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Bios 355 Flashcards

1
Q

Peripheral nerves

A

Efferent nerves

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2
Q

Autonomic nerves

A

Control everything but skeletal muscle

Sympathetic and parasympathetic branch

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3
Q

Somatic motor neurons

A 
Control skeletal muscle 
Single neuron 
Always excitatory 
Forms neural and muscular junction
NT is always Ach 
Target muscle expresses nicotinic cholinergic receptors 
No varicosities 
Neuromuscular junction is the synapse of a somatic motor neuron on a muscle fiber
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4
Q

Pre-ganglionic neurons

A

Can have many collateral axons that stimulate many post-ganglionic neurons

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5
Q

Sympathetic branch

A

Post ganglionic neuron releases norepinephrine at the target
Target expresses adrenergic receptors aka G-protein coupled receptors

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6
Q

Parasympathetic branch

A

Post-ganglionic neurons releases Ach onto the target

Target expresses the muscorinic cholinergic receptor (G-protein coupled receptor)

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7
Q

Sympathetic pre ganglion neurons

A

Originate in thoracic and lumbar regions of spinal cord

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8
Q

Parasympathetic pre ganglion neuron

A

Originate in sacral region of spinal cord

Cranial nerves

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9
Q

Adrenal medulla

A

Pre ganglionic sympathetic stimulates

Medulla are modified post ganglionic neurons

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10
Q

Post ganglionic neurons

A

Release epinephrine directly into blood

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11
Q

Cholinergic receptors

A

Bind Ach

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12
Q

Nicotinic cholinergic receptor

A

Ligand-gated Na channels

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13
Q

Muscorinic cholinergic receptor

A

G-protein coupled

Open Ca and potassium channels

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14
Q

Adrenergic receptors

A

G-protein coupled

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15
Q

Alpha adrenergic receptors

A 
Most common
Bind to NE 
Cause increase in Ca (smooth muscle contraction) 
Alpha 1: sympathetic target tissue 
activates phospholipase C
Cause contraction or secretion 
Alpha 2: GI tract and pancreas 
Decreases cAMP 
Cause relaxation (dilate)
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16
Q

Beta 1 adrenergic receptors

A

Cardiac/kidney
Respond to both NE and epinephrine
Increase in cAMP (intracellular signal)

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17
Q

Beta 2

A

In locations that lack sympathetic neurons
Respond to epinephrine
Increase cAMP
(Response: dilate vascular smooth muscle)

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18
Q

Beta 3

A

Adipose tissue
Increase cAMP
Bind to NE over epinephrine
Response: mobilize lipid storage

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19
Q

Properties of a sensory system

A
  1. Selective stimulus
  2. Receptor
  3. Receptor will convert the stimuli into a voltage change
  4. If voltage change exceeds threshold an AP is generated
  5. Afferent neuron delivers AP to the CNS
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20
Q

Chemoreceptors

A 
Taste 
Olfaction 
pH
Oxygen 
Glucose
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21
Q

Mechanoreceptors (physical or manual stimuli)

A 
Pressure 
Bending 
Tactile 
Hearing 
Blood pressure (baro receptors) 
Equilibrium 
Lung inflation/deflation 
Progress through the GI tract 
Proprioception (position of limbs) 
Osmolarity (water concentration)
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22
Q

Types of receptors (afferent sensors)

A 
Chemoreceptors (chemical)
Mechanoreceptors (physical)
Photo receptors (light)
Thermal receptors (heat)
Nociceptors (pain)
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23
Q

Tonic receptors

A

Continue to transmit signals as long as stimulus is present

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24
Q

Phasic receptors

A 
Habituate rapidly (cease firing AP if the stimulus is prolonged) 
Fire AP again when stimulus is removed
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25
Q

Tactile receptors

A

Skin
Viscera
Mechanosensative cation channels > Na influx > voltage change > initiates AP

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26
Q

Styles of tactile receptors

A 
Free nerve endings (variable responses) 
Meissner corpuscles (flutter/superficial/adapts rapidly)
Parcinion corpuscles (vibration/deeper layers of skin/phasic) 
Ruffini corpuscles (stretch/deep/tonic)
Merkel receptor (steady pressure/superficial/tonic)
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27
Q

