Cell signalling Flashcards
1
Q
what percent of CNS cells are neurons
A
10% of CNS cells
2
Q
can neurons continue devideing
A
No, terminaly differentiated (non-dividing)
3
Q
Roll of Cell body in neurons
A
Protein synthesis
4
Q
what part of the neuron is polarized
A
Dendrites and Axons
5
Q
roll of dendrites
A
signal reception
6
Q
Roll of axons
A
Singal transmission
7
Q
what does the internal system for protein transport do
A
Normal metabolic function
respond to injury
route for viral infection
8
Q
how much of the CNS is Glial
A
90%
9
Q
can glial cells devide
A
yes
10
Q
PNS glial cells
A
Schwann cells
11
Q
roll of schwann cells
A
Myelination in the PNS
12
Q
Glial cells in the CNS
A
Oligodendrocytes
Microglia
Astrocytes
13
Q
roll of oligodendrocytes
A
myelination in the CNS
14
Q
what are microglia cells like
A
MAcrophage-like
15
Q
roll of microglia
A
Phagocytic
16
Q
Roll of Astrocytes
A
REgulate extracellular fluid (remove K and neurotransmitters)
Buffering roll (homeostasis)
provide neurons metabolically
17
Q
what forms the blood brain barrier
A
AStrocytes surrounding brain capillaries
18
Q
what can lead to demyelination
A
Guillain-Barre syndrome
PEripheral nerve damage
Multiple Sclerosis (CNS)
19
Q
what is Guillain -Barre syndrome
A
Autoimmune disease resulting in demyelination of peripheral motor axons
20
Q
how does a neuron interact with microglia
A
- Microglia originally kept unreactive by neuron glycoprotein
- Neuronal injury releases intracellular ATP inducing motility (chemotaxis)
- Microglia remove damages neuronal debris
21
Q
action of microglia interaction with neuron
A
Not well understood
Makes contact with healthy neurons
PRuning unused dendrtes
22
Q
how does stuff move down the axon
A
Microtubules
23
Q
Anterograde transport
A
From cell body toward terminal
24
Q
motor protein for anterograde transport
A
Kinesins
25
what are Kinesins like
Myosin contractile proteins
26
speed of fast anterograde transport
400mm/day
27
speed of slow anterograde transport
.2-2.5mm/day
28
what does fast anterograde transport
Organelles such as neurotransmitter vesicles (Small)
29
what does Slow anterograde transport
structural proteins (large)
30
what does Retrograde transport
Dyeins
31
speed of retrograde trasport
fast (400mm/day)
32
what does Retrograde transport
Growth factors
| Virus... (bad)
33
how is herpes simplex virus Type I transmitted
via oral contact
34
how many people have herpes simplex virus type I
up to 75% of in adult population
35
symptoms of herpes simplex virus type I
usually asymptomatics
36
how is the Herpes simplex virus type I transmitted in the body
retrogradely to the trigeminal ganglion
37
what happens to Herpes simplex virus type I during latency
TRansciptionally quiet
38
what can happen if an infant gets herpes simplex virus type I
goes beyond trigeminal ganglion and causes encephalitis
39
how can Herpes Simplex VIrus Type I be activated
By fever, sun, cold, trauma, or stress
40
how does Herpes Simplex Virus Type I show symptoms
TRansmitted anterogradely to peripheral tissue, lips, palate, causing painful blisters
41
axonal transport roll in nerve regeneration
important
42
can damages CNS neurons regenerate
No
43
what happens to a damages CNA neuron
axons sprout, but do not reach target
44
what prevents surviign axons of the damages CNS neurons from reaching their target
Gliosis (Scare Formation
45
what inhibits axon regeneration in the CNS
astrocytes making chondroitin sulfate proteoglycan
46
CAn PNS nerve damage be recovered
can take place depending onseverity
47
what helps with PNS neuron recovery
Schwann cells promote axonal regeneration
48
how does PNS fucntional recovery matter
nerve injury from maxillofacial surgery (Tooth extraction/dental procedures)
49
severe nerve injury leads to
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
50
the closer the cell injury to the ganglion
the more severe the nerve injury
51
less sever nerve injury leads to
terminal and anterograde degeneration
| Chromatolysis
52
what is Chromatolysis associated with
associated with protein synthesis in an injured cell
53
what happens to the cell body in CHromatolysis
Cell body swell
| Eccentric nucleus
54
action of schwann cels in regernation
Schwann cells proliferate
production of laminin for substrate for regenerating axons
Schwann cell secrete NErve growth factor (NGF)
NGF transported to ganglion cell body
55
roll of NGF (nerve growth factor)
regulates gene expression and promotes sprouting
- microtubules and microfilaments (structural)
- neurotransmittter prudction
- ion channel
- neurotransmitter receptors
56
what happens to the cell body in severe and not severe cell injurt
cell body only injured in non-severe
57
what does Collateral sprouting do
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
58
what signals for collateral sprouting
dead neuron
| NGF transported via retrograde transport
59
how was collateral sprouting found
ipsilateral removal of trigeminal nerve
| eventually started gaining sensation past the midline
60
relationship between collateral sprouting and age
as you get older, you get less collateral sprouting
61
what does Neuronal polarity depend on
Distribution of channel types
62
High density of Na+ channels allong the axon support
Action Potential
63
High density of Ca++ channels along the axon supports
Synaptic release
64
what is a snyapse
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
65
typesof Synapses
Chemical
| Electrical (gap junction)
66
size of the cleft in the chemical synapse
10-20nm
67
what is found in the chemcial synaptic cleft
pre-synaptic vesicle release
| post-synaptic receptors
68
roll of electrical synapses
Fast and synchronization
69
commonness of electrical synapse
A few are found in the CNS but not common
