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Physio > neuronal structure and signaling > Flashcards

neuronal structure and signaling Flashcards

1
Q

neurons make up what % of CNS cells

A

10%

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2
Q

do neurons divide or differentiate?

A

no…terminally differentiated/non dividing

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3
Q

what is the exception to the non-dividing property of neurons

A

hippocampus neurogenesis (here there is learning and memory which requires continual replenishing of neurons)

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4
Q

the soma contains…

A

the nucleus (where protein synthesis occurs)

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5
Q

dendrite is the…

A

major INPUT process. graded potentials occur here.

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6
Q

the axon is the…

A

OUTPUT process for signalling

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7
Q

axon hillock is where

A

a.ps start…also called the initial segment

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8
Q

axon terminals are where

A

vesicles are stored

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9
Q

afferent neurons

A

are sensory/input neurons that send info to the CNS

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10
Q

afferent neuron cell bodies are located

A

OUTSIDE the CNS and are called GANGLIA

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11
Q

efferent neurons

A

are motor/output neurons that send infor to effector cells in the periphery

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12
Q

efferent neuron cell bodies are located

A

WITHIN the CNS (and project to outside of it)

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13
Q

interneurons

A

are located WITHIN the CNS and fn as integrators/switches

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14
Q

glial cells make up what % of cells in the CNS

A

90%

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15
Q

can glial cells undergo cell division

A

yes

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16
Q

glial cells in the CNS are called

A

oligodendrocytes

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17
Q

glial cells in the PNS are called

A

schwann cells

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18
Q

microglia are

A

phagocytic cells that are in the CNS

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19
Q

astrocytes

A

cells in the CNS that regulate the ecf (buffering role) and provide neurons metabolically (food) and surround the brain capillaries (forming the blood brain barrier)

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20
Q

schwann cells provide myelin to

A

one axon (many schwann cells per axon though)

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21
Q

oligodendrocytes provide myelin to

A

many axons

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22
Q

guillain-barre syndrome

A

demyelination of peripheral motor axons

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23
Q

unreactive state of microglia

A

neurons release glycoprotein CD200 to keep microglia (phagocytic cells) unreactive

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24
Q

following neuron injury what rxn takes place between the neuron and microglia

A

the neuron releases intracellular ATP and induces the motility/chemotaxis of microglial cells (to that area of injury)

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25
Q

movement of materials through axons occur through what component

A

microtubules w/in the axon

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26
Q

anterograde transport

A

from cell body to terminal via KINESINS

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27
Q

kinesins are

A

motor proteins that transport during anterograde transport

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28
Q

retrograde transport

A

from axon terminal to cell body via DYNEINS

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29
Q

retrograde transport can include the movement of…

A

growth factors or VIRUSES

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30
Q

herpes virus type I

A
  • transmitted via oral contact
  • first, virus transmitted RETROGRADELY to the trigeminal ganglia (and remains LATENT)
  • the virus can be activated by fever/sun/stress/trauma/cold and travel ANTEROGRADELY toward the periphery and result in a blister
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31
Q

in infants virus can…

A

go beyond the trigeminal ganglion and cause encephalitis

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32
Q

damaged CNS neurons

A

do not regenerate…they “sprout” but never reach their targets

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33
Q

why do sprouted CNS neurons never reach their targets

A

scar formation

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34
Q

what role do astrocytes have in nerve regeneration

A

they inhibit it by making chondroitin sulfate proteoglycans

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35
Q

in the PNS, is nerve regeneration possible

A

yes! some functional recovery can occur which is clinically significant in dental procedures in which nerve injury takes place.