Sensory cell v-gated Ca channels

A

Trp channels (transient receptor potential)

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28
Q

Two types of pain neurons

A 
Fast pain (delta fibers, fast  AP) 
Slow pain (c-fibers, slower AP)
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29
Q

Capsacius

A

Binds to trp channels

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30
Q

Chemoreceptors

A

Smell

Taste

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31
Q

Olfaction

A

Nasal epithelia olfactory receptors
G-protein coupled receptors
Activate (cause an increase in cAMP > cause ion channels to open)
Discrimination between different odorant molecules to the receptors
Lead to hippocampus and amygdala
Olfactory cortex
Smell evokes memory

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32
Q

Taste

A 
Salty 
Sweet
Sour 
Bitter 
Umami (savory) 
All non-spiking neurons
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33
Q

Bitter

A

Receptor is coupled to a G-protein
PLC
Type 2 taste receptor

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34
Q

PLC

A 
Liberates IP3 
IP3 binds to Ca channels on the ER
Channel opens 
Ca into cytoplasm 
Synaptic vesicle fuse and release NT
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35
Q

Sour

A 
Decrease in pH causes potassium channels to close 
Activates v-gated Ca channels 
Ca in 
Causes vesicles to fuse > release NT
Type 3 taste receptor
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36
Q

Salty

A

Receptor has open Na channels facing surface of tongue
Increase in NaCl in saliva, Na enters the sensor, Na influx causes depolarization
Activate v-gated Ca channels
Ca in
Synaptic vesicles fuse > release NT
Type 1 taste receptor

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37
Q

Sweet

A 
G-protein coupled receptor 
Activates adenylyl cyclase 
cAMP causes potassium channel to close 
Cause depolarization 
Activate v-gated Ca channels 
Ca in 
Synaptic vesicles fuse 
Release NT 
Type 2 taste receptor
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38
Q

Hearing

A

Mechanical receptor
Based on hair cells bending back and forth
Bending because of alternating pressure waves in the air

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39
Q

Pitch

A

Frequency

How many waves per second

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40
Q

Sounds transduction

A
  1. Sound waves
  2. Mechanical vibrations
  3. Fluid waves
  4. Bends the hair cells (mechanical)
  5. Converted to electrical signals
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41
Q

Hearing 2

A 
Sound waves (pressure) 
Tympanic membrane vibrates
Move the bones of middle ear 
Push oval window (membrane) 
Causes waves in the endolymph 
Organ of Corti 
Organ of Corti contains hair cells that transform the physical energy of the endolymph waves into electrical energy
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42
Q

Equilibrium

A 
Balance 
Position of body in space 
1. Gravity receptors 
2. Proprioceptors 
3. Visual
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43
Q

Vision

A
  1. Focus light
  2. Transduce light energy into electrical energy
  3. Neural processing
    Shorter wavelength = more energy
    Longer wavelength = less energy
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44
Q

Focusing

A

Regulates amount of light that reached photoreceptors
Pupils dilate
Decrease in aperture size and increase in depth of field
Lens is rounded (focus on objects close to you)
Ciliary muscles can pull on the lens > flattens (focus on objects farther away)

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45
Q

Photo transduction

A

Retina
Photo transducer
Synapse with bipolar cells
Synapse with ganglion cells
Axons of ganglion cells are bundled into optic nerve
Fovea > highest concentration of photoreceptors

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46
Q

Rods

A

Most common
Monochromatic
Very good at low light
Visual pigment rhodopsin

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47
Q

Cones

A

Concentrated in fovea
High acuity vision
Color vision (discriminate different wavelengths, red, blue, green)

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48
Q

Photoreceptors

A

Membrane disks

Folded membrane to increase surface area

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49
Q

Transduction mechanism: dark

A 
Photoreceptors have an open Na channel 
Depolarize 
Induce Ca influx 
NT release (glutamate) 
Increase AP
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50
Q

Transduction mechanism: light

A

Rhodopsin
>opsin (G-protein coupled receptor)
>retinal (organic carotenoid)

