tissue after injury
Oligodendrocytes
wrap neurons like electrical tape (“insulators”)
function
form myelin around CNS axons → myelin allows signals to travel faster
microglia
the brain’s security guards (“immune cells”)
function:
defend the nervous system
remove debris and damaged tissue
ependymal cells
help make the brain’s cushion fluid (“CSF makers”)
function:
line cavities in the brain
help produce cerebrospinal fluid (CSF)
concussion
temporary brain injury → usually not permanent neurological damage (shaken brain)
symptoms:
confusion
dizziness
headaches
stroke (CVA)
a blood vessel becomes blocked → no blood = no O2 = dead neurons
result:
brain tissue loses oxygen
brain cells die
common outcome:
paralysis
sensory deficits
alzheimer’s disease
progressive degeneration of the brain → brain slowly loses memory
symptoms:
memory loss
personality changes
dementia
cognitive decline
Association:
acetylcholine (ACh) deficiency
plaque accumulation
parkinson’s disease
casued by loss of dopomine-producing neurons
symptoms:
tremors
rigid movements
reduced facial expressions
w/o dopmine:
movement control worsens
edema
swelling caused by fluid accumulation in brain tissue → compressed brain
danger:
increased pressure inside the skull
chronic traumatic encephalopathy (CTE)
occurs after repeated head trauma → can cause long term neurological damage
symptoms:
memory loss
depression
aggression
dementia
brain atrophy
(common in boxers + football players)
cholinergic system
uses Acetylcholine (ACh) → neurotransmitter
nicotinic receptors (preganglionic)
found on ALL autonomic postganglionic neurons (1st synapse)
→ both sympathetic and parasympathetic preganglionic neurons release ACh onto nicotinic receptors
muscarinic receptors
found on parasympathetic target organs (ex: heart, smooth muscle, glands)
parasympathetic postganglionic neurons release ACh onto (MR)
parasympathetic end organ = M
adrenergic system
uses norepinephrine (NE) + epinephrine (Epi) → usually associated with sympathetic responses
alpha receptors (α)
usually excitatory + cause contraction (ex: blood vessel constriction)
excitatory = Epi + Ne
A = squeeze
beta- 1 receptors (β₁)
mainly found in the heart → “Be my #1 Lover”
excitatory = Epi + Ne
effects:
increased heart rate
increased force of concentration
B1 = 1 heart
beta-2 receptors (β₂)
usually inhibitory to smooth muscle → causes relaxation = MORE Epi
ex:
blood vessels (relaxation → vasodilation = more blood flow)
airways (relaxation → bronchodilation = more airflow)
→ opens tubes
dual control
most organs receive BOTH sympathetic and parasympathetic input → usually with opposite effects
ex: heart
sympathetic → speeds heart rate (fight or flight) = gas pedal
parasympathetic → slows heart rate = break pedal
sweat glands
only sympathetic → only uses ACh
blood vessels
most blood vessels only receive sympathetic innervation
salivary glands
recieve both sympathetic and parasympathetic input
→ both increase saliva, but they produce different types of saliva
adrenal medualla
instead of sending nerve signals, it releases hormones that reinforce sympathetic effects
→ it is a modified part of the sympathetic nervous system and releases:
80% epinephrine
20% norepinephrine
into the blood stream
CNS (central nervous system)
consists of the brain and the spinal cord
responsibilities:
processing information,
making decisions
learning and memory
creating responses
brain region = cerebral hemisphere (largest part of the brain)
function:
conscious thought
learning
memory
language
voluntary movement
neurons included:
astrocytes, oligodendrocytes, microglia, ependymal cells
PNS (peripheral nervous system)
consists of cranial nerves, spinal nerves, ganglia → everything outside of the brain + spinal cord
→ job is to carry information between the body and the CNS
components:
sensory neurons (afferent) + motor neurons (efferent)
motor = somatic NS + autonomic NS
sensory neuron (afferent)
carries INFO from body → CNS
ex:
touch
pain
temperature
vision
hearing
afferent = arrives at CNS
motor neuron (efferent)
carries COMMANDS CNS → body
ex:
move muscle
stimulate galnds
efferent = exit CNS
somatic nervous system (motor)
controls the skeletal muscle → conscious control
voluntary actions:
walking
writing
talking
autonomic nervous system
controls the cardiac/spinal muscle + glands → automatic control
involuntary actions:
heart rate
digestion
blood pressure
sweating
neurotransmitters:
acetylcholine(ACh)
Norepinephrine (NE)
sympathetic nervous system (autonomic)
fight or flight response → gas pedal
activated:
stress
fear
exercise
effects:
increase heart rate
pupil dilation
decreased digestion
increase blood flow to muscles
parasympathetic nervous system (autonomic)
rest and digest → break pedal
activated:
relaxation
effects:
decrease heart rate