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36
Q

what is the first response (in a timeline) of a nerve to a SEVERE nerve injury

A
  1. anterograde degeneration
  2. terminal degeneration
    (peripheral process of neuron lost…approaching the ganglia)
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37
Q

what is wallerian degeneration

A

anterograde degeneration (from terminal towards the ganglion)

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38
Q

what is transganglionic degeneration

A

central process of the neuron is lost (plus the ganglia and peripheral process)…this occurs later on in the severe nerve injury

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39
Q

what is transynaptic degeneration

A

some signal crosses the synapse (where another nerve is synapsing on the one that was injured) to degenerate the adjacent neuron

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40
Q

what is the nerve response to a LESS SEVERE injury

A

you get both terminal degeneration and anterograde degeneration but also get CHROMATOLYSIS

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41
Q

what is chromatolysis

A

a physiologic change in which the cell attempts to repair the periphery (via protein synthesis). the cell body swells to have an eccentric nucleus (nucleus pushed to the side?)

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42
Q

what is a schwann cell’s response to regeneration

A

the cells proliferate and produce LAMININ and NGF

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43
Q

what is the role of laminin in regeneration

A

schwann cells produce this as a substrate for regenerating axons to grow on

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44
Q

what is the role of NGF

A

nerve growth factor is secreted by schwann cells and is transported to the ganglion cell body of the adj non-injured nerve (retrograde). here it regulates gene expression and promotes the sprouting of the axons

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45
Q

NGF regulates the gene expression of what

A
  • microtubules/microfilaments (for nerve axon structure)
  • n.t
  • ion channels
  • n.t receptors
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46
Q

collateral sprouting

A

schwann cells release NGF which is retrogradely transported to nerve adj to injured neuron (?) and causes “collateral sprouts” to branch off towards the area of lost innervation

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47
Q

the older the patient (of nerve injury) the…

A

less transmedian regeneration/sprouting. negative correlation of age and recovery of function

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48
Q

synaptotagmin

A

a Ca2+ sensitive docking protein used for vesicle fusion and release in presynaptic neuron (Ca must have entered the axon terminal in order for this to occur)

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49
Q

4 ways what n.t can diffused

A
  1. uptake by astrocytes
  2. diffuse from synaptic cleft
  3. enzymes in synaptic cleft can degrade the n.t
  4. reuptake by the presynaptic neuron
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50
Q

synaptic integration

A

interactions b/w inputs on a neuron influence whether or not there will be an output/a.p by that neuron

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51
Q

temporal summation

A

adding together of PSP’s from one synaptic contact over time

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52
Q

spacial summation

A

adding together of PSP’s produced by different synpases

53
Q

what is a classical neurotransmitter

A

used for rapid communication (msec)…they act on the postsynaptic cell to produce an excitatory or inhibitory effect

54
Q

what are neuromodulators

A

can be co-released with n.ts. can amplify or dampen the synaptic activity. also can act on the presynaptic cell to alter the synthesis/release/uptake/metabolism of n.ts. the actions that they cause occur much slower than n.ts (min to days)

55
Q

acetylcholine is synthesized by

A

choline and acetyl co-A

56
Q

what enzyme makes acetylcholine

A

choline acetyletransferase

57
Q

what enzyme stops the action of Ach

A

acetylcholinesterase diffuses/degrades Ach

58
Q

what is another way for Ach action to stop

A

reuptake of choline by presynaptic neuron

59
Q

what neurons release ACh

A
  • all motor neurons
  • those in nucleus basalis and pons
  • pregang symp and psymp
  • all postgang psymp
60
Q

what is the ACh receptor type in the CNS

A

muscarinic receptor…EXCEPT postgang psymp (PNS)

61
Q

muscarinic ACh mechanism

A

ACh binds and (INDIRECTLY) causes g protein activation to open or close ion channels

62
Q

muscarinic receptors are blocked by

A

atropine

63
Q

what is the ACh receptor type in the PNS

A

nicotinic receptors (not many in the CNS)

64
Q

nicotinic ACh mechanism

A

ACh binds and DIRECTLY opens the ion channels (channel located in the ACh receptor)

65
Q

ACh nicotinic receptors are blocked by

A

curare (like at the neuromuscular jn)

66
Q

ACh neurons in the nucleus basalis/basal forebrain are for

A

cognitive fn

67
Q

ACh neurons in the pontine nuclei are for

A

sleep regulation

68
Q

myasthenia gravis

A

autoimmune disorder. ab made that target nicotinic receptors (ACh receptors). muscle weakness (neuromuscular jn).

