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physiology > Cell signalling > Flashcards

Cell signalling Flashcards

1
Q

what percent of CNS cells are neurons

A

10% of CNS cells

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2
Q

can neurons continue devideing

A

No, terminaly differentiated (non-dividing)

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3
Q

Roll of Cell body in neurons

A

Protein synthesis

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4
Q

what part of the neuron is polarized

A

Dendrites and Axons

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5
Q

roll of dendrites

A

signal reception

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6
Q

Roll of axons

A

Singal transmission

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7
Q

what does the internal system for protein transport do

A

Normal metabolic function
respond to injury
route for viral infection

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8
Q

how much of the CNS is Glial

A

90%

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9
Q

can glial cells devide

A

yes

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10
Q

PNS glial cells

A

Schwann cells

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11
Q

roll of schwann cells

A

Myelination in the PNS

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12
Q

Glial cells in the CNS

A

Oligodendrocytes
Microglia
Astrocytes

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13
Q

roll of oligodendrocytes

A

myelination in the CNS

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14
Q

what are microglia cells like

A

MAcrophage-like

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15
Q

roll of microglia

A

Phagocytic

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16
Q

Roll of Astrocytes

A

REgulate extracellular fluid (remove K and neurotransmitters)
Buffering roll (homeostasis)
provide neurons metabolically

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17
Q

what forms the blood brain barrier

A

AStrocytes surrounding brain capillaries

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18
Q

what can lead to demyelination

A

Guillain-Barre syndrome
PEripheral nerve damage
Multiple Sclerosis (CNS)

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19
Q

what is Guillain -Barre syndrome

A

Autoimmune disease resulting in demyelination of peripheral motor axons

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20
Q

how does a neuron interact with microglia

A
  1. Microglia originally kept unreactive by neuron glycoprotein
  2. Neuronal injury releases intracellular ATP inducing motility (chemotaxis)
  3. Microglia remove damages neuronal debris
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21
Q

action of microglia interaction with neuron

A

Not well understood
Makes contact with healthy neurons
PRuning unused dendrtes

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22
Q

how does stuff move down the axon

A

Microtubules

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23
Q

Anterograde transport

A

From cell body toward terminal

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24
Q

motor protein for anterograde transport

A

Kinesins

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25
Q

what are Kinesins like

A

Myosin contractile proteins

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26
Q

speed of fast anterograde transport

A

400mm/day

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27
Q

speed of slow anterograde transport

A

.2-2.5mm/day

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28
Q

what does fast anterograde transport

A

Organelles such as neurotransmitter vesicles (Small)

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29
Q

what does Slow anterograde transport

A

structural proteins (large)

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30
Q

what does Retrograde transport

A

Dyeins

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31
Q

speed of retrograde trasport

A

fast (400mm/day)

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32
Q

what does Retrograde transport

A

Growth factors

Virus… (bad)

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33
Q

how is herpes simplex virus Type I transmitted

A

via oral contact

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34
Q

how many people have herpes simplex virus type I

A

up to 75% of in adult population

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35
Q

symptoms of herpes simplex virus type I

A

usually asymptomatics

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36
Q

how is the Herpes simplex virus type I transmitted in the body

A

retrogradely to the trigeminal ganglion

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37
Q

what happens to Herpes simplex virus type I during latency

A

TRansciptionally quiet

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38
Q

what can happen if an infant gets herpes simplex virus type I

A

goes beyond trigeminal ganglion and causes encephalitis

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39
Q

how can Herpes Simplex VIrus Type I be activated

A

By fever, sun, cold, trauma, or stress

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40
Q

how does Herpes Simplex Virus Type I show symptoms

A

TRansmitted anterogradely to peripheral tissue, lips, palate, causing painful blisters

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41
Q

axonal transport roll in nerve regeneration

A

important

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42
Q

can damages CNS neurons regenerate

A

No

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43
Q

what happens to a damages CNA neuron

A

axons sprout, but do not reach target

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44
Q

what prevents surviign axons of the damages CNS neurons from reaching their target

A

Gliosis (Scare Formation

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45
Q

what inhibits axon regeneration in the CNS

A

astrocytes making chondroitin sulfate proteoglycan

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46
Q

CAn PNS nerve damage be recovered

A

can take place depending onseverity

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47
Q

what helps with PNS neuron recovery

A

Schwann cells promote axonal regeneration

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48
Q

how does PNS fucntional recovery matter

A

nerve injury from maxillofacial surgery (Tooth extraction/dental procedures)

