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physio- exam 1 > travers- neuronal structure & signalling > Flashcards

travers- neuronal structure & signalling Flashcards

1
Q

what is the only region of the brain where neurons have been shown to divide?

A

hippocampus

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2
Q

______ are the major input processes of neurons (respond w/graded potentials)

A

dendrites

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3
Q

the ______ of a neuron is the trigger zone for action potentials

A

axon hillock

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4
Q

where in the neuron are vesicles stored?

A

axon terminal (for release into the synaptic cleft)

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5
Q

which type of neuron has cell bodies outside the CNS?

A

afferent neurons (CBO in ganglia)

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6
Q

what type of cell makes up 90% of the CNS?

A

glial cells

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7
Q

_______ are the myelinating glia cells in the PNS

________ are the myelinating glia cells in the CNS

A

PNS- schwann cells

CNS- oligodendrocytes

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8
Q

list the functions of Astrocytes:

A

Regulate extracellular fluid, e.g. remove K+ and neurotransmitters: buffering role

Provide neurons metabolically (e.g. glucose)

Surround brain capillaries: form blood brain barrier

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9
Q

which myelinating glial cell can serve multiple neurons?

A

oligodendrocytes

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10
Q

what facilitates the Movement of proteins & other material from one part of neuron to another

A

Microtubules (structural components of axon)

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11
Q

what are the 2 forms of transport through a neuron?

A

Anterograde transport

Retrograde transport

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12
Q

_________ transport occurs from the cell body toward the terminal

A

anterograde

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13
Q

what type of motor protein does anterograde transport use?

A

kinesins

similar to myosin contractile proteins

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14
Q

what motor protein does retrograde transport use?

A

dynein

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15
Q

what is the downside to retrograde transport in neurons?

A

it can carry viruses (herpes, rabies, polio) toward the neuron body

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16
Q

what virus remains latent in trigeminal ganglion?

A

Herpes simplex virus type 1

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17
Q

During latency, the herpes simplex virus (type 1) is transcriptionally quiet except for a _________

A

latency associated transcript (LAT)

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18
Q

characteristics of CNS damage and nerve regeneration:

A

Damaged CNS neurons do not regenerate

Axons “sprout” but axons do not reach targets

Scar formation prevents surviving axons from reaching targets

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19
Q

when a CNS neuron is damaged, what substance do the astrocytes produce? what does this cause?

A

Astrocytes make chondroitin sulfate proteoglycans that inhibit neuron growth

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20
Q

what determines the recovery of a PNS injury?

A

severity of the injury

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21
Q

anterograde degeneration due to severe trauma is also known as “________” degeneration. What does this do to the neuron?

A

Wallerian degeneration

leads to neuron cell death, transganglionic degradation, and transynaptic degradation

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22
Q

what is the nerve response to a less severe injury?

A

terminal degradation and Chromatolysis

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23
Q

what is Chromatolysis?

A

the degradation of nissl bodies (granular bodies of rough ER)

associated with protein synthesis
cell body swells, eccentric nucleus

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24
Q

after injury, schwann cells proliferate and produce _______ for substrate for regenerating axons

A

laminin

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25
Q

schwann cells produce ________ which is transported to the ganglion cell body

A

NGF (neural growth factors)

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26
Q

what is the role of NGF in neuron regeneration?

A

NGF regulates gene expression and promotes sprouting

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27
Q

the release of NGF will ultimately lead to ________ sprouting

A

collateral

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28
Q

what explains Increased Crossed-midline Sensitivity after the removal of the trigeminal nerve?

A

collateral sprouting

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29
Q

there is a negative correlation between ______ and the recovery and function of nerve damage

A

age

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30
Q

what is a synapse?

A

An anatomically specialized junction between a neuron and another cell at which the electrical activity of the presynaptic neuron influences the electrical activity in the postsynaptic cell

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31
Q

what are the types of synapses?

A
  • Chemical vs electrical (also called gap junctions, rare in CNS)
  • Excitatory vs inhibitory
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32
Q

name the 3 types of chemical synapses

A

Axo-somatic

Axodendritic

Axo-axonic

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33
Q

what is the difference between temporal summation and spatial summation?

A

Temporal summation: adding together of PSP’s from one synaptic contact (over time)

Spatial summation: adding together of PSP’s produced by different synapses

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34
Q

a classical neurotransmitter can:

A

Functions in rapid communication (msec)

Act on postsynaptic cell to produce EPSP or IPSP

35
Q

____________ are often co-released with neurotransmitters

A

neuromodulators

36
Q

what is the role of neuromodulators?

A

May act postsynaptically to amplify or dampen on-going synaptic activity

May act on pre-synaptic cell to alter synthesis, release, uptake or metabolism of neurotransmitters

Actions can involve changes in DNA/protein synthesis or enzyme activity: can thus be much slower in action (min – days)

37
Q

how is acetylcholine synthesized?

A

Synthesized from choline and acetyl Co-enzyme A by choline acetyltransferase in synaptic terminal

38
Q

examples of neurons that release ACh:

A

Motor neurons

Neurons in nucleus basalis and pons

All preganglionic neurons (sympathetic & parasympathetic)

All postganglionic parasympathetic neurons

39
Q

what are the 2 main regions of the CNS that release ACh? what is the role of these 2 regions?

A
  • Basal forebrain (cognitive function)

- Pontine nuclei (sleep regulation)

40
Q

what are the types of ACh receptors? where are they found?

A
  • Muscarinic receptors: Mostly found in CNS

- Nicotinic receptors: Relatively few in central nervous system

41
Q

which ACh receptor triggers G protein that open or close ion channels?