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51
Q

Retina in the dark

A 
Cis-bond 
Tightly binds to opsin 
Photon strikes the retinal 
Absorbs energy 
Changes structure to trans-bond 
Can't bind to opsin
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52
Q

Retina in the light

A

Changes retinal
Frees the opsin receptor
Opsin binds to the G-protein
Activates G-protein

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53
Q

Afferent neurons (somatic motor neurons)

A

Control skeletal muscle

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54
Q

Muscle

A

Collection of muscle fibers (muscle cells)
100’s-1000’s of fibers
Each fiber is controlled independently

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55
Q

Myoblast

A

Myo = muscle
Blast = immature
Form myocytes

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56
Q

Fibers

A 
Attach to connective tissue 
Bundle fibers together 
Wrap around outer muscle 
Protect to the bone  
Increase strain on muscle > increase amount of connective tissue 
Protection
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57
Q

Skeletal muscle

A

Made of many muscle fibers

Wrapped by connective tissue for protection

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58
Q

Myofibrils

A

Bundles of contractile proteins

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59
Q

Sarcomere

A

Functional unit of myofibril

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60
Q

Sarcoplasmic reticulum

A

Modified ER
Wraps around myofibrils
Stores calcium
(Calcium is signal for contraction)

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61
Q

Transverse tubules

A

Invaginations of the plasma membrane

Conduct AP along the T-tubule and deliver info decay into the muscle fiber

62
Q

Glycogen granules

A

Glucose polymer

Energy store for skeletal muscle

63
Q

Contractile proteins

A

Actin (contraction)
Myosin (contraction)
Troponin (regulatory)

64
Q

Actin

A

Forms a polymer (can only pull) (microfilament)

65
Q

Myosin

A

Motor protein

66
Q

Myosin cycle

A
  1. Myosin is energized
    - phosphorylated
    - head is cocked
    - actin binding site exposed
  2. Myosin binds to actin
    - causes myosin to change shape (rotate)
    - pulls the actin
    - de phosphorylates
  3. In the new conformation it exposes an ATP binding site on the myosin
  4. ATP binds > myosin releases microfilament
  5. Activates the myosin ATPase
  6. Phosphorylates the myosin light chain > pushes the myosin into the cocked or energized conformation
67
Q

Neublin

A

Protein responsible for placing the microfilament in these parallel arrangement

68
Q

Dystrophin

A

Complex of protein
Attach to the desmin z-line
Span membrane
Attaches to connective tissue

69
Q

Force transduction

A
  1. Myosin pulls on the microfilament
  2. MF pulls on the z-line
  3. Z-line pulls on the dystrophin
  4. Dystrophin pulls on connective tissue
  5. Connective tissue pulls on bone
70
Q

Muscular dystrophy

A

Faulty protein in the dystrophin complex
Does not attach to connective tissue
Contraction tears fibers (chronic inflammation)

71
Q

Contraction

A

Sarcomere gets smaller

72
Q

Fine/crude control

A

Fine: 1:1 ratio of neuron to muscle fiber
Crude: 1:100 neuron to muscle fiber

73
Q

Regulation of skeletal muscle

A
  1. Somatic motor neuron fires AP
  2. Neuro muscular synapse
  3. Muscle fiber depolarizers
  4. AP will also follow the transverse tubules
  5. In the t-tubules are voltage sensors
  6. Activated DHP receptor can physically touch or interact with ryanodine receptor on the SR
  7. Open ryanodine receptor will permit Ca efflux from the SR > cytoplasm
  8. Troponin complex
  9. Continue as long as Ca is high
74
Q

Relaxation

A

Stop firing AP

Ca must be pumped out of the cytoplasm back into the SR

75
Q

Calsequestrin

A

Ca storage protein
Abundant inside SR
Increase the amount of Ca that can be stored

76
Q

McArdle’s disease

A 
Faulty glycogen breakdown 
Muscle fatigue 
Stiffness 
Pain 
Glycogen storage disease 
Cannot release glucose 
Low muscle power
77
Q

Rigor Mortis

A
  1. Heart stops
    - no oxygen delivery
    - no glucose delivery
  2. Cells begin to consume store of ATP
  3. Decrease in ATP > decrease in NaK-ATPase
  4. DHP receptors respond to the voltage change
  5. Muscle myosin with bind to MF (powerstroke)
  6. Without ATP > myosin cannot release MF, muscles become stiff
78
Q

