Exam 1 Flashcards
1
Q
Motor Unit
A
Motorneuron + fiber it innervates
1 action potential in muscle membrane (sarcolemma): 1 action potential in the muscle membrane
2
Q
Muscle Cell
A
Each muscle cell is innervated by 1 motor neuron, but neuron can branch
3
Q
Myosin
A
Motor protein
Thick filament
It’s head has a binding site for ATP and Actin
Denatured with heat
4
Q
Actin
A
Motor protein
Thin filament
5
Q
Power Stroke
A
Myosin head has been activated by the splitting of ATP into ADP and Pi, which remain bound. At this point, the myosin head has bonded to the actin, forming a cross bridge between the thick and thin filaments.
After the Pi group leaves the cross bridge, the myosin head changes its orientation producing a power stroke that moves the tin filament
6
Q
Activation of the myosin head
A
- The myosin head has an actin binding site and an ATP binding site, which serves as an ATPase to hydrolyze ATP.
- When ATP is hydrolyzed into ADP and Pi, the myosin head becomes activated and changes its orientation. It is now ready to bind to the actin subunits; at this point, ADP and Pi are still attached to the myosin head.
7
Q
Hot to regulate/control cross bridge cycle
A
tropomyosin- linear protein
troponin
8
Q
Troponin
A
Attached to tropomyosin
Intracellular Ca2+ binding protein.
When Ca2+ binds, troponin changes shape, dragging tropomyosin out of the way, which is blocking the actin binding site of the myosin
9
Q
Tropomyosin
A
blocks the actin binding site
10
Q
Muscle relaxation
A
The attachment of myosin cross bridge to actin must be prevented.
The position of the of the tropomyosin in the actin is such that it physically blocks the cross bridges from bonding to specific attachment sites in the actin. Thus, in order for the myosin cross bridges to attach to actin, the tropomyosin must be moved, requiring the interaction of troponin with Ca2+
A subunit of troponin binds to Ca2+, and as a result causes tropomyosin to change position in the thin filament
11
Q
Ca2+ in a relaxed muscle
A
Concentration of Ca2+ is low in the sarcoplasm because tropomyosin is blocking the attachment of crossbrigdes to actin.
12
Q
Overall equation glycolysis
A
Glucose + 2 NAD + 2 ADP+ 2Pi–> 2 pyretic acid + 2 NADH+2 ATP
13
Q
Formation of lactic acid
A
Pyretic acid–>Lactic acid
enzyme: Lactic acid dehydrogenase
NADH+H+ is oxidized
14
Q
First step glycolysis that’s regulated
A
glucose-->glucose-6-phosphate enzyme: hexokinase ATP--> ADP stimulated by glucose, inhabited by G-6-P (end-product inhibition) delta G= -7.5kcal/mol
15
Q
Second large step of regulation during glycolysis
A
Fructose-6-phosphate-->Fructose-1,6-bisphosphate enzyme: Phosphofructokinase (PFK) ATP-->ADP delta G= -3.4 kcal regulated by ATP levels, G6P inhibits, AMP stimulates, decreased pH (inhibits-allosteric) Citrate-inhibits
16
Q
Third large step of regulation during glycolysis
A
Phosphoenolpyruvate-->Pyruvate Enzyme: Pyruvate Kinase ADP+P-->ATP Delta G= -7.5 kcal/mol Regulated by: fructose 1,6 bisphosphate (stimulates) ATP inhibits alanine inhibits
17
Q
What is the significance of the Cori cycle between liver and muscle
A
With strenuous muscle activity, blood lactate levels increase. The liver can take up the lactate, convert it to glucose and release it into the blood stream to be used as an energy source for exercising muscles. This is an important energy source for exercising muscles and muscles recovering from exercise (to restore muscle glycogen).
18
Q
Explain how facilitated diffusion differs from simple diffusion and how active transport can be distinguished from passive transport.
A
Facilitated diffusion involves specific channels or carrier molecules to move impermeable molecules along their concentration gradient. Simple diffusion involves membrane-permeable substances moving along their gradients.
Active transport requires direct or indirect energy from ATP hydrolysis to move molecules against their concentration gradients. Passive transport is along the gradient.
19
Q
Competitive Inhibitors
A
same vmax, different km
20
Q
Noncompetitive Inhibitors
A
same km, reduced vmax
21
Q
Amino acid metabolism
A
Pyruvic acid Acetyl CoA Alpha-ketogluterate Succinct Acid Fumaric Acid Oxaloacetic Acid
22
Q
Energy yield (anaerobic)
A
32
23
Q
Corticospinal
A
motor efferent nerve that crosses over in the medulla going down to effector organ, starts in cerebral cortex
So, injury in spine can’t control anything below it on the same side.