69
Q

myasthenia gravis is treated with

A

acetylcholinesterase inhibitors to prolong the effect of ACh

70
Q

alzheimers disease and ACh

A

loss of neurons in nucleus basalis (which has Ach neurons) which leads to a decrease in cholinergic/Ach activity in cortex (CNS)….can’t be treated by actyl cholinesterase.

71
Q

biogenic amines are synthesized from

A

a.a…they include the catecholamines, serotonin, and histamine

72
Q

catecholamines include

A

dopamine, norepinephrine, and epinephrine

73
Q

catecholamines are synthesized from

A

a.a, tyrosine

74
Q

catecholamine release is dependent on

A

Ca2+

75
Q

termination of catecholamine action is through

A
  1. presyntaptic reuptake

2. degradation by MAO (monoamine oxidase)

76
Q

neurons for biogenic amines are found

A

in very limited locations

77
Q

receptors for biogenic amines are found

A

extensively in the CNS

78
Q

receptors for biogenic amines are

A

exclusively G-protein couples receptors

79
Q

dopamine neurons are found in the

A
  1. ventral tegmental area

2. substantia nigra

80
Q

in the VTA, dopamine is associated with

A

reward and addiction

81
Q

cocaine and amphetamine do what

A

prolong dopamine action at the synapse in the VTA

82
Q

in the substantia nigra, dopamine is associated with

A

the motor system

83
Q

loss of dopamine in the S.N results in

A

parkinson’s disease

84
Q

D1 vs D2 dopamine receptors

A

D1: activate adenylate cyclase–>a.p
D2: inhibit a.c–> hyperpolarization

85
Q

tardive dyskinesia

A

drugs that block D2 receptors can cause this.. presented as rhythmic oral movements.

86
Q

norepinephrine neurons are found

A
  1. locus ceruleus

2. brainstem

87
Q

norepinephrine neurons in the locus ceruleus are responsible for

A

attention and sleep

88
Q

norepinephrine neurons in the brainstem are responsible for

A

autonomic/homeostatic fns

89
Q

norepinephrine neurons include

A

postgang symp

90
Q

noepinephrine receptor type

A

noradrenergic (alpha and beta types)….g-protein coupled

91
Q

alpha NE receptors

A

type 1: release Ca=excitatory

type 2: open K channels/block Ca=inhibitory

92
Q

beta NE receptors

A

open Ca channels

93
Q

depending on receptor, NE effects are

A

very different

94
Q

serotonin is synthesized from

A

tryptophan

95
Q

serotonin neurons are located in

A
  1. rostral raphe nuclei

2. caudal raphe nuclei

96
Q

serotonin neurons in the rostal raphe nuclei are responsible for

A

sleep, mood, homeostasis

97
Q

serotonin neurons in the caudal raphe nuclei are responsible for

A

sensori-motor fn

98
Q

histamine is synthesized from

A

histadine (a.a)

99
Q

histamine neurons are found

A

small pop. of hypothalamic neurons

100
Q

histamine is responsible for

A

sleep-wakefullness

101
Q

histamine receptors are

A

g-protein coupled (H1-H4)

102
Q

what are the EXCITATORY amino acid n.ts

A

glutamate and aspartate

103
Q

excitatory a.a n.ts bind to what kind of receptors

A

ionotropic receptors and metabotropic receptors

104
Q

ionotropic receptors for the excitatory a.a n.ts have channels that….