Fatigue

A

Mechanism to prevent rigor

79
Q

Fatigue mechanisms

A
  1. Insufficient oxygen delivery to muscles
  2. High rates of ATP consumption
  3. High AP frequency in large muscles
  4. Decrease in Ca in SR
    Decrease in Ca release per AP
    Decrease in relative stimulation
    Decrease in ATP consumption
  5. Central fatigue
80
Q

Slow-twitch oxidative muscle

A 
Slow contraction speed 
Slow myosin ATPase 
Small diameter of fiber 
Long duration of contraction 
Low Ca-ATPase activity 
Resistant to fatigue 
Low power 
Lots of mitochondria 
Use lots of oxygen 
Red
81
Q

Fast-twitch oxidative muscle

A 
Fast contraction speed 
Fast myosin ATPase 
Medium diameter of fiber 
Short duration of contraction 
High Ca-ATPase activity 
Reasonably fatigue resistant 
High power 
Metabolism can switch depending on depend
Red
82
Q

Fast-twitch glycolytic

A 
Really fast contraction speed 
Fast myosin ATPase 
Large diameter of fiber 
Short duration of contraction 
High Ca-ATPase activity 
Fatigue easily 
Highest power 
Very few mitochondria glycolytic 
White (no myoglobin)
83
Q

Myosin-ATPase

A

Myosin cycle how quickly it can move along the MF

84
Q

Ca-ATPase

A

Rate at when you can decrease Ca and relax (relaxation speed)

85
Q

Myoglobin

A

Respiratory pigment
Higher affinity for oxygen than hemoglobin
Cause oxygen transfer from blood to muscle

86
Q

Large motor units

A 
High power 
Lower fidelity (control)
87
Q

Small motor units

A 
Lower power 
Higher fidelity (control)
88
Q

Tension

A
  1. Sarcomere length
  2. AP frequency
  3. Size of motor unit
  4. Motor unit recruitment
89
Q

Asynchronus recruitment

A

Rotate through the motor units
35-40% of fibers responding at the same time
Also a protection device to limit muscle damage

90
Q

Renshaw cells

A

Inhibitory interneurons (spinal cord)
Adapt quickly and stay responding
Permit higher frequency after initial stimulation
Release cells glycine as NT (inhibitory synapse with motor neuron)

91
Q

Strychnine

A

Blocks glycine receptors
Eliminates renshaw cells
Muscle spasms

92
Q

Clostridium tetani

A 
Produced tetanus toxin
Blocks inhibitory interneurons 
Prevents the release of the NT 
Muscle spasms 
Seizures 
Often fatal
93
Q

Muscle tetanus

A

Sustained contraction

94
Q

Clostridium botulinum

A 
Botulinum toxin 
Typically found in food 
Prevent Ach release at the neuro-muscular synapse 
Produce a paralysis 
Most deadly toxin 
Botox
95
Q

Tetani

A

Neurotoxin
Block release of inhibitory NT
Spasms/seizures

96
Q

Botulinum toxin

A

Prevents release of Ach at neuromuscular junctions

Muscle paralysis

97
Q

Duchenie muscle dystrophy

A 
Dystrophin malfunction 
Results in muscle tears > inflammation 
Large Ca influx 
Activates protease 
Muscle breakdown 
Death due to failure of respiratory muscles
98
Q

Anderson’s disease

A 
Glycogen storage disease 
Enzyme amylo transglucosidase (responsible for branching)
Forms large crystals 
Liver damage 
Fatal
99
Q

Endurance training

A

Increase in lactic acid (decrease in pH)

  1. Increase cardiac output
  2. Increase vascularization
  3. Increase fibers make more mitochondria > increase ATP production
100
Q

Strength training

A

Increase force required
Cause a release of transcription factor
Go to nucleus
Cause transcription of sarcomere proteins (more actin/myosin)
Produce more connective tissue (protection)
Increase muscle mass
Increase capacity for force