24
Q
Dorsal Colum
A
Fine touch, vibration, proprioception
Crosses over in the medulla so can’t feel fine touch/ vibration on the same side
25
Spinothalamic
Lateral- pain, temp
Anterior- crude touch
comes in at receptors and then crosses over immediately in spinal cord and goes up to medulla through midbrain to thalamus and then cerebral cortex.
Can't feel pain/temp below injury on the opposite side
26
GLUT4
insulin regulate heart, muscle, adipose unregulated after meals
27
SGLT-Na+ dependent
not reversible, flow in direction of Na+ (intestine, kidney)
| play a role in glucose in gut
28
Cerebral spinal fluid
Provides basic mechanical/immunological protection to brain inside skull
29
phospholipid
barriers, hydrophobic inside, hydrophilic outside
30
Glycolipid
serve as marker for cellular recognition
31
Transmembrane protein (integral protein)
significant in moving things across membranes (transport)
32
Cholesterol
in animal membranes, can enhance/inhibit membrane fluidity, can manipulate concentration
33
Glycoprotein
important in cell signaling, identity, defense
34
Cytoskeleton
microfilaments giving structure to cell-signaling pathways, way to connect inside and outside cell (actin) conduit between membrane and deeper environments
35
Cytoskeleton
microfilaments giving structure to cell-signaling pathways, way to connect inside and outside cell (actin) conduit between membrane and deeper environments
36
Hypotonic
fluid rushes in, cell bursts
37
Hypertonic
fluid rushes out, cell shrivels
38
Isotonic
nothing
39
Nernst Equation
Ex= RT/ZxF ln([X]o/[X]i) Equilibrium potential for the specific ion
40
GHK
Vm=RT/F ln(p[K+]o/[K+]i.... Resting Membrane Potential
41
CNS
brain + spinal cord
42
PNS
nerves, ganglia, nerve plexus, carry info in and out of CNS
43
Enteric NS
Gut+ intestine
44
afferent, sensory
conduct impulses from sensory receptors into CNS
45
efferent, motor
conduct impulses out of the CNS and serve the associate or integrative functions of the NS
46
association neurons or interneurons
located entirely within CNS and serve the associative or integrative functions of the NS
47
oligodendrocytes
form myelin sheath around CNS
48
schwann cells
form myelin sheaths around peripheral axons
49
satellite cells
support neuron cell bodies within the ganglia of PNS
50
microglia
migrate through the CNS and phagocytose foreign and degenerated material, derived from immune system established in development
51
Astrocytes
help to regulate external environment of neurons in the CNS, helps regulate NT metabolism, regulate K+ concentration in extracellular environment and H+ and pH ,regulate lactate metabolism
52
Ependymal cells
epithelial cells that line the ventricles of the brain and the central canal of the spinal cord, secrete fluid of Cerebral spinal fluid
53
Acetylcholine
Precursors acetyl co a + Choline
| Enzyme: choline acetyl transferase found in presynaptic terminal packaged into synaptic vesicles
54
Pesticides inhibit
ACHE
55
Acetylcholinesterase
splits into choline and acetate within the terminal of the extracellular space
56
Cholinergic Receptors
Nicotinic Acetylcholine Receptor (nAChR)
| Muscarinic AChR
57
Catecholamines
Dopamine, norepinephrine, epinephrine
58
Catecholamines are derived from
tyrosine
59
Serotonin is derived from
tryptophan and packaged and made in synaptic terminals
60
MAO
monoamine oxidase inside neurons of astrocytes breaks down serotonin in the liver
61
GABA and Glutamate
do most of the signaling in the CNS of humans
62
Glutamate is precursor to
GABA
63
GABA
ipsp
64
Glutamate
epsp
65
Overall mechanism of NT release
1. action potential reaches presynaptic terminal
2. Depolarization of presynaptic terminal opens ion channels allowing Ca2+ into cell
3. Ca2+t triggers release of NT from vesicles
4. NT binds to receptor sites on post synaptic membrane
5. Opening and closing of ion channels cause change in post-synaptic membrane potential
6. action potential propagates through next cell
7. NT is inactivated or transported back into presynpatic terminal
66
Overall mechanism of NT release
1. action potential reaches presynaptic terminal
2. Depolarization of presynaptic terminal opens ion channels allowing Ca2+ into cell
3. Ca2+t triggers release of NT from vesicles
4. NT binds to receptor sites on post synaptic membrane
5. Opening and closing of ion channels cause change in post-synaptic membrane potential
6. action potential propagates through next cell
7. NT is inactivated or transported back into presynpatic terminal
67
What is the functional significance of the dual innervation of many organs by the parasympathetic and sympathetic branches of the autonomic nervous system?
