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A-BIOL 1191 LECTURE > CH 12 > Flashcards

CH 12 Flashcards

1
Q

what two systems of the human body coordinate responses to stimuli and regulate and maintain homeostasis?

A

nervous and endocrine

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2
Q

how does the nervous system detect and respond to stimuli?

A
  • specialized cells
  • electrical and chemical means
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3
Q

what are the two divisions of the nervous system?

A
  • CNS
  • PNS
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4
Q

what does the PNS consist of?

A

the nerves branching out from the spinal cord

  • 12 cranial nerves
  • 31 spinal nerves
  • enteric plexuses in small intestine
  • sensory receptors in skin
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5
Q

what is the function of the PNS?

A
  • provides sensory input to the CNS
  • carries the responses from the CNS to effectors
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6
Q

what are types of sensory input?

A
  • somatic senses
  • special senses
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7
Q

what are somatic senses?

A
  • tactile
  • thermal
  • pain
  • proprioceptive
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8
Q

what are special senses?

A
  • smell
  • taste
  • vision
  • hearing
  • equilibrium
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9
Q

what are the different types of motor output?

A
  • skeletal muscle (somatic NS)
  • smooth muscle, cardiac muscle, glands (sym. and para. NS)
  • smooth muscle and glands of digestive canal (enteric plexuses)
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10
Q

what is the sensory fxn of the nervous system?

A

sensory receptors detect stimuli and send the information to the CNS through cranial and spinal nerves

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11
Q

what is the integrative fxn of the nervous system?

A

processes sensory info by analyzing it and deciding most appropriate responses

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12
Q

what is the motor fxn of the nervous system?

A

elicits appropriate motor response by activating effectors through the cranial and spinal nerves

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13
Q

what are the enteric plexuses?

A

network of neurons confined to digestive canal wall

  • helps regulate activity in digestive canal
  • can fxn independently
  • communicates w/ / regulated by other branches of autonomic nervous system
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14
Q

what does the CNS do?

A

processes info that comes from PNS and coordinates responses

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15
Q

what are the two types of cells that make up nervous system?

A

Neurons and Neuroglia

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16
Q

what are neurons?

A

cells that send and receive electrical signals (nerve impulses), possessing electrical excitability

  • cannot undergo mitosis when mature
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17
Q

what is the neuron’s cell body?

A
  • nucleus + other organelles required for gene expression where neurotransmitters are synthesized
  • receives stimuli and produces EPSPs and IPSPs through activation of ligand-gated ion channels.
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18
Q

why is gene expression required in neurons?

A

neurons must synthesize secretory proteins, enzymes, membrane proteins, cellular components, etc. to function

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19
Q

what is electrical excitability?

A

can respond to internal/external stimuli and generate action potentials

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20
Q

what are stimuli?

A

any change in environment that deviates organism from homeostasis, can initiate nerve impulse

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21
Q

what are Nissl bodies?

A

fragments of rER in neuron cell bodies that produce proteins

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22
Q

what are neurofibrils?

A

intermediate filaments that maintain a neuron’s shape

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23
Q

what are the neuron’s dendrites?

A

extensions from cell body that receive signals

  • highly branched, has dendritic spines, contains nissl bodies, mitochondria, ribosomes, etc.
  • Receive stimuli through activation of ligand-gated or mechanically gated ion channels; in sensory neurons, produce generator or receptor potentials; in motor neurons and interneurons, produce excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs)
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24
Q

what are dendritic spines?

A

even smaller extensions on individual dendrites that increase surface area for signal reception
- contains numerous receptor sites for binding neurotransmitters from other neurons

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25
Q

what is a neuron’s axon?

A

long cytoplasmic extension formed by microtubules and neurofibrils that propagates nerve impulses towards a postsynaptic cell

  • no nissl bodies in axons, no protein synthesis
  • Propagates nerve impulses from initial segment (or from dendrites of sensory neurons) to axon terminals in self-regenerating manner; impulse amplitude does not change as it propagates along axon
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26
Q

how do neurotransmitters go from cell body to axon terminal?

A

neurotransmitters are synthesized in cell body and transported in vesicles down microtubules in axon to axon termini

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27
Q

what are synaptic end bulbs?