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49
Q

severe nerve injury leads to

A

1st: Anterograde (wallerian Degeneration)- parts distal to lesion destroyed
and terminal degeneration -destruction of synapse
2. cell death
3. transganglionic degeneration - moves up the dendrites/ axons past the cell body
4. transynaptic degeneration - death of a CNS neuron

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50
Q

the closer the cell injury to the ganglion

A

the more severe the nerve injury

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51
Q

less sever nerve injury leads to

A

terminal and anterograde degeneration

Chromatolysis

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52
Q

what is Chromatolysis associated with

A

associated with protein synthesis in an injured cell

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53
Q

what happens to the cell body in CHromatolysis

A

Cell body swell

Eccentric nucleus

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54
Q

action of schwann cels in regernation

A

Schwann cells proliferate
production of laminin for substrate for regenerating axons
Schwann cell secrete NErve growth factor (NGF)
NGF transported to ganglion cell body

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55
Q

roll of NGF (nerve growth factor)

A

regulates gene expression and promotes sprouting

  • microtubules and microfilaments (structural)
  • neurotransmittter prudction
  • ion channel
  • neurotransmitter receptors
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56
Q

what happens to the cell body in severe and not severe cell injurt

A

cell body only injured in non-severe

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57
Q

what does Collateral sprouting do

A

when the cell of a ganglion dies, other cells of that ganglion can spout branches from its dendrites/axons to take over some of the sensory action/axonal action of the dead nerve

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58
Q

what signals for collateral sprouting

A

dead neuron

NGF transported via retrograde transport

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59
Q

how was collateral sprouting found

A

ipsilateral removal of trigeminal nerve

eventually started gaining sensation past the midline

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60
Q

relationship between collateral sprouting and age

A

as you get older, you get less collateral sprouting

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61
Q

what does Neuronal polarity depend on

A

Distribution of channel types

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62
Q

High density of Na+ channels allong the axon support

A

Action Potential

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63
Q

High density of Ca++ channels along the axon supports

A

Synaptic release

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64
Q

what is a snyapse

A

Anatomically specialized junctiton between a neuron and another cell at which electrical activety of the presynaptic neuron influences the electrical activity of the post synaptic cell

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65
Q

typesof Synapses

A

Chemical

Electrical (gap junction)

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66
Q

size of the cleft in the chemical synapse

A

10-20nm

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67
Q

what is found in the chemcial synaptic cleft

A

pre-synaptic vesicle release

post-synaptic receptors

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68
Q

roll of electrical synapses

A

Fast and synchronization

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69
Q

commonness of electrical synapse

A

A few are found in the CNS but not common

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70
Q

types of chemcial synapses

A

Axon-somatic
Axodendritic
Axo-axonic

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71
Q

Location of receptors

A

Postsynaptic- on the post synaptic neuron
Presynaptic- on the axon to be acted on by a different axon
autoreceptor- on the axon to be acted on by its own neurotransmitter

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72
Q

roll of presynaptic receptors

A

mediates pre-synaptic inhibition and excitiation

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73
Q

types of Postsynaptic receptors

A

Ionotropic

Metabotropic

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74
Q

what are ionotropic recetpors

A

ion channels directly gated

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75
Q

what are metabotropic receptors

A

G-protein/2nd messenger (indirect gating

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76
Q

what is Synaptotagmin

A

Ca++ sensitive docking proteins for vesicle fusion and release

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77
Q

what happens where a transmitter binds to a ionotropic receptor

A

gates (open/closes) the pore

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78
Q

sped of direct gating

A

very rapid, msec

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79
Q

what happens when a transmitter bind to a Indirect gate

A

Activates G protein
G protein activates 2nd messenger
2nd messenger activates gate in channel

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80
Q

speeed of indirect gating

A

can be msec to hours

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81
Q

what happens in an excitatory synapse

A

influx of cations Na, Ca, K

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82
Q

what happens in an inhibitory synapse

A

Influx of anions, Cl

efflux of K

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83
Q

size of the post synaptic potential

A

about .5 mV (need more than one to reach threshold

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84
Q

temporal summation

A

adding together of Post synaptic potential from one synaptic contact over time

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85
Q

spacial summation

A

adding together of post synaptic potential produced by different synapses

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86
Q

what might a drug do to synaptic junction

A
  • increase leakage of neurotransmitter to cytoplasm so its get broken down by enzymes
  • increase transmitter release into cleft
  • block transmitter release
  • inhibit transmitter synthesis
  • block transmitter reuptake
  • block cleft enzymes that metabolize transmitter
  • bind to receptor on postsynaptic membrane to block or mimic transmitter action
  • ihibit or stimulate second-messenger activity within postsynaptic cell
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87
Q

function of neurotransmitter

A

Rapid communication (msec)

