nervous system Flashcards
excitable cell
uses RMP to generate AP to communicate
action potential
generated through depolarization events
goes beyond -55mV
main steps for action potential *
1)stimulus
2)depolarization
3) repolarization
4)hyperpolarization
5)resting stage
step 1 action potential *
stimulus trigger depolarization making cell’s inside +,
-threshold -55mV
failed initiations
depolarization is under -55mV
step 2 action potential *
depol
-Na+ channels open, K+ is closed
-inside +
step 3 action potential *
repol
-K+ channels open, Na+ channels closed
inside -
step 4 action potential *
hyper
-also called relative refractory period
-overcorrection, too negative inside
hard to elicit AP b/c Na+ channels are closed
step 5 action potential *
RMP is restored
dendrites
soma projections site to communicate with other neurons
directing AP towards soma
myelin sheath
insulating layer around axon
ensures AP transmits fast along axon
myelin made of protein and fatty acids/phospholipid membrane
schwann cell
cell that surrounds axon, produces myelin, ensures that neuron stays alive
nodes of ranvier
myelin-sheath gaps, rich in ion channels, helps with fast production of AP
cause of direction of propagation of AP
refractory periods
saltatory conduction *
AP skip from node to node in myelinate neurons
-faster
types of PNS
somatomotor/somatic and autonomic
somatomotor
going to skeletal muscles to power voluntary movement
autonomic
going to automatic organs
unvoluntary
multiple sclerosis *
-autoimmune, progressive disease that attacks myeline sheath
-if nerve is connect to muscle, muscle can’t contract
-chronic inflammatory response on myelin sheath
parietal lobe
primary somatosensory cortex
-integrate sensory info
cerebellum
coordinated movement and balance
brainstem
midbrain, pons and medulla oblongata
controls basic function l
occipital lobe
primary visual cortex> vision + visual association areas
hypothalamus
controls endocrine functions (temp, thirst, food intake) using hormones
homeostasis
negative feedback
controls release of hormones from pituitary
synapses and types
site where neurons exchange info
-electrical and chemical
electrical synapse
cell-cell communication where neurons exchange ions through channels
chemical synapse
cell-cell communication using neurotransmitters
-no channels
synaptic vesicles
contain neurotransmitters that are released in synaptic cleft
pre-synaptic neuron
transmits info to synaptic cleft via its axon + axon terminals to dendrites of next neuron
synaptic cleft
small space between axon terminals of 1 neuron and dendrites of another
post-synaptic neuron
transmits info away from synaptic cleft from its dendrites towards its own soma
steps of synapsis *
1) AP depolarizes at pre-synaptic membrane
2) Ca enters the cell, which causes synaptic vesicles to fuse with pre-synaptic membrane
3) neurotransmitters are released from synaptic vesicle into synaptic cleft
4) neuro transmitters can then
bind to receptors on post-synaptic membrane
diffuse out of synapse down [] gradient
are broken down by enzymes
absorbed into presynaptic cell
5)neurotransmitter bind to ligand-gate receptor on post-synaptic membrane and causes depolarization or hyperpolarization
EPSPs/excitatory post-synaptic potentials *
-don’t produce AP
-localized
-brings neuron closer to AP
-decay and summed (stack on top of each other)
IPSPs/inhibitory sub-threshold potentials *
-localized
-graded + summed
-neuron further away from the AP/more negative
-decay
graded potentials
-determine if an action potential is generated
can be excitatory (+) or inhibitory (-)
axon hillock
trigger zone for AP
ways to strength EPSP
temporal or spatial summation
temporal summation
1 neuron fire repeatedly
spatial summation
many neurons fire at same time
events of NMJ *
- AP propagates down pre-synaptic neuron
- Ca channels open on pre-synaptic causes Ca to rush in pre-synaptic neuron
- Ca causes synaptic vesicles with ACh inside
- ACh is released in cleft then receptors on post-synaptic
- At NMJ, acetylcholinesterase breaks down to ACh into acetate + choline
fast transmission *
ACh binds to nicotinc receptors, they open allowing ions to rush in + depolarized the cell
nicotinic receptors *
receptors that bind ACh at NMJ
-ligand-gated receptor
-spans membrane of post synaptic cell (transmembrane receptor)
slow transmission *
ACh bind to muscarinic receptors, the receptors activate biochemicals reactions on cytoplasmic side of cell. then activate and opens ion channels in post-synaptic membrane
-longer process
musk;ah;rin;ick
muscarinic receptor *
-ligand-gated receptor
-not ion channel but lead to opening of ion channels
end plate current *
graded current in skeletal muscles
end plate potential *