A

swollen ends of axons in axon termini that form junctions with other cells

  • Inflow of Ca2+ caused by depolarizing phase of nerve impulse triggers exocytosis of neurotransmitter from synaptic vesicles
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28
Q

what are varicosities?

A

smaller swollen bumps at axon terminus

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29
Q

what is an axon hillock?

A

tapered region of cell body due to the cell narrowing into the axon
- large concentration of VGNCs in axon hillock
- where trigger zone is found

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30
Q

what is the trigger zone?

A

junction between a cell body’s axon hillock and an axon’s initial segment where nerve impulses (action potential) arises

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31
Q

what happens in the trigger zone?

A

integrates EPSPs and IPSPs and, if sum is depolarization that reaches threshold, initiates a nerve impulse

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32
Q

what is an axon’s initial segment?

A

the first part of the axon right after the cell body’s axon hillock

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33
Q

what is an axon collateral?

A

branchpoint of an axon, usually at right angles
- usually for somatic neurons

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34
Q

what are somatic spines?

A

spines on the neurolemma that increase surface area for signal exchange

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35
Q

what is an axon terminal?

A

end branch of an axon where synaptic vesicles undergo exocytosis to release neurotransmitters

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36
Q

what is the synapse?

A

the junction between a presynaptic neuron and a postsynaptic cell

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37
Q

what are the three structural classification of neurons?

A
  • multipolar: many dendrites, one axon
    – found in motor cortex of brain, cerebellum
  • bipolar: one dendrite, one axon
    – found in inner ear, retina, olfactory area of brain
  • pseudounipolar: one dendrite and axon continuous with each other (fused tgt) that emerges from cell body
    – found in posterior root ganglia and cranial nerves
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38
Q

where are the cell bodies of pseudounipolar neurons found?

A

found in ganglia of spinal and cranial nerves

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39
Q

what is the functional classification of neurons?

A
  • sensory: collect info from sensory organs through dendrites and send signal down their axons to CNS
  • motor: collect info from CNS through dendrites and send signal down their axons to effectors
  • interneurons: CNS neurons that take info from sensory neurons and relay signal directly to motor neurons (most are multipolar)
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40
Q

which functional classification of neurons plays key role in reflexes

A

interneurons allow for reflex arcs to occur without having to process sensory info in brain and spinal cord

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41
Q

what are the types of neuroglia in CNS?

A
  • astrocytes
  • oligodendrocytes
  • microglia
  • ependymal cells
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42
Q

what are the types of neuroglia in PNS?

A
  • Schwann cells
  • Satellite cells
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43
Q

what are neuroglia?

A

cells that fxn to support, nourish, protect, repair neurons

  • outnumbers neurons
  • continues to divide throughout organism’s lifetime
  • multiplies to fill in spaces formerly occupied by neurons due to injury/disease
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44
Q

what are the types of astrocytes?

A
  • protoplasmic astrocytes: short branched processes, found in grey matter
  • fibrous astrocytes: long unbranched processes, found in white matter
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45
Q

how do astrocytes get their star shape?

A

processes are formed by microfilaments supporting the cell

  • processes contact other structures(capillaries, neurons, etc.)
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46
Q

what are some functions astrocytes have?

A
  1. mechanical support (microfilaments)
  2. Blood-brain barrier - selective permeability
  3. embryonic neuronal development regulation
  4. chemical environment maintenance
  5. affects development of neural synapses
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47
Q

how do astrocytes form the Blood-Brain Barrier?

A
  • astrocytes wrap around capillaries and provide a physical barrier btwn substances in blood and the neurons
  • contributes to selective permeability through secreting substances that seal capillaries
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48
Q

what are oligodendrocytes?

A

neuroglia w/ processes that wrap around axons of CNS neurons to form myelin sheath
- oligodendrocyte itseld does not touch axons, so cannot regenerate axons if they are damaged

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49
Q

what is the function of myelin?

A

decreases the capacitance of the axolemma
- provides electrical insulation
- allows electrical signals to travel rapidly down myelinated axons

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50
Q

what is capacitance?

A

the ability to retain charge

myelinated axons have decreased ability to retain charge so it is easier for electrical signal to travel through

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51
Q

how do oligodendrocytes myelinate CNS axons?

A
  • each oligodendrocyte has ~15 processes that allows it to wrap to multiple CNS axons
  • lipids and proteins in the processes form the myelin sheath
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52
Q

why are infants less coordinated and slower to respond to stimuli than adults?

