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
unmylenated axons
 Axons < 2 µm in diameters usually
26
myelination | in CNS
each oligodendrocyte myelinates several CNS axons causing axons of CNS to appear white = White matter
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gray matter
high concentrations of cell bodies and dendrocyes without myelin sheaths in CNS
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 Uninsulated gap between adjacent Schwann cells is called
node of Ranvier (where electrical signall occur)
29
 Nerve Regeneration |  Occurs much more readily in
in PNS than CNS because oligodendrocytes produce proteins that inhibit regrowth and glial scars in CNS
30
 When axon in PNS is severed
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
31
neurotrophins
Chemicals that promote fetal nerve growth, are required for survival of many adult neurons, and are important in regeneration (promote regrowth of axons)
32
astrocytes
the most common glial cell; have numerous cytoplasmic processes that terminate in end feet which surround capillaries
33
astrocytes are involved in
 Inducing capillaries to form blood-brain barrier, Buffering K+ levels, Recycling NTs, Regulating adult neurogenesis , Taking up of glucose from blood, Synapse formation
34
BBB = Blood-brain barrier
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
35
RMP
 Resting Membrane Potential (RMP) |  At rest, all cells have a negative internal charge (resting membrane potential) & unequal distribution of ions
36
RMP results from:
 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
37
neurons have a RMP of
~ -70 mV
38
excitable cells
``` can discharge (alter) their RMP quickly  By rapid changes in permeability to ions ```
39
excitable ells results in
in the diffusion of ions down their electrochemical (electrical and chemical) gradient through ion channels
40
 Neurons & muscles does excitability to
generate & conduct impulses
41
 Membrane Potential (MP) Changes
 Changes in the potential difference across the membrane can be measured by placing 1 electrode inside cell & 1 outside
42
Depolarization
occurs when MP becomes more positive; Excitatory (excites nerve impulses)
43
Hyperpolarization
: MP becomes more negative than RMP; Inhibitory (inibits nerve impulses)
44
Hyperpolarization is caused by
 Caused by positive charges leaving the cell or negative charges entering the cell
45
 Repolarization:
MP returns to RMP
46
 Membrane Ion Channels |  MP changes occur by
by ion flow through membrane channels
47
Membrane Ion Channels
 Some channels are normally open (leak channels); |  Some channels are normally closed until opened
48
 Closed channels have
molecular gates that can be opened
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 Voltage-gated (VG) channels are opened by
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
 When ion channels are closed
the plasma membrane is less permeable
51
 Ion channels are specific for
a particular ion
52
model of a voltage gated ion channel
- look at image in pp - channel closed at resting membrane potential - channel open by depolarization (action potential) - channel inactivated during refactory period
53
The Action Potential (AP)
 Is a wave of MP change that sweeps along the axon from soma to synapse
54
AP wave is formed by:
rapid depolarization of the membrane by Na+ influx; followed by rapid repolarization by K+ efflux
55
 Mechanism of Action Potential
depolarization | repolarization
56
depolarization
 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
repolarization
 VG Na+ channels close; VG K+ channels open  Electrochemical gradient drives K+ outward  Repolarizes axon back to RMP
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 Depolarization & repolarization occur via
diffusion  Do not require active transport  After an AP, Na+/K+ pump extrudes Na+, recovers K+
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 How stimulus Intensity is Coded
 Increased stimulus intensity causes more APs to be fired, |  size of APs remains constant
60
Refractory Periods
Absolute refractory period | relative refractory period
61
 Absolute refractory period:
 Membrane cannot produce another AP because Na+ channels are inactivated
62
 Relative refractory period occurs when
VG K+ channels are open, making it harder to depolarize to threshold
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 Axonal Conduction – Cable Properties
 Refers to ability of axon to conduct current
64
 Axon cable properties are poor because
cytoplasm has high resistance (though resistance decreases as axon diameter increases) and current leaks out through ion channels
65
 Conduction in an Unmyelinated Axon |  After axon hillock reaches threshold & fires AP
its Na+ influx depolarizes adjacent regions to threshold generating a new AP, process repeats all along axon so AP amplitude is always same
66
 Conduction in an Unmyelinated Axon is
slow
67
 Conduction in Myelinated Axon
 Ions can not flow across myelinated membrane, thus no APs occur under myelin & no current leaks
68
 Gaps in myelin are called
Nodes of Ranvier
69
APs occur only at
at nodes; current from AP at 1 node can depolarize next node to threshold
70
 Conduction in Myelinated Axon is fast because
APs skip from node to node; called Saltatory conduction
71
 Synaptic Transmission – Synapse
 Synapse = a functional connection between a neuron (presynaptic) & another cell (postsynaptic)
72
 There are chemical & electrical synapses;
Synaptic transmission in chemicals is via neurotransmitters (NT), Electricals are rare in NS
73
 Electrical Synapsse
 Depolarization flows from presynaptic into postsynaptic cell through channels called gap junctions
74
 gap junctions
formed by connexin proteins
75
 Electrical Synapsse is found in
smooth & cardiac muscles, brain, and glial cells
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 Chemical Synapse
 Synaptic cleft separates terminal bouton of presynaptic from postsynaptic cell
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Chemical Synapse: | NTs are in
synaptic vesicles in presynaptic cell
78
Chemical Synapse: | vesicles fuse with
bouton membrane
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Chemical Synapse: | release NT by
exocytosis
80
Chemical Synapse: | amount of NT released depends upon
frequency of Aps
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 Synaptic Transmission
 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
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 Neurotransmitter Release |  Is rapid because
vesicles are already docked at release sites on bouton before APs arrive
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 docked vesicles are part of
fusion complex;  Ca2+ triggers exocytosis of vesicles  NT (ligand) diffuses across cleft  Binds to receptor proteins on postsynaptic membrane
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 Chemically-regulated ion channels open - depolarizing channel causes? - hyperpolarizing channels causes?