A

are permeable to cations (which allow for a depolarizing/excitatory effect): Na, K, Ca

105
Q

metatropic receptors are

A

g-protein coupled

106
Q

the NMDA receptor is what kind of receptor

A

ionotropic

107
Q

properties of NMDA receptors

A
  • involved in fns that last

- can be responsible for excitotoxicity (excessive excitation)

108
Q

the NMDA receptor is the synaptic mechanism for

A

long term potentiation

109
Q

what is long term potentiation (LTP)

A
  • before the LTP the stimulus is subthreshold
  • tetanic stimulation of a neuron occurs (high fq of stimulation of a neuron) causes…
  • an LTP…which is a long lasting increase in excitatory receptors in the post synaptic membrane and sensitivity of those receptors/cell to the excitatory n.t
110
Q

describe NMDA receptor mediated potentiation

A
  1. high fq a.p at presynaptic terminal
  2. glutamate (excitatory a.a) is released into cleft
  3. glutamate binds to both the AMPA receptor and NMDA receptor
  4. glutamate + AMPA-r= Na entry and post synaptic depolarization
  5. post synaptic depolarization causes the extracellular Mg-block to be RELEASED from the NMDA receptor allowing Ca INTO the postsynaptic cell through the NMDA receptor
  6. Ca that has just flowed into the postsynaptic cell activates 2nd messenger systems
  7. this cascade eventually causes the long term potentiation (or long lasting increase in glutamate receptors in the post synaptic cell and sensitivity to glutamate)
  8. this cascade (2nd messenger system) can also synthesize molecules that can be transported RETROGRADE to the presynaptic cell to increase glutamate synthesis
    - 7&8 lead to the long lasting increase in signalling b/w these 2 cells
111
Q

how does phosphorylation of the NMDA receptor influence LTP

A

phosphorylation permanently removes the Mg block on the NMDA receptor….which allows Ca to flow into the post synaptic cell

112
Q

how does Ca entry into the post synaptic cell (through the NMDA receptor) effect LTP

A

allows the second messenger system to be activated which can synthesize NO (nitric oxide). NO can then be retrogradely transported to the presynaptic cell to FACILITATE GLUTAMATE SYNTHESIS AND RELEASE

113
Q

what is the astrocytes role in the glutamate pathway

A

reuptake

114
Q

what is the glutamate reuptake pathway

A
  1. glutamate is released
  2. glutamate binds to the postsynaptic cell
  3. glutamate uptake by an ASTROCYTE
  4. the astrocyte converts the glutamate to glutamine
  5. glutamine is released from the astrocyte into the ecm
  6. neurons uptake the glutamine
  7. the neurons can then convert glutamine back to glutamate (to reuse)
115
Q

what are the inhibitory a.a n.ts

A

GABA (modified form of glutamate…in the CNS) and glycine

116
Q

what are the 2 receptors for GABA

A
  1. ionotropic receptor (GABA-a)

2. metabotropic receptor (GABA-b)

117
Q

what channel does the GABA-a receptor open

A

Cl-…which HYPERPOLARIZES THE CELL

118
Q

what channel does the GABA-b receptor open

A

K+….causing K+ to flow out of the cell (down its [ ] gradient) which will HYPERPOLARIZE the cell

119
Q

huntinton chorea is linked to what deficiency

A

GABA…since this is an inhibitory n.t, have trouble suppressing inhibitory effects on muscles (uncontrolled excitability) which= motor spasticity

120
Q

glycine (inhibitory n.t) opens what type of channels

A

Cl-

121
Q

the effects of glycine are inhibited by what

A

strychnine

122
Q

peptide neuromodulators are typically

A

released with other n.ts

123
Q

properties of peptide neuromodulators

A
  • synthesized in stroma and must be transported to be released (which takes more time than with n.ts)
  • their actions can last a long time
124
Q

actions of peptide neuromodulators are terminated by

A
  1. proteolysis

2. diffusion

125
Q

by what is NO synthesized

A

L-arginine–> NO by nitric oxide synthase

126
Q

is NO stored in vesicles

A

nope! its a gas so it freely diffuses across the membrane (doesn’t require a synapse)

127
Q

NO acts to

A

modulate other n.t release

-also plays a role in brain fns like LTP

128
Q

how does ATP act as an n.t

A

usually excitatory and co-released with other classic n.ts

Physio (9 decks)

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