A

myelination starts during fetal development and increases until maturity

  • electrical signals travel slower down axons in infants compared to adults
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53
Q

what are microglial cells?

A
  • small cells with spiny processes that fxn. as phagocytes to facilitate neuronal development and remove debris from damaged nervous tissue
  • important in repair of CNS neurons
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54
Q

what are ependymal cells?

A
  • neuroglia with cuboidal to columnar shape that has both microvilli and cilia
  • lines brain’s ventricles and central canal to form the blood-cerebrospinal fluid barrier
  • functions during sleep
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55
Q

what is the difference btwn microvilli and cilia?

A

cilia - beat to move substances over tissues, made of microtubules

microvilli - increase SA of cells/tissues, made of microfilaments

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56
Q

what are Schwann cells?

A

neuroglia that wrap around one PNS axon to form myelin sheath using its plasma membrane, or enclose ~20 unmyelinated neurons to support development and maintain their fxn

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57
Q

what is the difference btwn myelination in CNS and PNS?

A
  • Schwann cells can only wrap one myelinated PNS neuron per cell
  • the plasma membrane forms the myelin sheath
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58
Q

what is the neurolemma?

A

the outermost layer of Schwann cells, with its cell body

the neurolemma allows PNS neurons to regenerate b/c it touches the axon itself

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59
Q

what is the fxn. of the neurolemma?

A
  • regeneration
  • neurolemma can nourish and protect axon while it regenerates
  • CNS oligodendrocytes can’t do this b/c they can’t come into contact w/ damaged axons
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60
Q

what are satellite cells?

A

flat cells that wrap around PNS ganglia

  • providing mechanical support to PNS nervous tissue
  • regulating substance exchange btwn PNS cell bodies and IF
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61
Q

what type of transport do ion channels perform?

A

facilitated diffusion
- hydrophilic surface provided by channels allow ions to move through plasma membrane rapidly

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62
Q

what transporter is responsible for the negative resting membrane potential?

A
  • Na+-K+ ATPase
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63
Q

what are the types of gated ion channels?

A
  • Leak channels
  • Ligand-gated ion channels
  • Mechanically-gated ion channels
  • Voltage-gated ion channels
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64
Q

what are leak channels?

A
  • found in all cells, including neurons
  • randomly open and close, no signals needed
  • K+LCs&raquo_space; Na+LCs ; contributes to the negative resting potential (b/c K+ leads to hyperpolarization)
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65
Q

what are ligand-gated ion channels?

A
  • found mainly in dendrites of neurons, cell bodies of motor and interneurons
  • need ligand (neurotransmitter, hormone,etc.)
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66
Q

what is a ligand?

A

a molecule that can bind to a receptor, which changes the physiology of the thing it binds to

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67
Q

what are mechanically-gated ion channels?

A
  • opens/closes in response to mechanical signal (ex. stretching of tissues, touch, pressure)
  • found in auditory receptors in ears, touch receptors in skin
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68
Q

what are voltage-gated ion channels?

A
  • open in response to changes in membrane potential
  • located in plasma membranes of electrically-excitable cells (neuron’s axons)
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69
Q

what maintains the -70mV resting potential of human cells?

A

unequal ion distribution is due to:

  • Na+-K+ ATPase (3Na out, 2K in)
  • higher propn. of K+ leak channels than Na+ leak channels
  • counterion of K+ are anionic macromolecules which can’t leave cell b/c they are important metabolic intermediates
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70
Q

when is the number of negative and positive charges in a soln. equal?

A

during equilibrium

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71
Q

describe the conc. gradient of Na+ and the direction it tends to go

A

[Na+] outside cell&raquo_space;> [Na+] inside

Na+ tends to go into the cell

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72
Q

what is the counterion to Na+?

A

Cl-

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73
Q

describe the conc. gradient of K+ and the direction it tends to go

A

[K+] inside cell&raquo_space;» [K+] outside

K+ tends to go out the cell

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74
Q

what is the counterion to K+?

A

anionic MACROmolecules

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75
Q

what is an action potential?

A

rapid depolarization followed by rapid repolarization

76
Q

what is a graded potential?

A

a SMALL change in membrane potential that occurs over a relatively short distance

77
Q

when is a cell depolarized?