generated by end plante current, could lead to an AP
motor end plate *
area on skeletal muscle plasma membrane where axon terminal communicate with the muscle
RMP in muscle cell
resting membrane potential -90mV
myasthenia gravis *
autoimmune neuromuscular disease
muscle weakness caused by antibodies binding to nicotinic receptors, blocking bind of ACh
muscle
bundles of fascicles
fascicles
bundles of muscle cells/fibers
sarcolemma
plasma membrane of skeletal muscle cell
transverse tubules
indentations in sarcolemma
terminal cisternae
sis; turn;ee
sections of sarcoplasmic reticulum
the triad
t tubules and terminal cisternae
myofibrils *
bundles of organelles in skeletal muscle fibers
made up of myofilaments
myofilaments *
proteins, colour depends on thickness (thin or thick)
arranged in sarcomeres
cause straited look
sarcomeres *
-repeating units of contractile proteins
-contractile unit of myofibril
-shorten during contraction
thick myofilament *
made of bundles of myosin
length same during contraction
anchored to m-line
thin myofilament *
3 associated proteins
actin, tropomyosin, troponin
length same during contraction
myosin *
head acts as actin + ATP binding site
ATP binding site has enzyme, ATPase, to break down ATP
head changes to adapt to generate contraction
actin *
Each has a myosin binding siteeach has binding spot
troponin *
3 protein complex attached to actin tropomyosin
holds tropomyosin over myosin binding site on actin
3 subunits
troponin A, C,T
a-binds to actin
c-Ca
T-tropomyosin
sequence of sliding filaments *
1.contraction is triggered
2.myosin head binds to actin > forming cross-bridge
3. myosin head changes shape leading to power-stroke to occur
4. thin myofilament slides past thick myofilament, moves towards m-line
5.z-lines come closer together
excitation-contraction coupling vs. sliding filament theory
- AP causes the release of Ca ions from sarcoplasmic reticulum leading cross-bridge, power shroke and muscle contraction
-sarcomeres shorten
steps of excitation-contraction coupling *
- AP generated at end plate of muscle cell
- AP propagates over sarcolemma and down t-tubules
- voltages sensors on t-tubule detects AP and changes shape
- Voltage sensors from SR open Ca channels and releases Ca
- Ca binds to troponin pulling tropomyosin off myosin binding site on actin
- myosin attaches to actin + power stroke occurs
- thin filament slides over thick filament and muscle contracts
8.Ca is actively pumped back in SR by Ca ATPase
9.when Ca is ‘removed’, tropomyosin cover myosin binding site - muscle relaxes
Energized state -ATP’s role *
step 1
ATPase breaks down ATP to release energy to activate myosin head
If Ca is presence during excitation-contraction coupling, -ATP’s role *
ATP releases CA so it binds to troponin C
-This then exposes myosin binding site on actin., myosin head binds causing a cross-bridge to form
no Ca=no cross bridge
Power stroke *
myosin head’s shape changes releasing ATPase
-myosin head pulls on actin causing thin myofilament moves towards m-line and shortening of sarcomere
detachment *
When ATPase site on myosin is empty, new ATP binds to myosin head and resumes low energy conformation
Rigor Mortis *
3-4h after death
death stops ATP production b/c no o2
no ATP, actin-myosin cross-bridge can’t detach from ATPase site on myosin so no Ca back in SR. This then causes more cross bridges to form because Ca binds to troponin C
constant contraction
is rigor mortis permanent
no because decomposing cause cross-bridges to break and protein to denature
^ temp makes rigor mortis happen faster
motor unit
motor neuron and all muscle fibers it innervates
muscle twitch
a contraction in response to 1 AP on the motor neuron
latent period during a muscle twitch *
a short delay from the time when AP was generate to when muscle tension can be measured
-it takes for calcium to be released from the SR into the cytoplasm, reach and bind to troponin C, cause tropomyosin to expose the myosin binding sites on actin to form of cross-bridges
contraction period during a muscle twitch *
when muscle generates tension because cycling of cross bridges
relaxation period during a muscle twitch *
when muscle returns to normal lengths
why does relaxation take so long? *
Ca to be pumped back in SR by Ca ATPase takes long
whys is muscle movement smooth but a twitch isn’t *
the scattered arrangement of skeletal muscle cell ensure smooth contraction because diff motor unit fires asynchronously
grading muscle contraction *
increase in muscle contraction force through motor unit recruitment and/or summation of twitches
Summation of twitch contraction *
increase AP frequency accumulates force of contract (think of so many AP going on top of each other to get more force)
