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reflex
autonomic involuntary nervous system response to an internal or external stimulus
what feedback system do reflexes use?
negative feedback system
what are components of the negative feedback system?
receptor
afferent pathway
CNS
efferent pathway
effector organ
receptor
a structure at the end of a sensory neuron that receives information
afferent pathway
sensory neuron that carries the information from the receptor to the CNS
CNS
brain and spinal cord that processes/integrates the information from the afferent pathway and relays information on how the body should respond to the initial response
efferent pathway
a motor neuron that carries information from the CNS to effector organ
effector organ
usually a muscle or gland that responds to the initial response
monosynaptic
involves one synapse between an afferent and efferent neuron
ipsilateral reflexes
reflexes that occur entirely on one side of the body
contralateral reflex
involve afferent neurons on one side of the body and efferent neurons on the other side of the body
stretch reflex
the tendon stretching activates stretch receptors(intrafusal fibers)
ex: patellar jerk reflex
what do physicians look for when testing reflexes?
they look for evenness on both sides, if it is not even there can be spinal cord damage
if spinal cord is damaged how does this impact reflexes?
at the site of damage: reflex will be weak or absent
above damaged area: will likely not be affected
below damaged area: reflexes may be exaggerated due to loss of inhibitory signals
where do axons from alpha motor neurons exit from?
the ventral horn of the spinal cord
neuromuscular junction (NMJ)
the junction/synapse between the motor neuron (axon terminus) and the innervated skeletal muscle (motor endplate)
motor unit
one motor neuron plus all of the individual muscle cells that it makes a synapse with
what is the first step to initiate movement?
an action potential initiates within the alpha motor neurons and is propagated to axon terminus
second step of initiating movement?
cell is depolarized which opens voltage-gated Ca++ channels and extracellular Ca++ enters the presynaptic terminus signaling exocytosis of ACh
third step of movement?
ACh diffuses across the NMJ synaptic cleft and binds to nicotinic ACh receptors on the motor endplate of the muscle cell which causes a conformation and opens channels
fourth step?
Na+ now flows and the inward drive of Na+ causes the motor endplate to depolarize leading to an excitatory endplate potential and bringing nearby voltage-gated Na+ channels to a threshold which triggers an AP
fifth step?
AP spreads along t-tubules and triggers Ca++ release from SR which signals protein interactions to causes muscle cell shortening
what does acetylcholinesterase do?
degrades ACh which prevents ACh from repeatedly stimulating the muscle and assures a single muscle contraction for each motor neuron action potential
how much ACh is released?
a large amount is released from alpha motor neurons to get EPP to threshold
what is tubocurarine?
a poison that blocks nicotinic receptor, so ACh can’t bind, which blocks NMJ signaling and leads to paralysis in prey
skeletal muscles
long multinucleate cells that extend from one tendon to the other tendon
what specialized proteins are in muscle cells?
actin and myosin
sarcomere
a single unit of a series of actin/myosin
why do muscle cells look striped?
as sarcomeres align along the length it gives it the striped look
excitation/contraction coupling
elevated Ca++ levels lead to molecular events that cause muscle cell shortening
tropomyosin
a regulatory protein that is typically originated across the thin filament actin that inhibits myosin from interacting and “cross-bridging”
myosin
motor protein
troponin
when Ca++ binds it induces a conformational change which leads to tropomyosin also change shape (this change exposes binding sites for myosin to interact with)
how long does cross-bridge cycling last?
until enough Ca++ is pumped back into the SR to cause troponin to return back to its original shape
cross-bridge cycle
calcium dependent interaction of actin and myosin during muscle contraction,
what parts of muscle contraction is ATP required for?
“recocking” of the myosin head group (in preparation for next powerstroke
pumping of Ca++ back into the SR by the smooth ER Ca++ ATPase
what happens if there is no ATP present?
the actin and myosin bond cannot be broken and muscles become locked in position (rigor mortis)
what are the three major methods to affect the amount and efficiency of cross-bridging?
position the muscle closer to the optimal length
increase AP frequency along single neuron via treppe, summation, and tetany
recruitment
recruitment
adding more units to the contraction
EMG
a measurement of electrical changes on the skin surface that result from AP’s generated in the muscle cells underlying the skin
if there is a stronger contraction how will the EMG read it?
the EMG wave will generate a larger amplitude
what happens when an individual muscle cell is brought to threshold?
the cell completes an “all-or-none” twitch
what happens when there are additional motor neurons stimulated?
more motor units will be added to the contraction and more cross-bridging/strength will be produced
series elastic elements
composed of elastic-like connective tissue and are located on the ends of sarcomeres
what does a single action potential do?
releases the same amount of Ca++, so if the stimulations are spaced apart well then the twitch will produce the same strength
treppe
occurs when stimulations are close enough together to produce a stronger contraction, but far enough apart to allow muscle tension to return completely to baseline
what are potential explanations for the treppe effect?
not enough time has elapsed between twitches so not enough Ca++ was pumped back into SR so there is a buildup of Ca++ and more cross-bridges to be uncovered
increase in muscle temperature due to increased activity may also improve the speed of cross-bridge
summation
when the subsequent AP’s stimulate contractions before the muscle has completely relaxed from the first contraction will have a second stronger twitch because it is stacked on the first (refractory period does not interfere with stimulation)
tetany
when the muscle is stimulated with a series of stimulations so close together that no relaxation occurs between contractions, muscle has achieved maximum contractile force
length-tension relationship
muscle has to be at optimal length to contract the strongest because actin and myosin overlap is ideal for cross-bridge intercation
what happens if a muscle is too short?
it has a weak contraction because the degree of overlap of the actin and myosin filaments is too great, so the opposing actins interfere with each other as they slide towards each other for contraction
what if a muscle is stretched too long?
it has a weak contraction because there is little overlap of the actin and myosin filaments