A

if the resting membrane potential becomes more positive than resting

  • Na+ transported in
78
Q

when is a cell hyperpolarized?

A

if the resting membrane potential becomes more negative than resting

  • K+ transported out
  • Cl- transported in
79
Q

what determines the amplitude of the membrane potential?

A

the intensity of the stimulus

80
Q

what does “graded” mean in the context of graded potentials?

A

the magnitude of the change in membrane potential varies with the intensity of the stimulus

81
Q

what happens when a stimulus’s intensity is WEAK?

A

fewer ligand- or mechanically- gated ion channels will open

82
Q

what happens when a stimulus’s intensity is STRONG?

A

more ligand- or mechanically- gated ion channels will open

83
Q

why do electrical signals decrease in strength as distance from initiating stimulus increases?

A

leak channels which randomly open and close make it easier for charges to dissipate through them, eventually returning the membrane potential to resting

84
Q

where do graded potentials change the membrane potential?

A

close to where signal starts

graded potentials change the local membrane potential only

85
Q

why do graded potentials change the local membrane potential only?

A

the current produced when the ion channels open during a graded potential spread a short distance but die out due to the charges dissipating through the leak channels

86
Q

what is decremental conduction?

A

electrical signalling occurs over a short distance (a few mm) due to leak channels allowing charge to dissipate as distance increases

87
Q

what are postsynaptic potentials?

A

graded potentials happening in the dendrites and cell body

88
Q

what are receptor potentials?

A

graded potentials happening in the sensory receptors

89
Q

what is summation?

A

multiple graded potentials add up in strength to produce a stronger electrical signal that travel farther and opens more ion channels

90
Q

what are the phases of an action potential?

A
  • depolarization
  • repolarization
  • after-hyperpolarization (sometimes)
91
Q

how are action potentials all-or-none?

A

action potentials cannot be stimulated if a stimulus is below a threshold (-55mV)

once a stimulus reaches threshold, the amplitude of the resulting action potential is the same

stronger stimuli=/= stronger AP

92
Q

what is a subthreshold stimulus?

A

stimulus weaker than threshold of -55mV

93
Q

what is a threshold stimulus?

A

stimulus that is -55mV

94
Q

what is a suprathreshold stimulus?

A

stimulus that is strong enough to depolarize above threshold

95
Q

what happens when a threshold stimulus is received?

A
  1. depolarization
    – VGNCs open, Na+ into cell
    –NAKATPase continuously effluxes Na+ out of cell
  2. Repolarization
    – VGKCs open same time as VGNCs but more slowly, K+ out of cell
96
Q

why does after-hyperpolarization occur in some neurons?

A
  • VGNCs can be deactivated, VGKCs CANNOT
  • higher [VGKCs] and [K+ LKs] in membrane compared to Na+, more K+ leaves than Na+ enters
97
Q

how is resting membrane potential restored after after-hyperpolarization?

A

Constant action of Na+-K+ ATPase restores the resting membrane potential

98
Q

Resting state

A
  • VGNCs closed
  • VGKCs closed
  • -70mV
99
Q

Depolarizing Phase

A
  • when threshold reached
  • VGNCs open
  • VGKCs open slowly
  • Na+ rushes in cell
100
Q

Repolarizing phase begins

A
  • VGNCs inactivated by inactivating particle (abs. refractory period)
  • VGKCs still open
  • K+ goes out cell
101
Q

Repolarization phase continues

A
  • K+ outflow continues
  • resting membrane potential restored
  • VGNCs close, inactivation gates open
  • return to resting potential when VGKCs close
102
Q

what is a refractory period?

A

length of time in which cell can’t respond / less responsive to new signals

103
Q

what is the absolute refractory period?

A

busy period

  • refractory period due to VGNC inactivation
  • VGNC open but plugged in by inactivating particle
  • new depolarizing signal cannot open VGNCs b/c already open
104
Q

what is the relative refractory period

A

tired period

  • refractory period due to after-hyperpolarization
  • VGNCs closed
  • membrane potential more negative
  • stronger stimulus needed to reach threshold and trigger new AP
105
Q

why are refractory periods important?

A
  • permits cell to complete response that is already in progress
  • provides time for cell to return to resting potential before initiating new responses to new stimuli
  • permits cell to only successively respond to signals that are strong enough to reach threshold
106
Q

are action potentials decremental?

