Lecture 6 ch7 Nervous system Flashcards

1
Q

The nervous system is divided into?

A
  • central nervous system

- peripheral nervous system (PNS)

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2
Q

CNS

A
  • central nervous system

- brain and spinal cord

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3
Q

PNS

A

 Peripheral nervous system (PNS)

 = network of nerves and ganglia carrying signals into and out of the CNS; cranial & spinal nerves

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4
Q

Nervous system consists of 2 kinds of cells

A

 Neurons & supporting cells (= glial cells)

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5
Q

neurons

A

functional units of NS

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6
Q

supporting cells

A

maintain homeostasis

 Are 5X more common than neurons

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7
Q

neurons have a

A

cell body that contains nucleus, dendrites, & axon

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8
Q

Neurons  Gather & transmit information by:

A
  1. Responding to stimuli, 2. sending and receiving electrochemical impulses, and 3. Releasing and receiving chemical messages
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9
Q

cell body

A

enlarged portion of neuron; makes macromolecules

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10
Q

groups of cell bodies in CNS are called? in PNS?

A

n CNS are called nuclei; in PNS are called ganglia (both carry out common function)

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11
Q

dendrites

A

branched processes extending from the cell body’s cytoplasm; receive information, convey it to cell body

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12
Q

axons

A

longest process; conduct impulses away from cell body

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13
Q

functional classification of neurons

A
  • sensory/afferent

- motor/efferent

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14
Q

sensory/afferent neurons

A

conduct impulses into CNS

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15
Q

motor/efferent neurons

A

carry impulses out of CNS

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16
Q

somatic motor eurons

A

responsible for reflexive and voluntary muscle control

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17
Q

autonomic motor neurons

A

responsible for smooth and cardiac muscle control and glands

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18
Q

 Association/ Interneurons

A

integrate NS activity; located entirely inside CNS

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19
Q

 Supporting/Glial Cells

 PNS

A

has Schwann & satellite cells

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20
Q

 Schwann cells

A

myelinate PNS axons

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21
Q

Supporting/Glial Cells

 CNS

A

oligodendrocytes, microglia (phagocytes), astrocytes (environmental regulators), & ependymal cells

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22
Q

 Ependymal cells

A

are neural stem cells

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23
Q

 Other glial cells are involved in

A

NS maintenance

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24
Q

 Myelination

in PNS

A

each Schwann cell myelinates 1mm of 1 axon by wrapping round & round axon = sheath of Schwann; Electrically insulates axon

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25
Q

unmylenated axons

A

 Axons < 2 µm in diameters usually

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26
Q

myelination

in CNS

A

each oligodendrocyte myelinates several CNS axons causing axons of CNS to appear white = White matter

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27
Q

gray matter

A

high concentrations of cell bodies and dendrocyes without myelin sheaths in CNS

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28
Q

 Uninsulated gap between adjacent Schwann cells is called

A

node of Ranvier (where electrical signall occur)

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29
Q

 Nerve Regeneration

 Occurs much more readily in

A

in PNS than CNS because oligodendrocytes produce proteins that inhibit regrowth and glial scars in CNS

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30
Q

 When axon in PNS is severed

A

distal part of axon degenerates and surviving Schwann cells form regeneration tube and the tube releases chemicals that attract growing axon and guides regrowing axon to synaptic site

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31
Q

neurotrophins

A

Chemicals that promote fetal nerve growth, are required for survival of many adult neurons, and are important in regeneration (promote regrowth of axons)

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32
Q

astrocytes

A

the most common glial cell; have numerous cytoplasmic processes that terminate in end feet which surround capillaries

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33
Q

astrocytes are involved in

A

 Inducing capillaries to form blood-brain barrier, Buffering K+ levels, Recycling NTs, Regulating adult neurogenesis , Taking up of glucose from blood, Synapse formation

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34
Q

BBB = Blood-brain barrier

A

Allows only certain compounds to enter brain; Formed by capillary specializations in brain that are not as leaky as those in body, Do not have gaps between adjacent cells, Closed by tight junctions

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35
Q

RMP

A

 Resting Membrane Potential (RMP)

 At rest, all cells have a negative internal charge (resting membrane potential) & unequal distribution of ions

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36
Q

RMP results from:

A

 Large anions being trapped inside cell
 Na+/K+ pump
 limited permeability keeps Na+ high outside cell
 K+ is very permeable & is high inside cell because it is attracted by negative charges inside

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37
Q

neurons have a RMP of

A

~ -70 mV

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38
Q

excitable cells

A
can discharge (alter) their RMP quickly
	By rapid changes in permeability to ions
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39
Q

excitable ells results in

A

in the diffusion of ions down their electrochemical (electrical and chemical) gradient through ion channels

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40
Q

 Neurons & muscles does excitability to

A

generate & conduct impulses

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41
Q

 Membrane Potential (MP) Changes

A

 Changes in the potential difference across the membrane can be measured by placing 1 electrode inside cell & 1 outside

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42
Q

Depolarization

A

occurs when MP becomes more positive; Excitatory (excites nerve impulses)