101
Q

Protective reflexes

A
  1. Muscle tensions > protection (Golgi tendon organ)
  2. Muscle stretch (muscle spindles) > maintain length
  3. Joint capsules (proprioceptors) > joint position
102
Q

Muscle spindles

A 
Modified muscle fiber (intrafusal fibers) 
Intrafusal fibers link to connective tissue 
Neuro sensor (stretch receptor)
103
Q

Stretch

A

Neuron fired an AP
Goes to spinal cord
Synapse with the alpha-somatic motor neurons

104
Q

Golgi tendon organ

A

Mechano sensor (measure pressure)
Increase force generated by muscle pull on the tendon with more force
Increase AP frequency on sensor
Axon goes to the spinal cord
Make an inhibitory synapse with alpha-somatic motor neurons

105
Q

Antagonist muscles around a movable joint

A

Form myotatic units

Stimulation of one will cause a reciprocal inhibition of the other through interneurons

106
Q

Smooth muscle

A

Not associated with a bone
Associated with hollow organs (tubes)
Can create peristaltic forces to force movements
Can maintain force (does not fatigue)
Surrounds blood vessels, GI tract, reproductive tract, urinary tract, bladders, sphincter
Control movement through systems

107
Q

Regulation of smooth muscle

A
  1. Autonomic nervous system
  2. Paracrine control (changes in the environment)
  3. Stretch activation (peristalsis)
108
Q

Smooth muscle continued

A 
Actin/myosin 
No troponin 
(Still relies on Ca as signal) 
Less myosin per unit area 
Lower ATPase activity (cycling rate is low > slow contractions)
109
Q

SM fibers

A
  1. Single unit smooth muscle (fibers are electrically coupled to one another, gap junctions)
  2. Multi-unit smooth muscle
    Cells are not electrically coupled
    Each fiber requires individual stimulation
110
Q

SM contraction

A
  1. Increase in Ca
  2. Ca binds to calmodublin (protein)
  3. CaM binds and activates the myosin light chain kinase (phosphorylate myosin)
  4. Activates myosin
111
Q

SM relaxation

A
  1. Ca-ATPase at PM
  2. Na/Ca exchange
    Decrease Ca
    CaM releases Ca
    Stops activation of MLCK
    Myosin light chain phosphate removes the phosphate from myosin
112
Q

Cardiac muscle

A

Myogenic (muscle mistakes the AP) (pacemaker)
Fibers are small (easy to get fuel and oxygen, does not fatigue, high rate of oxygen consumption)
All cardiac myocytes are electrically coupled
1 AP = 1 heart beat

113
Q

Myogenic

A 
Specialized cells (sinoatrial node) 
Cells of SA node have an unstable resting membrane voltage
114
Q

If channel (funny channel)

A

Open Na channel
always cause depolarization
Reach threshold

115
Q

AP Route (CM)

A
  1. Starts in SA node
  2. AP spreads to the atrial myocytes (atrium contracts)
  3. From the atrial cells for AP is funneled through the AV node
  4. AV node has a very slow conduction velocity (AP is slow, gives time for the atria to contract and relax before stimulation the ventricles
  5. AP then passes down the septum following high conduction bundle of his
  6. AP spreads through the ventricular myocytes following the Purkinje fibers (high conduction)
  7. Ventricle contracts
116
Q

Fibrulation

A

AP route is too erratic

117
Q

Sympathetic (cardiac muscle)

A 
NE
Beta 1 adrenergic receptors 
Increase cAMP
Cause a decrease in potassium conductance 
Depolarize
Faster to threshold (more AP/min)
Increase HR
118
Q

Parasympathetic (cardiac muscle)

A

Release Ach
SA expresses muscorinic cholinergic receptor
Activated G-protein > binds to potassium channel
Increase potassium conductance
Take longer to reach threshold
Decrease AP/unit time (decrease HR)

119
Q

AP frequency in cardiac at rest

A

Athlete: 45 beats/min
Elderly: 90 beats/min
Max: 200 beats/min

120
Q

Limits of AP frequency in cardiac muscle

A

If Na channel (slower conductance)
Prevent reaching threshold too fast
Also refractory period at the end