Enables a wide dynamic range of activity of the organs to precisely regulate. Activity can change with the reduction of input from one system, or the addition of the input from the other system.
68
Joe Schmoe suffered a stroke that led to difficulty swallowing, as well as deficits with parotid gland salivation and taste sensation in the posterior regions of his tongue. The clinicians determined that there was likely damage to which cranial nerve?
Glossopharyngeal (CN IX)
69
9. Allison has a rare condition that leads to a higher than normal concentration of potassium in her extracellular fluid. You measure the ion concentrations of the three major ions, noted in the table below. What effect does her condition have on neuron function? Be specific and complete.
Allison’s equilibrium potential for K+ will be -57 mV (instead of -88.88mV. This will make the resting membrane potential (if all permeabilities remain the same) less negative than normal, making her excitable cells (neurons, muscle, etc) more likely to reach threshold for any given stimulus and would reduce the afterhyperpolarization phase of action potentials, shortening the refractory period.
70
CN I
Olfactory
| *nose
71
CN II
Optic Sensory
| *eye, retina into optic nerve, crosses to opposite site
72
CN III
Oculomotor
* all eye muscles except those in IV, VI
* carries some afferent information info from eyes
73
CN IV
Trochlear motor
| *superior oblique muscle of he eye, motor function to eye
74
CN V
Trigeminal sensory
*face, sinuses, teeth, etc.
motor
*muscles of mastication, innervates facial muscles like in novocain, regulates chewing
75
CN VI
Abducent motor
| *External rectus muscle of the eye
76
CN VII
Facial motor
*muscles of the face
intermediate motor
*submaxillary & sublingual gland (lip, cheek)
sensory
*anterior part of the tongue&soft palate, closing eyelid when laying
77
CN VIII
Vestibulocochlear sensory
| *inner ear, major auditory nerve, balance
78
CN IX
```
Glossopharyngeal
motor
*pharyngeal musculature
sensory
*posterior part of tongue, tonsil, pharynx
```
79
CN X
Vagus motor
*heart, lungs, bronchi, GI tract
Sensory
*heart, lungs, bronchi, trachea, larynx, pharynx GI tract
80
CN XI
Accessory motor
| *sternocleidomastoid and trapezius muscles (muscles of neck and jaw)
81
CN XII
Hypoglossal motor
| *muscles of tongue
82
CN XII
Hypoglossal motor
| *muscles of tongue
83
A 2 M solution of NaCl and 2 M glucose solution are separated by a membrane permeable to water but not to the solutes. What happens? Why
Glucose doesn’t dissociate in water, but NaCl does. Therefore on the glucose side of the membrane, there will be 2 osmoles of glucose, but on the NaCl side there will be 2 osmoles of Na+ and 2 osmoles of Cl- for a total of 4 osmoles. Thus the water will move from the glucose side of the membrane toward the NaCl side of the membrane, because the NaCl side has a greater number of moles/kg solvent
84
The four types of tissue are
epithelial, muscle, nervous, and connective
85
A noncompetitive enzyme inhibitor alters the Vmax without changing the Km.
True
86
A paper published in 2001 described a reduction in GLUT4 transporters on the plasma membrane of slow muscle fibers in patients with Type 2 diabetes. What are the consequences of this result?
In Type 2 diabetes, fewer GLUT4 receptors (carrier transport consequences), glucose in the blood won’t be able to be uptaked normally by slow twitch muscles, leading to faster fatigue under exercise. Metabolically, glycogen levels will decrease because will be used for energy so muscle will be compromised because glycogen stores are lowered and so the cell will be pushed towards lactate and gluconeogensis under these conditions.
87
What is the main function served by the formation of lactic acid during anaerobic metabolism? How is this function accomplished during aerobic respiration?