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43
Q

Hyperpolarization

A

: MP becomes more negative than RMP; Inhibitory (inibits nerve impulses)

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44
Q

Hyperpolarization is caused by

A

 Caused by positive charges leaving the cell or negative charges entering the cell

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45
Q

 Repolarization:

A

MP returns to RMP

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46
Q

 Membrane Ion Channels

 MP changes occur by

A

by ion flow through membrane channels

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47
Q

Membrane Ion Channels

A

 Some channels are normally open (leak channels);

 Some channels are normally closed until opened

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48
Q

 Closed channels have

A

molecular gates that can be opened

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49
Q

 Voltage-gated (VG) channels are opened by

A

depolarization
 1 type of K+ channel is always open
 other types are VG & is closed in resting cell
 Some Na+ channels are VG; closed in resting cells
 but sometimes flicker open randomly allowing leaks

50
Q

 When ion channels are closed

A

the plasma membrane is less permeable

51
Q

 Ion channels are specific for

A

a particular ion

52
Q

model of a voltage gated ion channel

A
  • look at image in pp
  • channel closed at resting membrane potential
  • channel open by depolarization (action potential)
  • channel inactivated during refactory period
53
Q

The Action Potential (AP)

A

 Is a wave of MP change that sweeps along the axon from soma to synapse

54
Q

AP wave is formed by:

A

rapid depolarization of the membrane by Na+ influx; followed by rapid repolarization by K+ efflux

55
Q

 Mechanism of Action Potential

A

depolarization

repolarization

56
Q

depolarization

A

 At threshold, VG Na+ channels open
 Na+ driven inward by its electrochemical gradient
 This adds to depolarization, opens more channels; positive feedback loop
 Causes a rapid change in MP from –70 to +30 mV

57
Q

repolarization

A

 VG Na+ channels close; VG K+ channels open
 Electrochemical gradient drives K+ outward
 Repolarizes axon back to RMP

58
Q

 Depolarization & repolarization occur via

A

diffusion
 Do not require active transport
 After an AP, Na+/K+ pump extrudes Na+, recovers K+

59
Q

 How stimulus Intensity is Coded

A

 Increased stimulus intensity causes more APs to be fired,

 size of APs remains constant

60
Q

Refractory Periods

A

Absolute refractory period

relative refractory period

61
Q

 Absolute refractory period:

A

 Membrane cannot produce another AP because Na+ channels are inactivated

62
Q

 Relative refractory period occurs when

A

VG K+ channels are open, making it harder to depolarize to threshold

63
Q

 Axonal Conduction – Cable Properties

A

 Refers to ability of axon to conduct current

64
Q

 Axon cable properties are poor because

A

cytoplasm has high resistance (though resistance decreases as axon diameter increases) and current leaks out through ion channels

65
Q

 Conduction in an Unmyelinated Axon

 After axon hillock reaches threshold & fires AP

A

its Na+ influx depolarizes adjacent regions to threshold generating a new AP, process repeats all along axon so AP amplitude is always same

66
Q

 Conduction in an Unmyelinated Axon is

A

slow

67
Q

 Conduction in Myelinated Axon

A

 Ions can not flow across myelinated membrane, thus no APs occur under myelin & no current leaks

68
Q

 Gaps in myelin are called

A

Nodes of Ranvier

69
Q

APs occur only at

A

at nodes; current from AP at 1 node can depolarize next node to threshold

70
Q

 Conduction in Myelinated Axon is fast because

A

APs skip from node to node; called Saltatory conduction

71
Q

 Synaptic Transmission – Synapse

A

 Synapse = a functional connection between a neuron (presynaptic) & another cell (postsynaptic)

72
Q

 There are chemical & electrical synapses;

A

Synaptic transmission in chemicals is via neurotransmitters (NT), Electricals are rare in NS

73
Q

 Electrical Synapsse

A

 Depolarization flows from presynaptic into postsynaptic cell through channels called gap junctions

74
Q

 gap junctions

A

formed by connexin proteins

75
Q

 Electrical Synapsse is found in

A

smooth & cardiac muscles, brain, and glial cells

76
Q

 Chemical Synapse

A

 Synaptic cleft separates terminal bouton of presynaptic from postsynaptic cell

77
Q

Chemical Synapse:

NTs are in

A

synaptic vesicles in presynaptic cell

78
Q

Chemical Synapse:

vesicles fuse with

A

bouton membrane

79
Q

Chemical Synapse:

release NT by

A

exocytosis

80
Q

Chemical Synapse:

amount of NT released depends upon

A

frequency of Aps

81
Q

 Synaptic Transmission

A

 APs travel down axon to depolarize bouton
 opens VG Ca2+ channels in bouton
 Ca2+ driven in by electrochemical gradient
 triggers exocytosis of vesicles; release of NTs

82
Q

 Neurotransmitter Release

 Is rapid because

A

vesicles are already docked at release sites on bouton before APs arrive

83
Q

 docked vesicles are part of

A

fusion complex;
 Ca2+ triggers exocytosis of vesicles
 NT (ligand) diffuses across cleft
 Binds to receptor proteins on postsynaptic membrane