A

Muscarinic receptors

42
Q

how do nicotinic receptors cause changes in the postsynaptic cell?

A

ACh binding opens ion channel within receptor

Channel permeable to Na+ and K+, therefore depolarizing

43
Q

_________ is an autoimmune disorder in which individual makes antibodies to nicotinic receptors

A

Myasthenia gravis

44
Q

how is myasthenia gravis treated?

A

Treated with acetylcholinisterase inhibitors

45
Q

which ACh receptor disorder is the most common form of dementia?

A

Alzheimers disease

46
Q

what are Biogenic Amines synthesized from?

A

amino acids

47
Q

what are the 3 bionegic amines that are classified as Catecholamines? what amino acid are they produced from?

A

dopamine, norepinephrine, epinephrine

-Synthesized from the amino acid tyrosine

48
Q

describe the life cycle of catecholamines:

A

1) Synthesis- Presynaptic terminal
- Stored in vesicles

2) Release- Ca++ dependent

3) Termination of action
a. presynaptic neuron re-uptake
b. degradation

49
Q

______ is a common molecule that can breakdown catecholamines

A

Monoamine oxidase

MAO

50
Q

T/F: Receptors for catecholamines are almost exclusively G-protein coupled receptors

A

true

51
Q

Catecholamines are associated with what neurological diseases?

A

Parkinsons’s disease, depression, schizophrenia

52
Q

what are the 2 structures of the CNS that produce dopamine?

A

Ventral tegmental area

Substantia nigra

53
Q

the ventral tegmental area associated with ________ and _________

A

reward and addiction

54
Q

the substantia nigra is associated with the ______ system

A

motor

55
Q

there are ______ dopamine receptor subtypes. All are G-protein coupled

A

five

56
Q

what is the main effect from activation of D1 (dopamine 1) receptors? D2?

A

D1: activate adenylate cyclase

D2: inhibit adenylate cyclase (leading to hyperpolarization)

57
Q

what condition is often associated with the D2 receptors of patients receiving dopamine blocking drugs?

A

Tardive Dyskinesia

58
Q

T/F: Norepinerphrine requires presence of additional enzymes for synthesis from Epinephrine

A

FALSE-

Epinerphrine requires presence of additional enzymes for synthesis from norepinephrine

59
Q

NE neurons include:

A

Sympathetic postganglionic neurons (and some CNS)

60
Q

Epinephrin neurons include:

A

Adrenal gland (medulla) as circulating hormone (not much in CNS)

61
Q

catacholamine and other biogenic amine receptors are almost all _________ coupled

A

g-protein

62
Q

what are the 2 different types of alpha NE receptors? what is their function?

A

α1 (intracellular release Ca++): excitatory

α2 inhibitory via opening K+ channels or blocking Ca

63
Q

how do beta NE receptors function?

A

beta receptors: (ß1, ß2 ,ß3): open Ca++ channels

64
Q

NE can have very different effect on tissue depending on what?

A

the receptor type (alpha 1 or 2, beta)

65
Q

what regions of the CNS use Norepinephrin?

A

Locus ceruleus- attention/sleep

Other brainstem groups- Autonomic & homeostatic functions

66
Q

Serotonin is involved with which CNS structures? what is the role of these structures?

A

Rostal raphe nuclei
-Sleep, mood, homeostatic function

Caudal raphe nuclei
-Sensori-motor function

67
Q

T/F: serotonin is involved in many functions ranging from sensorimotor systems to cognitive function

A

true

68
Q

Histamine is derived from amino acid ______

A

Histidine

69
Q

histamine is involved in the control of _____________ cycles in the CNS

A

sleep-wakefulness

70
Q

what are the “Excitatory Amino Acids”?

A

glutamate & aspartate

Glutamate: most common excitatory neurotransmitter

71
Q

Glutamate & aspartate bind to several classes of _________receptors

A

ionotropic

72
Q

Amino acid neurotransmitter receptors are also a class of _________ receptors, which are g-protien coupled

A

metabotropic receptors

73
Q

the N-methyl-D-aspartate (NMDA) receptors are the Synaptic mechanism of _______________

A

Long term potentiation

-functions that last (memory formation, chronic pain)

74
Q

what factors promote long term potentiation?

A
  • Phosphorylation of NMDA receptor (removal of Mg+ block)

- Calcium entry into cell via NMDA receptor

75
Q

what is the Major inhibitory neurotransmitter in CNS?

A

GABA (gamma-amminobutyric acid)

76
Q

GABA is a modified form of what?

A

Glutamate

77
Q

What type of receptor is GABAa? what effect does it have? what about GABAb?

A

GABAA : ionotropic receptor
—-opens Cl- channel

GABAB receptor: metabotropic receptor
—-opens K+ channels

78
Q

what disease is linked to a GABA deficiency?

A

Huntington chorea

79
Q

characteristics of glycine:

A

Amino Acid neurotransmitter

A) Inhibitory neurotransmitter (mostly spinal cord)

B) Receptor opens Cl- channels

C) Blocked by strychnine

80
Q

________ function as neuromodulators

hint: they are formed by the linking of 2 base units

A

peptides

81
Q

what is the only gaseous neurotransmitter? what are its effects?

A

Nitric oxide (NO)

Can modulate neurotransmitter release, e.g. glutamate & GABA

82
Q

the neurotransmitter ______ is usually excitatory, and is co-released with other classical neurotransmitters

A

ATP

83
Q

how does calcium entry due to NDMA receptors lead to long term potentiation?

A

Phosphorylation of AMPA receptors

Increase number of AMPA receptors

Synthesis of retrograde messenger nitric oxide (NO)

physio- exam 1 (8 decks)

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