A

NO; they must not lose strength as they are propagated from the trigger zone down an axon

107
Q

what are the two types of signal propagation for action potentials?

A
  • continuous conduction
  • saltatory conduction
108
Q

what is continuous conduction

A

nerve impulses are propagated continuously in unmyelinated neuron’s axolemma

  • VG ion channels are relatively evenly distributed along axolemma of unmyelinated neurons
  • AP is continuously generated along axon’s length
109
Q

what is saltatory conduction

A

nerve impulses are propagated discontinuously in myelinated neuron’s axolemma

  • VG ion channels unevenly distributed along axolemma
  • myelin sheath is interrupted by nodes of Ranvier in both CNS and PNS myelinated neurons
  • nerve impulse appears to jump from node to node
110
Q

what are nodes of Ranvier?

A

unmyelinated portions of myelinated axons where VGNCs are concentrated

  • AP travels rapidly along myelin sheaths and when they hit nodes of Ranvier, they are regenerated, travel along next myelin sheath until hit next node
111
Q

How is it possible signals are propagated in one direction only?

A
  • all previous areas that took part in an AP are in refractory period, so AP has no choice but to continue on to part w/ no refractory period
  • abs. refractory period at peak depolarization: VGNCs inactivated therefore can’t respond to new signal
112
Q

what factors determine the speed a signal is propagated?

A
  • myelination
  • axon diameter
  • temperature
113
Q

how does myelination affect the speed a signal is propagated?

A

signals travel faster through myelinated neurons

114
Q

how does axon diameter affect the speed a signal is propagated?

A

signals travel faster through axolemma of large diameter neurons
- absolute refractory period is very brief (~0.4ms)
- larger surface area for signal transmission

115
Q

how does temperature affect the speed a signal is propagated?

A

signals travel faster at higher temperatures because molecular motion is increased

116
Q

what are the structural types of synapses?

A
  • axodendritic synapse (btwn axon and dendrite)
  • axosomatic synapse (btwn axon and cell body)
  • axo-axonal synapse (btwn presynaptic axon and postsynaptic axon)
117
Q

what are the types of synapses?

A
  • electrical synapses
  • chemical synapses
118
Q

what are electrical synapses?

A
  • adjacent neurons are directly connected via gap junctions w/ connexons that act as tunnels connecting cytosol tgt.
  • sharing of cytosol leads to rapid diffusion of ions, faster and direct communication
  • permits coordination/synchronization of neuron function, large groups of neurons can produce APs in unison due to gap jxns.
  • found in heart, skeletal muscle
119
Q

what are chemical synapses?

A

presynaptic and postsynaptic cells are separated by a synaptic cleft
- neurotransmitters released by presynaptic cell act as ligands for receptors at postsynaptic cell

120
Q

how are signals transmitted at chemical synapses?

A
  • nerve impulse travels to synaptic bulb
  • depol. occurs and opens VGCCs
  • increased [Ca2+] triggers exocytosis of synaptic vesicles
  • neurotransmitters released into synaptic cleft
  • neurotransmitters bind to receptors on postsynaptic cell
  • postsynaptic potentials are initiated
  • postsynaptic cell’s physiology changes
121
Q

what are postsynaptic potentials?

A

changes in membrane potential/voltage of the postsynaptic cell

122
Q

what keeps the signal transduction moving in one direction in synapses?

A
  • receptors can only be found on postsynaptic cells
  • signal cannot go back because presynaptic neurons do not have receptors
  • only synaptic end bulbs of presynaptic neurons can release neurotransmitter
123
Q

what are the structural types of receptors?

A
  • Ionptropic (Excitatory)
  • Ionotropic (Inhibitory)
  • Metabotropic
124
Q

what are Ionotropic receptors?

A
  • receptor IS a ligand-gated ion channel
  • NT binding site and ion channel are components of the same protein
  • when NT binds, the ion channel opens
  • can be inhibitory/excitatory
125
Q

what is an excitatory postsynaptic potential (EPSP)?

A

action potential resulting from the depolarization caused by the opening of the ligand-gated ion channel

126
Q

what is an inhibitory postsynaptic potential (IPSP)?

A

action potential resulting from the hyperpolarization of the ligand-gated ion channel

127
Q

what are metabotropic receptors?