increase motor unit recruitment *
more are recruited because more load or more force is needed
Treppe *
increase of force of contraction because increase AP frequency in a stair like fashion
unfused tetanus *
frequency of AP allows for partial relaxation, tension in muscle plateaus
complete tetanus *
AP frequency is so high that there is no relaxation between twitches
absolute refractory period *
no AP can be elicited
2Na can’t be fired one on top of other
this is during depolarization and repolarization period
What is the direction in which an action potential propagates?
towards the axon terminals
Pathology
causes and effects of disease
two main types of brain cells
glial cells and neurons
difference between AP and graded potentials
The amplitude of a graded potential varies with the power of the stimulus, whereas the size of an action potential is all-or-none, regardless of stimulation strength.
non excitable cells
cells that do not generate action potential
somatic motor system
also called somatic nervous system
part of PNS
coordinates voluntary movement
motor neurons
used in voluntary action
CNS
communicates skeletal muscle cells at NMJ
proprioception *
the position of the limbs
brain knowing the positions of limbs b/c of receptors in muscles that sends signals back to brain
corticospinal tract
-major pathway from primary motor cortex to motor neurons that innervates muscle cells
-most nerve fibers cross contralaterally and then synapse with the lower motor neurons
muscle receptors *
muscle spindles and golgi tendon organs
what do muscle spindles do *
-increase AP frequency in motor neuron which causes twitch summation
-increase motor unit recruitment
-when muscle stretches, AP is sent to brain, brain uses proprioception
-responsible got velocity (length changes and frequency)
-has intrafusal fibers: detect length changes
Golgi tendon organs *
Signals information about the load and force applied to a muscle
Links muscles and tendon
Detects muscles tension
sensory innervation of muscle spindles *
primary (Ia) and secondary afferens (II)
primary afferen *
provides info about length changes and velocity to CNS
firing rate depends on rate of change of muscle length
secondary afferon *
provides info about change in length to CNS
firing rates doesn’t depend on rate of change of muscle length
alpha motor neurons *
innervate extrafusal fibers
generate power
part of a motor unit
gamma motor neurons *
innervate intrafusal fibers
don’t generate contraction
keep muscle spindle sensitive to stretching
alpha-gamma co-activation *
When CNS tells a muscle to contract, simultaneously alpha motor neurons contract and gamma motor neurons contract to maintain stretch on central region
-this tells brain about positioning
reflex arc *
- pain receptors send sensory info to CNS via afferent pathway
- afferent neuron synapses with interneuron in spinal cord
- interneuron synapses with efferent neuron
- info is sent to effector organ using efferent neuron
- effector organ reacts
afferent vs, efferent
sensory, go to CNS
motor, go away from CNS, to organ
sympathetic division (SYN)
ANS
responsible for activating body functions innervated in fight, flight or freeze
increase heart rate and blood pressure, dilates, airways, decrease blood flow and NRG to gut
parasympathetic division (PSYN)
stores and conserves NRG
rest and relax
decrease heart rate and BP, directs blood flow to gut
differences between SNS and PSNS *
SNS
-nerves exit spinal cord in T and L region
-axon of pregnanglionic neuron is short while post is longer a myelinates
-autonomic ganglion is close to CNS
-neurotransmitter in target organ is (no)epinephrine
PSNS
-exits at brain stem and sacral region
-axon pregnanglionic neuron is long while post is shorter and unmyelinated
-autonomic ganglion is close to target organ
-neurotransmitter in target organ is ACh
acetylcholine *
released at autonomic ganglion
binds to nicotinic receptors on dendrites of post ganglionic neurons
can use fast and slow transmission
binds to muscarinic receptors
adrenergic receptor *
add-rah-ner-gerik
receptors on target organs for epinephrine
2 types
alpha and beta adrenergic receptors
alpha adrenergic receptors response *
smooth muscle + vasoconstriction
beta adrenergic receptors response *
vasodilation, smooth muscle relaxation, bronchodilation, + excitatory cardiac function
Extrafusal muscle fiber *
normal contractile fibers
somatosensory systems
detects sensations of touch, temp, pain
usually in skin
What are the two major ascending sensory pathways? *
dorsal column system and spinothalamic tract
Sensory cortex *
-As info comes from thalamus, it is sent to a diff region on the somatosensory cortex (homunculus).