increase digestion
increase saliva
promotes waste elimination
has nicotinic/muscarinic receptors
acetylcholine → degraded by the enzyme cholinesterase
major excitatory NT that helps learn
glutamate, most common excitatory NT
affects mood, food intake, reproductive behaviors
serotonin → tryptophan derived
excess of this NT leads to schizophrenia
dopamine → deficiency leads to parkinson’s
an anti-seizure NT
GABA → xanax and valium also bind to receptors, reduce anxiety, and induce sleep
hyperpolarizes membrane in muscle (espically)
glycine → major inhibitory NT in spinal cord/brain stem
has alpha and beta receptors
epinephrine/norepinephrine → includes a1, a2, b1, b2, and b3
muscle fiber
one muscle
very large cell
has many nuclei
filled with myofibrils
myofibril
long tubes inside the muscle fiber → made of repeating units called saromeres
sacromere
the functional unit of contraction
→ sarcomere = smallest part that actually shortens (physically)
thick filament
also known as myosin → which is the motor protein that pulls on the actin
contains:
head
tail
ATPase site
actin-binding site
(the mover)
thin filament
contains 3 proteins:
actin
tropomyosin
troponin
actin
the “rope” that myosin grabs
tropomyosin
blocks the binding sites on actin → acts as a cover
troponin
binds the Ca2+ → calcium sensor
binded:
tropomyosin moves away
myosin can attach
A band
dark band
contains thick filament
A = All myosin
I band
light band
contains thin filaments
I = Thin
Z line
end of a sarcomere (sarcomere to sarcomere)
M line
middle of sarcomere
H zones
center region containing only myosin → gets smaller during contraction
sliding filament theory
muscle shortens due to:
thin filaments sliding
thick filaments pulling
→ NONE of the filaments themselves get shortened
during contraction:
Z lines move closer together
I band decreases
H zone decreases
A band stays the same
neuromuscular junction (NMJ)
this is where a motor neuron meets a muscle fiber
action potential travels down to α-motor neuron
voltage-gated Ca2+ channels open
Ca2+ enter nerve terminal
ACh released
ACh binds ACh receptors on muscle
Na+ enters muscle
muscle action potential begins
(skeletal muscle = 1 motor neuron)
(smooth/cardica muscle = 2 motor neuron)
excitation-contraction coupling
this explains how an electrical signal becomes a contraction
sequence:
motor neuron AP
ACh released
muscle AP produced
AP spreads across sarcolemma
AP enters T-tubles
Ca2+ released from SR
cross-bridge cycling
contraction
T-tubules
carry action potential deep into the muscle → electrical tunnels
sarcoplasmic reticulum (SR)
stores calcium
DHP + Ryanodine receptors
DHP = voltage-sensitive cork
sequence:
action potential enters T-tubles
DHP receptors senses voltage
ryanodine receptors opens
Ca2+ released from SR
(electricity in → calcium out)
SERCA pumps
after contraction → Ca2+ must be removed
SERCA pumps:
uses ATP
pump Ca2+ back into sarcoplasmic reticulum (SR)
results:
troponin loses Ca2+
tropomyosin covers actin again
muscle relaxes
cross-brige cycle
Needs: ATP + Ca2+ (without either = contraction stops)
sequence:
Ca2+ exposes binding site
myosin binds actin
power stroke occurs
ATP binds myosin
ATP splits → re-cock myosin head
(repeats as long as ATP + Ca2+ are present)
motor unit
1 motor neuron + all muscle fibers it controls
→ more force = turn on MORE motor units
ex: lift pencil → few motor units
lift heavy backpack → many motor units
load-recruitment relationship
more motor unit recruitment
(heavier weight = more nerves activated)
length-tension relationship
maximum force occurs when actin and myosin overlap optimally
too short → filaments overlap too much
top stretched → filaments barely touch
both reduce force
(best force occurs in the middle range)
force-velocity relationship
no load = fastest contraction
heavy load = slower contraction
maximum load = no movement
greater than maximal load = muscle lengthens while active
(eccentrics contractions)
isometric
force generated
NO length change
ex: holding a dumbbell still
MIDDLE GROUND → NEUTRAL
concentric
muscle shorten
ex: lifting a bicep curl
lifting UP
eccentric
muscle lengthens while producing force
most damaging type of contraction
ex: lowering a dumbbell + walking down stairs
lifting DOWN
muscle fiber types
type I, type 2a, type 2x, type 2b
type I
red fibers → slow oxdiative
characteristics:
lots of mitochondria
lots of myoglobin
uses oxygen
fatigue resistant
ex: marathon runners + posture muscles
type 2a
red fibers → fast oxidative
characteristics:
faster than type I
fairly resistant to fatigue
ex: balance of speed + endurance
type 2x
white fibers → fast glycolytic
characteristics:
very powerful
uses glycogen
fatigues quickly
ex: sprinting + jumping
type 2b
white fiber → glycolytic
characteristic:
fastest
rapid fatigue
ex: ONLY FOUND IN ANIMALS