A
  • NOT ion channels
  • G protein-coupled receptors (GPCRs): neurotransmitter binding site lacks an ion channel as part of its structure but is coupled to a separate ion channel by a G protein
  • NT binds to a transmembrane receptor
  • receptor binds and activates a G protein (GTP-binding protein)
  • activated G protein mat directly affect ion channel or sends second messengers in cytosol to affect ion channel
128
Q

how can one neurotransmitter have different effects on cells?

A

it can bind to different kinds of receptors

129
Q

why cannot neurotransmitters be left in the synapse?

A
  • signal will continue otherwise
  • sometimes effects are not needed for long time
130
Q

what are ways to remove neurotransmitters from the synapse

A
  • diffusion out of synapse
  • enzymatic degradation
  • neurotransmitter reuptake
131
Q

how can neurotransmitters return to presynaptic neurons?

A

Active transporters act as reuptake proteins that pump neurotransmitters back to recycle them

132
Q

what are the two classes of neurotransmitters?

A
  • small-molecule transmitters
  • neuropeptides
133
Q

what are some examples of small-molecule neurotransmitters?

A
  • ACh
  • Amino Acids (Glutamate, Glycine)
  • Biogenic Amines (Adrenaline, Dopamine)
  • ATP, purines
  • NO
  • CO
134
Q

what is ACh’s effect

A

PNS
- excitatory in NMJs
— binding of ACh to ionotropic receptors opens cation channels
- inhibitory in other synapses

CNS
- memory, cognition

135
Q

what is the function of acetylcholinesterase?

A

inactivates ACh by degrading it into acetate and choline fragments

136
Q

what is Glutamate’s effect?

A

excitatory in CNS

  • binding of the neurotransmitter to ionotropic receptors opens cation channels
  • The consequent inflow of cations (mainly Na+ ions) produces an EPSP
137
Q

what is GABA’s effect?

A

inhibitory in CNS only

  • binding of GABA to ionotropic receptors opens Cl− channels, producing an IPSP
138
Q

what is Glycine’s effect?

A

inhibitory in spinal cord

  • binding of glycine to ionotropic receptors opens Cl− channels
139
Q

how does GABA work?

A

GABA binds to ionotropic receptors and opens Cl- channels
- results in hyperpolarization of postsynaptic cells
- antianxiety drugs (Valium) enhance GABA’s effects

140
Q

what kinds of receptors do biogenic amines (adrenaline, dopamine, etc.) usually act on?

A

metabotropic receptors

  • biogenic amines act as 1st messengers for metabotropic receptors which activate g-proteins that send 2nd messengers which activate other proteins (like ion channels)
141
Q

what are catecholamines?

A

molecules that has:

  • 6C catechol ring
  • amine group
142
Q

what effect does norepinephrine have?

A
  • arousal/awakening from deep sleep
  • regulating mood
  • dreaming
143
Q

what effect does epinephrine have?

A

regulates fight-or-flight response (sympathetic nervous system)

144
Q

what effect does dopamine have?

A
  • regulates mood
  • addictive behaviours
  • pleasure responses
  • regulate skeletal muscle tone and some aspects of movement due to contraction of skeletal muscles
145
Q

how are biogenic amines (like the catecholamines) removed from the synaptic cleft?

A
  • reuptake
  • degraded by COMT or MAO
146
Q

what is COMT?

A

catechol-O-methyltransferase

  • degrades catecholamines, removing them from synaptic cleft
147
Q

what is MAO?

A

monoamine oxidase

  • degrades catecholamines, removing them from synaptic cleft
148
Q

what effect does serotonin have?

A
  • sensory perception
  • mood regulation
  • body temp. regulating
  • sleep induction
149
Q

where is serotonin concentrated in?

A

the raphe nucleus of the brain

150
Q

what effect do ATP and other purines have?

A
  • CNS and PNS
  • usually released with other NTs
  • Most of the synaptic vesicles that contain ATP also contain another neurotransmitter
151
Q

what neurotransmitter do sympathetic neurons release ATP with?

A

norepinephrine

152
Q

what neurotransmitter do parasympathetic neurons release ATP with?

A

acetylcholine

153
Q

what effect does nitric oxide (NO) have?

A
  • excitatory neurotransmitter in brain, SC, suprarenal glands, blood vessels, penis
  • vasodilation, increased blood flow
  • Viagra enhances vasodilatory effect in penis
154
Q

what synthesizes NO on demand?