-Left part of body interpreted on right side of sensory cortex viceversa
optic nerve
transmitting visual info from retina to brain
retina cells
rod cell and cone cell
receptor cells>no AP
rod cell
sensitive to light, function in low light
1 photo pigment- don’t detect colour
retina +around fovea
cone cell
best under bright light
3 types > each with diff photo pigment
s cones short wave length blue
m-cones medium -green
lcones long-red
also called bulbous
Vision in low light and complete darkness
complete darkness, membrane will depolarize and rod cells will release neurotransmitters that inhibits bi polar cells (inhibitory N)
with little light, membrane hyperpolarize and rod cells will stop releasing neurotransmitters> see some things but not in great detail
vision in the light
cones become hyperpolarized by closes Na channels and turn off production of inhibitory neurotransmitters.
This allows more bipolar cells to be depolarized and release neurotransmitters onto ganglion nerve causing AP to reach vision center in brain
saccades
eye movement that is rapid, jerky
ex. reading
smooth pursuit
smooth eye movement to keep moving object focused
vestibular ocular reflex VOR
eye movement focused on object but head is moving
vergences
eye movement when something is towards (eyes converge) or away (eyes diverge)
semi-circular canals
3 loop shape inner ear
maintains balance and spatial orientation
resonance
standing wave bends membrane of cochlear duct to the point where there is max vibration for a frequency
steps to hearing sound*
1)outer ear brings sound along ear canal to tympanic membrane then middle ear
2)vibration go to malleus >incus and stapes
3)when stapes move, it pushes on oval window generating waves in perilymph fluid of cochlea
4)pressure waves travel through cochlea fluid causing basilar membrane to vibrate
5)mechanical NRG is converted to nerve signals
6)standing wave forms at basilar membrane (apex low frequency, base high frequency)
7)movement of basilar membrane is detected by hair cells> have stereocilia that bend when there are vibrations
8)the bending opens ion channel > depolarization of hair cells
9)triggers AP in auditory nerve fibers and transmitted to brain
anterior semicircular canal
detects forward and backward head movement
posterior semicircular canal
detects head tilts towards the shoulders
lateral/horizontal semicircular canal
detects head movements >turns head L and R
utricle
detects horizontal line acceleration and head tilts in horizontal phase
has otoliths and bend. this sends out different amount of neurotransmitters that stimulate sensory nerve and signals brain
otoliths
hair cells topped with Ca carbonate crystals
saccule
detects vertical linear acceleration and head tilts in vertical plane
has otoliths and bend. this sends out different amount of neurotransmitters that stimulate sensory nerve and signals brain
tropomyosin
Partially covers the myosin binding site at rest
free nerve endings
detect various stimuli bc of unspecialized cells
ruffini/bulbous corpuscles
in dermis of skin
detect sustained pressure
tactile/Meissner corpuscles
-in hairless skin (glabrous)
-detect light touch and low frequency vibrations
sensitive to texture and fine touch
pacinian/ lammilar corpuscles
-deep in dermis
-detect deep pressure and high frequency
-sensitive to mechanical changes
hair follicles
produce hair
detect mechanical stimuli like hair moving
