Physiology Lab Quiz #2

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?

1. receptor

2. afferent pathway

3. CNS

4. efferent pathway

5. 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?

1. “recocking” of the myosin head group (in preparation for next powerstroke

2. 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?

1. position the muscle closer to the optimal length

2. increase AP frequency along single neuron via treppe, summation, and tetany

3. 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?

1. 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

2. 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