Review set 7 Flashcards
TWO major divisions of nervous system
CNS (Central = brain + spinal cord) and PNS (Peripheral = motor/ sensory nerves OUTSIDE of CNS)
Nerves made up of cells called
neurons
neurons:
carry rapid, electrical impulses
Sensory/ Afferent: signals from body TO CNS
Relay (interneurons): signals within CNS
Motor/ Efferent: carry signals FROM CNS to “effectors” (muscles/
glands)
Draw Neuron Structure and identfiy
- Dendrites: short, branched fibers (branching off the cell body)
receive chemical signals (from sensory receptors or other neurons)
and transform them into electrical signals which are sent to cell body
(into neuron) - Cell body (soma): nucleus & cytoplasm + organelles - metabolism and summation of input signals
- Axon: long nerve fibers
carry signals away from cell body to the end of the axon/ axon terminal/ synaptic terminal buttons (where neurotransmitters are released for communication with other neurons or effectors)
LOOK AT THE SLIDE
Schwann cells:
supporting cells that form an insulating layer on the axon called a myelin (mainly lipid) sheath (increases the speed of the signal along axon - saltatory conduction)
Nodes of Ranvier:
spaces in between the Schwann cells (contain membrane proteins - Na+/ K+ channels and pumps)
Neurons and Action Potentials
- Neuron “at rest” maintains resting potential (-70mV charge by sodium-potassium pump: 3Na+ out for every 2 K+ in – active transport)
- Signals/ stimuli received by dendrites
- Cell body “sums” all stimuli together (excitatory and inhibitory)
- IF stimuli “sum” to a more positive charge (more excitatory/ depolarization)
and reach threshold potential (-50mV) an action potential WILL be generated - In an action potential:
Depolarization, Repolarization, Resting potential restored.
Depolarization
(Na+ channels open and Na+ rushes INTO axon, causing more Na+ channels open – domino effect down the axon – membrane potential becomes more POSITIVE)
Repolarization
K+ channels open and K+ rushes OUT of axon – domino effect down the axon – membrane potential becomes more NEGATIVE
resting potential restored
by sodium-potassium pump: 3 Na+ OUT for every 2 K+ IN): This period called refractory period (another action potential cannot be fired until this period is complete)
In myelinated neurons what changes
action potentials travel FASTER down the axon because ion channels ONLY BETWEEN myelinated portions (Nodes of Ranvier) - SALTATORY CONDUCTION
Synaptic transmission
- An action potential arrives at the axon terminal/ synaptic knob (of presynaptic cell)
- Calcium channels open and calcium ions rush INTO the axon terminal/ synaptic knob.
- Calcium ions interact with vesicles (containing neurotransmitter) stored in the axon terminal, causing them to migrate to and fuse with the membrane of the axon terminal/ synaptic knob.
- Neurotransmitter is released (exocytosis) into the synaptic cleft (space between neurons/ neurons and effectors) and DIFFUSES across cleft
- Neurotransmitters bind to protein channels on the post-synaptic membrane (dendrites etc.).
- Protein channels open (due to change in 3 structure) and:
A. Na+ ions rush into the post-synaptic cell (causing depolarization: excitatory due to neurotransmitter Acetylcholine/ Ach) OR
B. Cl- ions rush into the post-synaptic cell (causing hyperpolarization: inhibitory) - Enzymes (such as acetylcholinesterase) break down neurotransmitters (closing ion channels on postsynaptic membrane) and their pieces diffuse back into presynaptic neuron to be assembled into vesicles again
Note: Neurotransmitter NEVER enters a postsynaptic cell!
Acetylcholine causes what?
Ach is released at the neuromuscular junction to trigger depolarization in muscle cell fibers (to cause muscle contraction)
Ach binds to nicotinic/ cholinergic receptors on muscle fibre membranes
Neonicotinoid everything you need to know
bind IRREVERSIBLY (forever) to Ach receptors (nicotinic receptors) on muscle cell membranes in insects (different composition than in humans) and BLOCK NORMAL Ach BINDING Acetylcholinesterase (AchE) is NOT able to break down neonicotinoid pesticides, so they STAY bound to receptors and insects UNABLE to generate their OWN muscle contractions = paralyzed = death Reduce honey bee and bird populations though, so…
Striated Skeletal Muscle Fiber Structure:
- Many nucleii (polynucleated)
- Many mitochondria (lots of ATP needed for muscle contraction)
- Myoglobin (stores oxygen for ATP production)
- Cell membrane (sarcolemma)
- Internal folded membrane structures (sarcoplasmic reticulum – stores Ca2+ ions)
- Myofibrils (divided into sarcomeres = functional/ contractile units: Z line to Z line) made of myofilaments = contractile proteins (actin = thin; myosin = thick)
Actin vs Myosin
Actin vs Myosin
Thin contractile protein filaments - appear as lighter bands vs Thick contractile protein filaments- appear as darker bands
Contain myosin-bidning sites vs Contain “heads” that have actin binding sites
Form helical structures vs Form shaft like structures with protruding “heads”
Regulated by the proteins troponin and tropomyosin vs “heads” are called cross-bridges and contain ATP binding sites, ATPase Enzyme
Diagram a muscle fiber
Check from Ms. Mann slide
Contraction of skeletal muscle
- Action potential from motor neuron sends Ach to muscle cell, which causes sodium ions to rush into muscle fiber, generating muscle action potential
- Muscle action potential causes release of Ca2+ ions from sarcoplasmic reticulum
- Calcium ions bind to troponin on actin filaments, causing it to change shape and move tropomyosin to expose myosin binding sites (on actin filaments)
- Myosin heads hydrolyze ATP and use energy to bind to actin filaments/ form a cross-bridge with actin
- Myosin heads release ADP, causing head to bend forward (SLIDING actin filaments IN toward sarcomere center over myosin
filaments): POWER STROKE = SHORTENS SARCOMERE! - ATP binds to myosin, breaking the cross-bridges
- ATP is hydrolyzed (by enzyme), causing myosin heads to change shape and swivel back, binding to NEXT binding site on actin
- Movement of myosin heads causes actin filaments to SLIDE over myosin filaments – shortening length of sarcomere (distance between Z lines)
Note: Actin and myosin filaments do NOT change their length during muscle contraction (they simply SLIDE PAST EACH OTHER) - This cycle of myosin binding and ATP hydrolysis continues (shortening sarcomere/ contracting muscle) as long as ATP and calcium levels remain high in sarcoplasm (cytoplasm of muscle cell)
Movement of the body requires muscles to work in
antagonistic pairs (such as the biceps and triceps in the elbow joint -a synovial joint)
Draw a Elbow and label it
CHECK IT WITH MS. MANN SLIDE
Cartilage
absorbs compression; reduces friction between bones
Synovial Fluid
Provides nutrients to cartilage; reduces friction
Joint capsule
Surrounds and seals joint cavity, limits range of motion promotes stability
Tendons
Attach muscles (triceps and Biceps) to bones
Ligaments
Connect radius ulna and humerus (bone to bone)
Biceps
Muscles hat contract to provide flexion (bending) of the arm
Triceps
Muscles that contract to provide extension (straightening) of the arm (biceps and triceps are antagonistics)