84
Q

 Chemically-regulated ion channels open

  • depolarizing channel causes?
  • hyperpolarizing channels causes?
A

 Depolarizing channels cause EPSPs (excitatory postsynaptic potentials)
 Hyperpolarizing channels cause IPSPs (inhibitory postsynaptic potentials)
 These affect VG channels in postsynaptic cell

85
Q

 EPSPs & IPSPs

A

summate (add up) and if MP in postsynaptic cell reaches threshold, a new AP is generated

86
Q

 Acetylcholine (ACh)

A

 Most widely used NT; at all neuromuscular junctions, used in brain

87
Q

 Acetylcholine (ACh) Used in ANS where can be

A

excitatory or inhibitory depending on receptor subtype Nicotinic or muscarinic

88
Q

 Ligand-Operated Channels

A

 Ion channel runs through receptor

 Opens when ligand (NT) binds

89
Q

 Nicotinic ACh Channel

A

 Formed by 5 polypeptide subunits; 2 subunits contain ACh binding sites; Opens when 2 AChs bind; Permits diffusion of Na+ into and K+ out of postsynaptic cell; Inward flow of Na+ dominates; produces EPSPs

90
Q

 G Protein-Operated Channels

A

 Receptor is not part of the ion channel

 is a 1 subunit membrane polypeptide that activates channel indirectly through G-proteins

91
Q

 Muscarinic ACh Channel

A

 Binding of 1 ACh activates G-protein cascade
 Different subunit activation causes different results
 opens some K+ channels, causing hyperpolarization
 closes some K+ channels in other organs, causing depolarization

92
Q

 Acetylcholinesterase (AChE)

A

 Inactivates ACh, terminating its action; located in cleft

93
Q

 Neurotransmitters – Neuromuscular Junction (NMJ)

A

synapse between somatic motor neuron and skeletal muscle cells; use acetylcholine as NT; large synapses on skeletal muscle are termed end plates or neuromuscular junctions

94
Q

NMJ functions

A

 Produce large EPSPs called end-plate potentials; open VG channels beneath end plate; cause muscle contraction
 Curare blocks ACh action at NMJ

95
Q

 Monoamine NTs

A

 Include serotonin, norepinephrine, & dopamine,

 Receptors activate G-protein cascade to affect ion channels

96
Q

 Serotonin is derived from

A

tryptophan

97
Q

Norepi & dopamine are derived from

A

from tyrosine

 Called catecholamines

98
Q

Monoamine NTs  After release

A

are mostly inactivated by: Presynaptic reuptake, & breakdown by monoamine oxidase (MAO);

99
Q

MAO inhibitors

A

antidepressants

100
Q

Serotonin

A

 Involved in regulation of mood, behavior, appetite, & cerebral circulation; LSD (the drug acid) is structurally similar

101
Q

 SSRIs

A

(serotonin-specific reuptake inhibitors) include antidepressants; Prozac, Zolof, Paxil, Luvox = Block reuptake of serotonin, prolonging its action

102
Q

 Dopamine

A

 Involved in motor control & emotional reward

103
Q

 Degeneration of dopamine motor system neurons causes

A

Parkinson’s disease

104
Q

Dopamine reward system

A

involved in addiction

105
Q

 Schizophrenia treated by

A

anti-dopamine drugs

106
Q

 Norepinephrine (NE)

A

 Used in PNS & CNS
 In PNS is a sympathetic NT
 In CNS affects general level of arousal

107
Q

 Amphetamines stimulate

A

NE pathways

108
Q

 Amino Acids NTs

A

 Glutamic acid & aspartic acid are major CNS excitatory NTs

109
Q

 Glycine

A

is an inhibitory NT
 Opens Cl- channels which hyperpolarize
 Strychnine blocks glycine receptors

110
Q

 GABA (gamma-aminobutyric acid) is

A

is most common NT in brain

 Inhibitory, opens Cl- channels

111
Q

 Synaptic Integration – EPSPs

A
	Graded in magnitude
	Have no threshold
	Cause depolarization
	Summate
	Have no refractory period
112
Q

 Spatial Summation

A

 Cable properties cause EPSPs to fade quickly over time & distance

113
Q

 Spatial summation takes place when

A

EPSPs from different synapses occur in postsynaptic cell at same time

114
Q

 Temporal summation occurs because

A

EPSPs that occur closely in time can sum before they fade

115
Q

 Synaptic Plasticity

A

 Repeated use of a synapse can increase its ease of transmission
 = synaptic facilitation

116
Q

 High frequency stimulation often causes enhanced excitability
 Called

A

long-term potentiation

 Believed to underlie learning

117
Q

 Repeated use of a synapse can also decrease its ease of transmission

A

synaptic depression

118
Q

Synaptic Inhibition

A

 Postsynaptic inhibition

 Presynaptic inhibition:

119
Q

 Postsynaptic inhibition

A

 GABA & glycine produce IPSPs
 IPSPs dampen EPSPs
 Making it harder to reach threshold

120
Q

 Presynaptic inhibition:

A

 Occurs when 1 neuron synapses onto axon or bouton of another neuron, inhibiting release of its NT