When oxygen is not available in sufficient amounts, the NADH (+ H+) produced in glycolysis is oxidized in the cytoplasm by donating its electrons to pyruvic acid. This results in the reformation of NAD and the addition of 2 hydrogen atoms to pyruvic acid, which is thus reduced. This addition of 2 hydrogen atoms to pyruvic acid produces lactic acid. In anaerobic respiration the last electron acceptor is an organic molecule, wheras in aerobic respiration the last electron acceptor is an atom of oxygen. Yields a net 2 ATP produced by glycolysis per glucose molecule.
88
Lactic acid metabolism
The main function served by the formation of lactic acid during anaerobic metabolism is to generate a form of sugar that can be broken down continuously to generate cellular energy in the form of ATP. During anaerobic respiration, without the presence of oxygen, pyruvate is converted into lactic acid by
In order for glycolysis to continue, there must be adequate amounts of NAD available to accept hydrogen atoms. Therefore, the NADH produced in glycolysis must become oxidized by donating its electron to another molecule. In aerobic respiration this other molecule is located in the mitochondria and ultimately passes its electrons to oxygen during the ETC when oxygen is the final electron acceptor.
89
If you experimentally increase the permeability of an axonal membrane to sodium ions, the equilibrium potential for sodium in the cell will
remain unchanged, because equilibrium is independent of permeability
90
The equilibrium potential of an ion is the potential
which just balances the concentration difference of the ion across the membrane.
91
The equilibrium potential of an ion represents
the electrical charge just required to balance the concentration difference of one specific ion across the membrane.
92
The Nernst Equation
Tells us the Equilibrium Potential of an ion
| =25mV*ln[out/in]
93
The Nernst equation ______ be used to calculate the membrane potential because ______
cannot; it tells you only what the equilibrium potential for an individual ion is, not what the summed effect of all ions is on the
94
The membrane of a typical resting neuron is largely impermeable to
Na+
95
In a squid giant axon, if one reduced the external concentration of Na+ around a neuron, the membrane potential would quickly
stays the same
96
Knee Jerk
Summary of events:
1. Passive stretch of a muscle (produced by tapping its tendon) stretches the spindle (intrafusal) fibers
2. Stretching of a spindle distorts its central (bag or chain) region, which stimulates dendritic endings of sensory neurons
3. Action potentials are conducted by afferent (sensory) nerve fibers into the spinal cord on the dorsal roots of the spinal nerve
4. Axons of sensory neurons synapse with dendrites and cell bodies of somatic motor neurons located in the ventral horn gray matter of the spinal cord.
5. Efferent nerve impulses in the axons of alpha motor neurons in the ventral roots of spinal nerves are conducted to the ordinary (Extrafusal) muscle fibers
6. Release of acetylcholine from the endings of the alpha motor neurons stimulates the contraction of the extrafusal fibers and thus the whole muscle
7. Contraction of the muscle relieves the stretch of its spindles thus decreasing activity in the spindle afferent nerve fibers.
97
Monosynaptic stretch reflex
1. Striking ligament, stretches tendon and quadriceps femoris muscle
2. Spindle is stretched activating sensory neuron
3. Sensory neuron activates alpha motor neuron.
4. Alpha motor neuron stimulates extrafusal muscle fibers to contract in the spinal cord
98
Reciprocal innervation
Afferent impulses from muscle spindles stimulates alpha motor neurons to the agonist muscle (the extensor) directly, but (via an inhibitory interneuron) they inhibit activity in the alpha motor neuron to the antagonist muscle
99
Energy usage during light exercise
25% Vo2max
| aerobic respiration of fatty acids
100
Energy usage during moderate exercise
Both fatty acids and glucose (including muscle glycogen
101
Energy usage during Intense exercise
2/3 from glucose (esp glycogen
102
Muscle fiber types
1. Slow-twitch IA and Fast oxidative IIA (human
2. Fast-twitch white (II)
3. Fast-twitch (IIX)-
103
Slow-twitch IA and Fast oxidative IIA
higher resistance to fatigue, lots of myoglobin
104
Fast-twitch white (II)
faster myosin ATPase, less myoglobin, anaerobic , lots of glycogen
105
Fast-twitch (IIX)-
faster myosin ATPase, less myoglobin, anaerobic, fatigue rapidly
106
Voluntary control
Upper motor neuron, crosses over at corticospinal tract so at medulla.
107
Smooth muscle
Mechanism: sliding muscle
arrangement of myofibrils is very different not striated because no rigid organization.
Actin filaments attach along dense bodies, different locations and planes so good when contraction.
*HIGHER actin concentration
*orientation of myosin is perpendicular instead of helical
108
Two types of smooth muscle
1. Single unit smooth muscle
| 2. Multiunit smooth muscle
109
Contraction of Smooth muscle
v. different than skeletal muscle.