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88
Q

action of neurotransmitters

A

Acts on postsynaptic cell to produce Excitatory PSP or Inhibitory PSP

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89
Q

when are neuromodulators released

A

Co-released with neurotransmitter

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90
Q

action of Neuromodulators

A
  • act postsynaptically to amplify/dampen on going synaptic activity
  • act on pre-synaptic cell to alter synth, release, uptake, or metabolism of neurotransmitter
  • can change protein synth or enzyme activity
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91
Q

speed of Neuromodulators

A

slow min-days

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92
Q

where is Acetylecholine synthesized and stored in the cell

A

in the synaptic terminal and stored in vesicles

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93
Q

what is acetylecholine synthesized from

A

Choline and acetyl Co-A

94
Q

how is Acetylcholine action stopped

A

diffusion and degradation

95
Q

what degrades acetylecholine

A

Acetylcholinesterase

96
Q

what happens to choline from degraded acetylecholin

A

re-uptake by presynaptic neuron for re-synthesis

97
Q

generally where is acetylcholine located in the nervous system

A

in a limited number of neurons with widespread projuctions

98
Q

receptors for Acetylcholine

A

Nicotinic

Muscarinic

99
Q

Function/disease of AcetyleCholine

A

Myasthenia gravis

Alzheimers disease

100
Q

percise location of ACh neurons in the CNS

A

BAsal Forebrain
Pontine Nuclei
lower Brainstem

101
Q

ACh roll in BAsal forebrain

A

Cognitive function

102
Q

ACh roll in Pontine Nuclei

A

Sleep regulation

103
Q

Lower brainstem Cholinergic neurons

A

Motor Neurons
Preganglionic sympa
preganglionic parasympa
Postganglionic Parasympa

104
Q

Cholingergic motor neurons

A

Oromotor nuclei

105
Q

preganglionic parasympa cholingeric neurons

A

Pre-salivary neurons in brain stem

106
Q

Postganglionic parasympa cells in brain stem

A

Salivary cell innervation

107
Q

what kind of receptor is a nicotinic receptor

A

Ionotropic

108
Q

what does the nicotinic receptor bind to

A

Nicotine

109
Q

where is nicotinic receptors found

A

In the CNS nd PNS

110
Q

what happens when ACh binds to Nicotinic receptors

A

opens ion channel within receptor allowing Na and K to pass

111
Q

what happens with Nicotinic recetpors in the neuromuscular junction

A

Depolarization

112
Q

what blocks Nicotinic receptors

A

Curare

113
Q

what kind of recetpor is Muscarinic recepors

A

Metabotropic

114
Q

what does muscarinic receptors bind

A

Muscarine ( a point in mushrooms)

115
Q

where are Msucarinic receptors found

A

In the CNS and PNS

parasympathetic postganglionic synapse (salivary glands)

116
Q

what does Binding of ACh to Muscarinic receptors do

A

Triggers G protein that open or close ion channels leading to depolarization or hyperpolarization

117
Q

what blocks Muscarinic receptors

A

Atropine

118
Q

what is Myasthenia Gravis

A

Autoimmune disorder where individuals make antibodies to nicotinic receptors, eventually degrading them

119
Q

symptoms of Myasthenia gravis

A

Weak Muscles

120
Q

treating Myasthenia gravis

A

Acetylcholinisterase inhibitors

121
Q

the most common form of dementia

A

Alzheimer’s disease

122
Q

what is all involved in alzheimer’s disease

A

many neuronal populations

123
Q

Alzheimer’s disease is caused by what

A

Loss of neurons in nucleus basalis, leadin gto decrease in cholinergic activity in cortex

124
Q

what are biogenic amines synthesized from

A

Amino acids

125
Q

Catecholamines

A

Dopamine
Norepinephrine
Epinephrine

126
Q

what are Catecholamines synthesized from

A

Amino acid Tyrosine

127
Q

where are CAtecholamines Syntheized and storeed

A

In presynaptic terminal and stored in vesicles

128
Q

how is CAtecholamines released

A

Ca++ depended

129
Q

how is the action of Catecholamines stoped

A

presynaptic neuron re-uptake
Diffusion
Degradation

130
Q

what degrades CAtecholamines

A

Monoamine OXidase (MAO)