121
Q

Unique feature of cardiac AP

A
  1. Myogenic
  2. Electrically coupled through gap junctions
  3. Coordinated transfer of the AP through the heart
  4. Depolarization phase is both v-gated Na channel and v-gated Ca channel
  5. Long depolarization phase (time for significant Ca influx)
  6. Myocytes are small (efficient, do not fatigue, high rates of O2 delivery)
  7. Low AP freq. (cannot induce tetanus)
122
Q

EKG waves

A 
P wave: atrial depolarization 
PQ interval: time to pass through the AV node 
Q: AP traveling down bundle of His 
R: Purkinje fibers 
S: radiating to myocytes 
T wave: ventricular repolarization
123
Q

What you can see from an EKG

A

HR
Rhythm
Conduction velocity
Size (mass) position

124
Q

Third degree heart blocks

A

Ventricular depolarization does not follow every atrial depolarization
Start contracting independently of one another
Tissue damage
Enlargement of heart

125
Q

Regulation in the force of cardiac muscle contraction

A

Do not sum cardiac fibers
Force of contraction is proportional to the amount of Ca
Increase Ca influx > increase force of contraction

126
Q

Regulation of Ca

A
  1. Catecholamines (NE, epi)

2. Mechano sensors (stretch activation)

127
Q

Catecholamines (sympathetic stimulation)

A

NE can be released from sympathetic post-ganglionic varicosities onto ventricles
Epi can be released into blood steam by adrenal medulla
Both NE and epi bind to beta 1 adrenergic receptors

128
Q

Targets for PKA in cardiac tissue

A
  1. PKA phosphorylate L-type Ca channels (increase conductance and open probability)
  2. PKA phosphorylates phospholambam (binds and increases the activity of the Ca-ATPase)
  3. PKA phosphorylates Troponin C (decrease Ca affinity, starts relaxation phase faster)
129
Q

Physical or stretch activation to increase force of contraction

A
  1. Length-tension curve (overlap between MF and myosin)
  2. Mechanosensative sensors
    Increase stretch
    Activate sensors
    Increase Ca influx = greater force
130
Q

Stroke volume

A

Volume of blood pumped per beat (SV = EDV - ESV)

131
Q

End diastolic volume (EDV)

A

Volume of blood in ventricle at the end of relaxation

Blood return rate

132
Q

End systolic volume (ESV)

A

Volume of blood in the ventricle at the end of contraction

133
Q

Cardiac output

A

Volume of blood pumped per minute

SV x HR

134
Q

Atherosclerosis

A

Decrease in stroke volume

In order to maintain C.O. HR must increase

135
Q

Heart attack

A

Cardiac proteins (Troponin isoform) in blood = damaged cells in heart = Heart attack

136
Q

Receptive field

A

The region within which a sensory neuron can sense a stimulus

137
Q

Primary sensory neuron

A

The sensory neuron that takes information from the sensory receptor into the spinal cord

138
Q

Inflammatory pain

A

Increases sensitivity to pain at sites of tissue damage

139
Q

Referred pain

A

Pain that is felt in a location away from the actual site of stimulus

140
Q

Gate control theory

A

AB fibers carry sensory information about mechanical stimuli to help block pain transmission
Ex: running a bumped elbow or skin lessens your pain

141
Q

Bipolar neuron

A

Neuron with a single axon and single dendrite

142
Q

Ganglion cells

A

Neurons of the eye whose axons form the optic nerve

Lie on surface of retina

143
Q

Optic nerve

A

Cranial nerve 2

Transmits impulses to the brain from the retina

144
Q

Visual fields (receptive fields) of ganglion cells

A

Each ganglion cell receives info from a particular area of the retina

145
Q

Z disks
M disks
Titin

A

Attachment site for thin filaments
Attachment site for thick filaments
Stabilizes the position of the contractile filament and its elasticity returns stretched muscles to their resting length

146
Q

Isotonic contraction

A

Contraction that creates force and movement

147
Q

Isometric contraction

A

Contractions that create force without movement

148
Q

Alpha motor neurons

A

Neurons that innervate extrafusual fibers and cause contraction

149
Q

Gamma motor neurons

A

Small neurons that innervate intrafusal fibers within muscle spindles

150
Q

Myotatic unit

A

Collection of pathways controlling a single joint

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