A

NOS: nitric oxide synthase

  • NOS catalyzes NO formation from arginine
  • NO formed as needed, not in advance
155
Q

why is NO highly reactive?

A

NO is a free radical, one unpaired e- on N, stable for ~10s

156
Q

what effect does carbon monoxide (CO) have?

A
  • excitatory
  • formed as needed, not in advance
  • vasodilation
  • affects memory
  • affects olfactory and optic sensing (smelling and seeing)
  • affects thermoregulation
  • affects inflammation
  • affects release of insulin
157
Q

what are neuropeptides?

A

molecules made of 3-40 amino acids linked by peptide bonds (secondary structures)

158
Q

what effect do neuropeptides have?

A
  • may be inhibitory/excitatory
  • binds to metabotropic receptors in CNS/PNS
159
Q

what effect do enkephalins have?

A
  • analgesics (pain-relieving molecules)
  • decreases Substance P release as part of analgesic effect
160
Q

what effect do endorphins and dynorphins have?

A
  • acts as analgesics (pain-relieving molecules)
    by increasing release of opioids
  • endorphins (not dynorphins) decreases Substance P release as part of analgesic effect
161
Q

what effect does Substance P have?

A
  • enhances pain perception (opposite of analgesics)
  • released from PNS neurons that input stimuli from pain receptors to CNS

Found in sensory neurons, spinal cord pathways, and parts of brain associated with pain

162
Q

why is damage to CNS irreparable generally?

A
  • neuroglia (like oligodendrocytes) inhibit repair and regeneration
  • lack of cell division stimulation by growth factors (which were present during fetal development)
  • astrocytes fill in nervous tissue with connective tissue after injury, causing scar tissue formation that inhibits growth of neurons
163
Q

why do astrocytes inhibit neurogenesis?

A

after axonal damage, nearby astrocytes proliferate rapidly, forming a type of scar tissue that acts as a physical barrier to regeneration

164
Q

what does repair in PNS depend on?

A
  • whether cell body is intact
  • whether Schwann cells are still functional
  • the degree of scar tissue formation, if it forms too rapidly or not
165
Q

how does repair of neurons occur in PNS?

A

24-48hrs after injury:
- Nissl bodies fragment

3-5days after injury:
- myelin degrades, distal portion of axon swells and fragments while neurolemma remains
- macrophages (not microglia) phagocytize debris
- RNA and protein synthesis increase to support new axon formation
- Schwann cells multiply and surround new axon, forming regeneration tube

166
Q

what is chromatolysis?

A

The breakdown of Nissl bodies into finely granular masses in the cell body of a neuron whose axon has been damaged

167
Q

what is Wallerian degradation?

A

Degeneration of the portion of the axon and myelin sheath of a neuron distal to the site of injury.

168
Q

what is multiple sclerosis?

A
  • progressive degeneration of myelin sheath into scleroses (hardened plaques) in CNS, causing motor dysfunction and pain
  • autoimmune disorder with unknown biological mechanism
  • more common in women
  • more common in white people
  • common in Canada
169
Q

The buzzing of the alarm clock woke Carrie. She stretched, yawned, and started to salivate as she smelled the brewing coffee. She could feel her stomach rumble. List the divisions of the nervous system that are involved in each of these actions.

A

Smelling the coffee and hearing the alarm are somatic sensory, stretching and yawning are somatic motor, salivating is autonomic (parasympathetic) motor, stomach rumble is enteric motor.

170
Q

Baby Ming is learning to crawl. He also likes to pull himself onto window sills, gnawing on the painted wood of his century-old home as he looks out the windows. Lately his mother, an anatomy and physiology student, has noticed some odd behavior and took Ming to the pediatrician. Blood work determined that Ming had a high level of lead in his blood, ingested from the old leaded paint on the window sill. The doctor indicated that lead poisoning is a type of demyelination disorder. Why should Ming’s mother be concerned?

A

Demyelinaton or destruction of the myelin sheath can lead to multiple problems, especially in infants and children whose myelin sheaths are still in the process of developing. The affected axons deteriorate, which will interfere with function in both the CNS and PNS. There will be lack of sensation and loss of motor control with less rapid and less coordinated body responses. Damage to the axons in the CNS can be permanent and Ming’s brain development may be irreversibly affected.