131
Q

what does MAO inhibitors do

A

prolongs activity of Catecholamines

132
Q

use of MAO inhibitors

A

therapeutic for mood disorders

133
Q

how is Dopamine synthesized

A

L-Dopa and dopa decarboxylase in synaptic terminal

134
Q

Location of Dopamine in Nervous system

A

Limited CNS neurons

135
Q

Receptors for Dopamine

A

D1 and D2

136
Q

what type of receptors are dopamine receptors

A

Indirect, G-protein coupled

137
Q

function/disease of Dopamine

A

Motor function/dysfucntion
- parkinson’s disease
- tardive dyskinesia
Addiction

138
Q

Nucleus for Dopamine

A

Ventral tegmental area

Substantia nigra

139
Q

what is the Ventral tegmental area associated with

A

Reward and addicition

140
Q

action of coke and amphetamine

A

prolong dopamine action at synapse in Tentral tegmental area

141
Q

what does the substantia nigra associated with

A

Motor system

142
Q

loss of dopamine at the substantia nigra leads to

A

PArkinsons’ disease

143
Q

treating parkinsons

A

L-dopa given

144
Q

action of D1

A

activate adenylate cyclase

145
Q

action of D2

A

Inhibit adenylate cyclase (leading to hyperpolarization)

146
Q

what do prescribed antidepressents and antiemetics bind to

A

Block D2 receptors

147
Q

what can prescribed D2 blockers cause

A

Tardive Dyskinesia

148
Q

how often do people get Targive Dysinesia

A

20-50% in patients receiving dopamine blocking drugs

149
Q

what does Targive reflec

A

Delayed onset

150
Q

is Tardive Dyskinesia more common in old

A

yes

151
Q

symptoms of Tardive dyskinesia

A

PResented as rhythmic oral movements (oral-buccal-lingual stereotopy)

152
Q

How is Norepinephrine synthesized

A

Dopamine acted on by Dopamine decarboxylase

153
Q

where is NE synthesized

A

In the synaptic terminal

154
Q

how is NE action stopped

A

MAO
Diffusion
re-uptake

155
Q

location of NE in the nervous system

A

NE neuron include sympathetic postgnaglionic neurons

Some CNS neurons with lost of projections

156
Q

Recptors for NE

A

G protein coupled receptors (alpha and BEta)

157
Q

Function/disease of NE

A

many autonomic and homeostatic function

158
Q

nucleus for NE

A

Locus Ceruleus

other brainstem

159
Q

Affect of NE depends partly on

A

what receptor type it binds to

160
Q

action of locus ceruleus for NE

A

attention/sleep

161
Q

action of brainstem groups of NE

A

autonomic and homeostatic fucntion

162
Q

action of alpha 1 NE receptor

A

Intracellular release Ca++ (excitation)

163
Q

action of alpha 2 NE receptor

A

Opening K+ channels or blocking Ca++ (inhibitor

164
Q

action of beta NE receptor

A

opens Ca++ channels

165
Q

why is epinephrine combined with local anesthetics

A

restrict diffusion of anesthetic

166
Q

what NE receptor does Smooth muscle have

A

Lots of Alpha 1, little beta 2

167
Q

NE action on smooth muscle alpha 1 and beta 2 leads to

A

alpha 1: contraction

beta 2: dilation

168
Q

NE action of BEta 1 of heart leads to

A

contraction

169
Q

what is Serotonin synthesized from

A

typtophan

170
Q

where is serotonin found

A

raphe nuclei in brinastem

171
Q

recetpors for serotonin

A

G-protein coupled recetpros (16 subtypes

172
Q

what serotonin synapse is the target of mood-altering drugs

A

5-HT

173
Q

functions of serotonin

A

Range from sensorimotor system to cognitive function (mood)

174
Q

what is Histamine derived from

A

Amino acid Histidine

175
Q

where is Histamine found

A

In small population of hypothalamic neurons

176
Q

what recetpors respond to Histamine

A

G-protein coupled

177
Q

roll of Histamine

A

Sleep-wakefulness

178
Q

How common are the neurons that synthesizecatecholamine ligands

A

very limited in location

179
Q

where are receptors for catecholamines generally found

A

Throughout the CNS

180
Q

What type of receptor is normal for Catecholamines

A

G-protein coupled with many subtypes to open and close ion channels

181
Q

general function of Catecholamines

A

Arousal/attention, feeding, movement, cognitive function (many)

182
Q

dissorders of catecholamines leads to

A

Motor Dysfunction: Parkinson’s, tardive dyskinesia

Cognitive disorders: depression, schizophrenia, addiction

183
Q

what are the excitable amino acid neurotransmitters

A

Glutamate and aspartate

184
Q

the most common excitatory neurotransmitter

A

Glutamate

185
Q

what receptrors do amino acid neurotransmitters bind

A

Ionotropic : AMPA, Kainate, NMDA
- premeable to Na, K, and Ca++
also metabotropic receptors (G-protein)