 Depolarizing channels cause EPSPs (excitatory postsynaptic potentials)  Hyperpolarizing channels cause IPSPs (inhibitory postsynaptic potentials)  These affect VG channels in postsynaptic cell
85
 EPSPs & IPSPs
summate (add up) and if MP in postsynaptic cell reaches threshold, a new AP is generated
86
 Acetylcholine (ACh)
 Most widely used NT; at all neuromuscular junctions, used in brain
87
 Acetylcholine (ACh) Used in ANS where can be
excitatory or inhibitory depending on receptor subtype Nicotinic or muscarinic
88
 Ligand-Operated Channels
 Ion channel runs through receptor |  Opens when ligand (NT) binds
89
 Nicotinic ACh Channel
 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
 G Protein-Operated Channels
 Receptor is not part of the ion channel |  is a 1 subunit membrane polypeptide that activates channel indirectly through G-proteins
91
 Muscarinic ACh Channel
 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
 Acetylcholinesterase (AChE)
 Inactivates ACh, terminating its action; located in cleft
93
 Neurotransmitters – Neuromuscular Junction (NMJ)
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
NMJ functions
 Produce large EPSPs called end-plate potentials; open VG channels beneath end plate; cause muscle contraction  Curare blocks ACh action at NMJ
95
 Monoamine NTs
 Include serotonin, norepinephrine, & dopamine, |  Receptors activate G-protein cascade to affect ion channels
96
 Serotonin is derived from
tryptophan
97
Norepi & dopamine are derived from
from tyrosine |  Called catecholamines
98
Monoamine NTs  After release
are mostly inactivated by: Presynaptic reuptake, & breakdown by monoamine oxidase (MAO);
99
MAO inhibitors
antidepressants
100
Serotonin
 Involved in regulation of mood, behavior, appetite, & cerebral circulation; LSD (the drug acid) is structurally similar
101
 SSRIs
(serotonin-specific reuptake inhibitors) include antidepressants; Prozac, Zolof, Paxil, Luvox = Block reuptake of serotonin, prolonging its action
102
 Dopamine
 Involved in motor control & emotional reward
103
 Degeneration of dopamine motor system neurons causes
Parkinson's disease
104
Dopamine reward system
involved in addiction
105
 Schizophrenia treated by
anti-dopamine drugs
106
 Norepinephrine (NE)
 Used in PNS & CNS  In PNS is a sympathetic NT  In CNS affects general level of arousal
107
 Amphetamines stimulate
NE pathways
108
 Amino Acids NTs
 Glutamic acid & aspartic acid are major CNS excitatory NTs
109
 Glycine
is an inhibitory NT  Opens Cl- channels which hyperpolarize  Strychnine blocks glycine receptors
110
 GABA (gamma-aminobutyric acid) is
is most common NT in brain |  Inhibitory, opens Cl- channels
111
 Synaptic Integration – EPSPs
```  Graded in magnitude  Have no threshold  Cause depolarization  Summate  Have no refractory period ```
112
 Spatial Summation
 Cable properties cause EPSPs to fade quickly over time & distance
113
 Spatial summation takes place when
EPSPs from different synapses occur in postsynaptic cell at same time
114
 Temporal summation occurs because
EPSPs that occur closely in time can sum before they fade
115
 Synaptic Plasticity
 Repeated use of a synapse can increase its ease of transmission  = synaptic facilitation
116
 High frequency stimulation often causes enhanced excitability  Called
long-term potentiation |  Believed to underlie learning
117
 Repeated use of a synapse can also decrease its ease of transmission
synaptic depression
118
Synaptic Inhibition
 Postsynaptic inhibition |  Presynaptic inhibition:
119
 Postsynaptic inhibition
 GABA & glycine produce IPSPs  IPSPs dampen EPSPs  Making it harder to reach threshold
120
 Presynaptic inhibition:
 Occurs when 1 neuron synapses onto axon or bouton of another neuron, inhibiting release of its NT