171
Q

As a torture procedure for his enemies, mad scientist Dr. Moro is trying to develop a drug that will enhance the effects of substance P. What cellular mechanisms could he enlist to design such a drug?

A

Dr. Moro could develop a drug that: (1) is an agonist of substance P; (2) blocks the breakdown of substance P; (3) blocks the reuptake of substance P; (4) promotes the release of substance P; (5) suppresses the release of enkephalins.

172
Q

What is the role of the neurolemma in regeneration?

A

neurolemma provides a regeneration tube that guides regrowth of a severed axon

173
Q

why does a person who injures axons of a nerve in an upper limb, for example, have a good chance of regaining nerve function?

A

Most nerves in the PNS consist of processes that are covered with a neurolemma

174
Q

what is the function of a regeneration tube?

A

tube guides growth of a new axon from the proximal area across the injured area into the distal area previously occupied by the original axon

  • new axons cannot grow if the gap at the site of injury is too large or if the gap becomes filled with collagen fibers
175
Q

Suppose that the net summation of the EPSPs and IPSPs is a depolarization that brings the membrane potential of the trigger zone of the postsynaptic neuron to −60 mV. Will a nerve impulse occur in the postsynaptic neuron?

A

Since −60 mV is below threshold, a nerve impulse will not occur in the postsynaptic neuron.

176
Q

why can subsequent stimuli more easily generate nerve impulse through summation following an EPSP?

A

because the neuron is partially depolarized, making it more likely to reach threshold when next EPSP occurs

177
Q

How can the neurotransmitter acetylcholine (ACh) be excitatory at some synapses and inhibitory at others?

A

At some excitatory synapses, ACh binds to ionotropic receptors with cation channels that open and subsequently generate EPSPs in the postsynaptic cell. At some inhibitory synapses, ACh binds to metabotropic receptors coupled to G proteins that open K+ channels, resulting in the formation of IPSPs in the postsynaptic cell.

178
Q

what are the membrane proteins that perform neurotransmitter uptake called?

A

neurotransmitter transporters

179
Q

why can’t nerve impulses travel from presynaptic neurons to postsynaptic cells directly?

A

synaptic cleft prevents direct contact, IF fills the cleft

180
Q

why do chemical synapses relay signals slower than electrical synapses?

A

time required for processes at a chemical synapse to occur leads to a synaptic delay

181
Q

can action potentials experience EPSPs/IPSPs?

A

No, action potentials are in axon and always consist of depolarizing phase followed by repolarizing phase and return to resting membrane potential

182
Q

can amplitude vary in graded potentials?

A

yes, intensity/strength of stimuli can vary, leading to variation in amplitude whereas APs are all-or-none only

183
Q

How can your sensory systems detect stimuli of differing intensities if all nerve impulses are the same size? Why does a light touch feel different from firmer pressure?

A

A light touch generates a low frequency of nerve impulses. A firmer pressure elicits nerve impulses that pass down the axon at a higher frequency. (frequency of nerve impulses)

A firm pressure stimulates a larger number of pressure-sensitive neurons than does a light touch. (# of activated sensory neurons)

184
Q

Given the existence of leak channels for both K+ and Na+, could the membrane repolarize if the voltage-gated K+ channels did not exist?

A

Yes, because the leak channels would still allow K+ to exit more rapidly than Na+ could enter the axon. Some mammalian myelinated axons have only a few voltage-gated K+ channels.

185
Q

how can nerve impulses keep their strength and not die out like in graded potentials?

A

nerve impulses are propagated along the axolemma, meaning the nerve impulse that travels along the membrane is not the same nerve impulse the whole time, but new impulses being made along the axon

(imagine long row of dominoes, each domino is different)

186
Q

can another nerve impulse be initiated in relative refractory periods?

A

yes, it just has to be a larger-than-normal stimulus to overcome the hyperpolarized state of the axolemma

187
Q

Will a nerve impulse occur in response to a hyperpolarizing graded potential that spreads from the dendrites or cell body to the trigger zone of the axon of a neuron?

A

An action potential will not occur in response to a hyperpolarizing graded potential because a hyperpolarizing graded potential causes the membrane potential to become inside more negative and, therefore, farther away from threshold (−55 mV)

A-BIOL 1191 LECTURE (4 decks)

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