186
Q

full name for the NMDA REceptor

A

N-methyl-D-Asparate

187
Q

what is the roll of the NMDA receptor

A

involved in functions that loast: memory formation, chronic pain

188
Q

what type of cell death is the NMDA REceptor associated with

A

Excitotoxicity

189
Q

what causes excitotoxicity

A 
excessive activation (epilepsy, trauma, stroke)
Intracellular Ca++ reaching toxic levels (Excited to death)
190
Q

what is the synaptic mechansism of long term potentiaion

A

the NMDA Receptor

191
Q

the most common excitatory neurotransmitter

A

Glutamate

192
Q

are amino-acids excitatory or inhibitory

A

both

193
Q

tetanic stimulation

A

rapid stimulus on pre-synaptic side

194
Q

how does long term potentiation occure

A

there is tetanic stimulation then to the point were even one AP is strong enough to create an AP in the post synaptic cell
-synapse is changed by the NMDA receptor (long term change in the synapse)

195
Q

How does NMDA mediated Potentiation occur

A
  • High-frequency AP in presynaptic cell
  • Glutamate is released
  • Glutamate binds to both AMPA receptor and NMDA receptor
  • AMPA lets Na in, depolarizaing the membrane by 20-30mV
  • NMDA lets out Mg++ due to the depolarization and CA++ enters to activate the second messenger system
  • long lasting increase in glutamate receptors and sensitivty
  • long lasting increase in glutamate synth via retrograde messsenger
196
Q

Depolarization via AMPA/Kainate receptors leads to what

A

Removal of Mg+ black (LTP_

197
Q

Calcium enrey into cell via NMDA receptor leads to

A

Phosphorylation of NMDA receptor
Phosphorylation of AMPA receptors
INCreased AMPA
Synth of retrograde messenger NO

198
Q

what does NO do for LTP

A

facilitates glutamate synth/release pre-synaptically

199
Q

how long is LTP

A

variable time duration

200
Q

Glutamate REuptake PAthway

A 
Glutamate release
Postsynaptic binding
Uptake by astrocyte (glutamate transporter)
Conversion to glutamine
Glutamine release
Neuronal glutamine uptake
Conversion to glutamate
201
Q

Inhibitory amino acid

A

GABA (gamm-amminobutyric acid) - main

Glycine

202
Q

what is GABA made from

A

modified form of glutamate

203
Q

receptors for GABA

A

GABA A

GABA B

204
Q

what type of receptor if GABA A

A

ionotropic that opens Cl- channel

205
Q

what type of receptor is GABA B

A

metabotropic to open K channels

206
Q

disease of GABA deficit

A

Huntington Chorea

207
Q

what is Huntington chorea

A

form of motor spasticity from GABA deficit

208
Q

where does Glycine normally inhibit

A

in the spinal cord

209
Q

action of Glycine

A

opens Cl- channels

210
Q

what blocks Glycine

A

by strychnine

211
Q

stychnine leads to

A

Convulsions

212
Q

how are peptides form

A

by a peptide link between 2+ amino acids

213
Q

how many peptide neurotransmitters are there

A

80ish

214
Q

examples of PEptides neurotransmitters

A

endogenous opioids
Substance P
neuropeptide Y

215
Q

roll of endogenous opoids

A

pain

216
Q

roll ofsubstance P

A

Pain

217
Q

roll of Neuropeptide Y

A

Feding

218
Q

when are peptides released

A

co-released with other neurotransmitters

219
Q

where are peptides synthesized

A

Synth in soma (must be transported)

220
Q

function of peptides

A

neuromodulator

221
Q

action length of peptides

A

lasts a long time

222
Q

how are peptide actions terminated

A

Proteolysis and diffusion

223
Q

how does Presynpatic modulation of opoids occur

A

opiods bind to a Mu opioid receptor on the presynaptic cell.

This leads to more inhibition of the postsynaptic cell

224
Q

how is NO synthesized

A

L-arginine to NO by nitric oxide synthase

225
Q

how is NO stored

A

Not in vesicles

226
Q

how is NO transmitted

A

free diffusible across membranes (no synapse)

227
Q

Roll of NO gas

A

modulates neurotransmitter release (glutamate and gaba)

plays a roll in numberous brain fucntion (LTP)

228
Q

is ATP excitatory or inhibitor

A

Usually excitatory (taste)

229
Q

how is ATP released

A

Usually co-released with classical neurotransmitters

230
Q

how is ATP stored

A

not always stored in vesicles (Taste)

231
Q

how is ATP released

A

from hemichannels (like gap channels

232
Q

what creceptors does ATP act on

A

Family of P2 receprots

  • P2X: ionotropic
  • P2Y: metabotropic

physiology (32 decks)

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