When smooth muscle is stimulated:
1. Fire action potentials along a muscle membrane.
2. Voltage gated Ca channels open and allow influx into cytoplasm of smooth muscle.
3. Ca binds to Calmodulin which activates myosin-light chain (MLCP)
4. PHOSPHORYLATION OF CROSS BRIDGE LEADS TO CONTRACTION
5. DEPHOSPHORYLATION OF CROSS BRIDGE LEADS TO RELAXATION
slower than skeletal muscle e
110
What neurotransmitter is released by preganglionic neurons of the sympathetic nervous system?
Acetylcholine
111
What neurotransmitter is released by the post-ganglionic neurons emerging from the sympathetic chain ganglia neurons?
Norepinephrine
112
. A victim of a car accident suffered a spinal cord lesion on the right side of the thoracic part of the spinal cord, at T6. What specific defects in sensation and motor function result (lists are fine)?
Motor and fine touch deficits in right side
| Paint/temp deficits on left
113
Sympathetic Neuron
short preganglionic neuron that releases ACh to nAChR then a long post-ganglionic neuron that releases NE to alpha1,2 and beta1,2 receptors to smooth muscle
114
Parasympathetic Neuron
long pre-ganglionic neurons that releases ACh to nAChR then a short post-synaptic neuron that releases ACh to mAChR to smooth muscle
115
somatic NS neuron
heavily myelinated axon releasing ACh to skeletal muscle
116
How does ATP participate in the cross-bridge cycle of skeletal muscle contraction? A diagram might be the best way to answer this question.
1. ATP binds to myosin head allowing it to dissociate from actin.
2. ATP is hydrolyzed by myosin-ATPase to ADP +Pi
3. Pi binds to myosin head→ conformational change to “cocked position”
4. Myosin head binds to actin filament
5. Pi leaves myosin head, conformational change→ power stroke
6. ADP leaves myosin head to allow another molecule to bind.
117
lymphatic system
Immune defsnse, filtraton of interstitial fluid + return to blood, transport of absorbed fats from small intestine into blood stream
118
What is the mechanism by which an action potential on a muscle membrane is transduced into a physical contraction (ie. excitation-contraction coupling)? A flow chart or diagram is fine.
ACh release across synapse→ binds to nAChR at motor end plate→ voltage gated Na+ channels open→ depolarization conducted by more Na+ channels down sarcolemma to T-tubules→ voltage gated Ca++ channels open, mechanically coupled to calcium release channels in sarcoplasmic reticulum, increased sarcoplasmic Ca++ → Ca++ binds to troponin to move tropomyosin out of the way of myosin binding sites on actin → cross bridge cycle (contraction).
To end contraction: cross-bridge cycle must cease. The calcium release channels will close, so Ca++ can’t passively diffusie out of the terminal cisternae. Ca++ in cytoplasm must then be moved against a concentration gradient back into the lumen of the sarcoplasmic reticulum. The active transport pumps for Ca++ are in the family of sarcoplasmic/endoplasmic reticulum Ca++ ATPase (or SERCA pumps) that accumulate Ca++ so it is sequestered from the cytoplasm. Thus preventing Ca++ from binding to troponin, so that tropomyosin can resume its position tha tblocks the myosin heads from bindign to actin. ATP is required for this part too!
119
somatic NS neuron
heavily myelinated axon releasing ACh to skeletal muscle
120
How do skeletal muscles respond to varying loads
By recruiting increasingly large motor units (somatic motor neuron and the muscle fiber it innervates) as load increases. Muscle fibers are stimulated rapidly and asynchronously in order to produce smooth, sustained contractions through summation of electrical signals. Filaments overlap, thin filaments over and between the thick filament. I H band get shorter during contraction.
121
Contrast skeletal and smooth muscle
```
Skeletal
Sarcomeres are basic unit of contraction
Myosin filaments parallel to thick filament
Excitation-contraction via tropnin
somatic
Individually innervated
```
Smooth
Actin anchored to dense bodies +cell walls in a less organized fashion
Myosin filaments perpendicular to thick filaments
Excitation-contraction via calmodulin and myosin ligh chain phosphorylation
Autonomic
Gap junctions (functional syncytium, except motor unit)
122
List three physiological adaptations of skeletal muscles to endurance training that illustrates the plasticity of the tissue
Increased myoglobin content
Increased size and number of mitochondria
Improved efficiency in extracting oxygen from blood