70
types of chemcial synapses
Axon-somatic
Axodendritic
Axo-axonic
71
Location of receptors
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
72
roll of presynaptic receptors
mediates pre-synaptic inhibition and excitiation
73
types of Postsynaptic receptors
Ionotropic
| Metabotropic
74
what are ionotropic recetpors
ion channels directly gated
75
what are metabotropic receptors
G-protein/2nd messenger (indirect gating
76
what is Synaptotagmin
Ca++ sensitive docking proteins for vesicle fusion and release
77
what happens where a transmitter binds to a ionotropic receptor
gates (open/closes) the pore
78
sped of direct gating
very rapid, msec
79
what happens when a transmitter bind to a Indirect gate
Activates G protein
G protein activates 2nd messenger
2nd messenger activates gate in channel
80
speeed of indirect gating
can be msec to hours
81
what happens in an excitatory synapse
influx of cations Na, Ca, K
82
what happens in an inhibitory synapse
Influx of anions, Cl
| efflux of K
83
size of the post synaptic potential
about .5 mV (need more than one to reach threshold
84
temporal summation
adding together of Post synaptic potential from one synaptic contact over time
85
spacial summation
adding together of post synaptic potential produced by different synapses
86
what might a drug do to synaptic junction
- 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
87
function of neurotransmitter
Rapid communication (msec)
88
action of neurotransmitters
Acts on postsynaptic cell to produce Excitatory PSP or Inhibitory PSP
89
when are neuromodulators released
Co-released with neurotransmitter
90
action of Neuromodulators
- 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
91
speed of Neuromodulators
slow min-days
92
where is Acetylecholine synthesized and stored in the cell
in the synaptic terminal and stored in vesicles
93
what is acetylecholine synthesized from
Choline and acetyl Co-A
94
how is Acetylcholine action stopped
diffusion and degradation
95
what degrades acetylecholine
Acetylcholinesterase
96
what happens to choline from degraded acetylecholin
re-uptake by presynaptic neuron for re-synthesis
97
generally where is acetylcholine located in the nervous system
in a limited number of neurons with widespread projuctions
98
receptors for Acetylcholine
Nicotinic
| Muscarinic
99
Function/disease of AcetyleCholine
Myasthenia gravis
| Alzheimers disease
100
percise location of ACh neurons in the CNS
BAsal Forebrain
Pontine Nuclei
lower Brainstem
101
ACh roll in BAsal forebrain
Cognitive function
102
ACh roll in Pontine Nuclei
Sleep regulation
103
Lower brainstem Cholinergic neurons
Motor Neurons
Preganglionic sympa
preganglionic parasympa
Postganglionic Parasympa
104
Cholingergic motor neurons
Oromotor nuclei
105
preganglionic parasympa cholingeric neurons
Pre-salivary neurons in brain stem
106
Postganglionic parasympa cells in brain stem
Salivary cell innervation
107
what kind of receptor is a nicotinic receptor
Ionotropic
108
what does the nicotinic receptor bind to
Nicotine
109
where is nicotinic receptors found
In the CNS nd PNS
110
what happens when ACh binds to Nicotinic receptors
opens ion channel within receptor allowing Na and K to pass
111
what happens with Nicotinic recetpors in the neuromuscular junction
Depolarization
112
what blocks Nicotinic receptors
Curare
113
what kind of recetpor is Muscarinic recepors
Metabotropic
114
what does muscarinic receptors bind
Muscarine ( a point in mushrooms)
115
where are Msucarinic receptors found
In the CNS and PNS
| parasympathetic postganglionic synapse (salivary glands)
116
what does Binding of ACh to Muscarinic receptors do
Triggers G protein that open or close ion channels leading to depolarization or hyperpolarization
117
what blocks Muscarinic receptors
Atropine
118
what is Myasthenia Gravis
Autoimmune disorder where individuals make antibodies to nicotinic receptors, eventually degrading them
119
symptoms of Myasthenia gravis
Weak Muscles
120
treating Myasthenia gravis
Acetylcholinisterase inhibitors
121
the most common form of dementia
Alzheimer's disease
122
what is all involved in alzheimer's disease
many neuronal populations
123
Alzheimer's disease is caused by what
Loss of neurons in nucleus basalis, leadin gto decrease in cholinergic activity in cortex
124
what are biogenic amines synthesized from
Amino acids
125
Catecholamines
Dopamine
Norepinephrine
Epinephrine
126
what are Catecholamines synthesized from
Amino acid Tyrosine
127
where are CAtecholamines Syntheized and storeed
In presynaptic terminal and stored in vesicles
128
how is CAtecholamines released
Ca++ depended
129
how is the action of Catecholamines stoped
presynaptic neuron re-uptake
Diffusion
Degradation
130
what degrades CAtecholamines
Monoamine OXidase (MAO)
131
what does MAO inhibitors do
prolongs activity of Catecholamines
132
use of MAO inhibitors
therapeutic for mood disorders
133
how is Dopamine synthesized
L-Dopa and dopa decarboxylase in synaptic terminal
134
Location of Dopamine in Nervous system
Limited CNS neurons
135
Receptors for Dopamine
D1 and D2
136
what type of receptors are dopamine receptors
Indirect, G-protein coupled
137
function/disease of Dopamine
Motor function/dysfucntion
- parkinson's disease
- tardive dyskinesia
Addiction
138
Nucleus for Dopamine
Ventral tegmental area
| Substantia nigra
139
what is the Ventral tegmental area associated with
Reward and addicition
140
action of coke and amphetamine
prolong dopamine action at synapse in Tentral tegmental area
141
what does the substantia nigra associated with
Motor system
142
loss of dopamine at the substantia nigra leads to
PArkinsons' disease
143
treating parkinsons
L-dopa given
144
action of D1
activate adenylate cyclase
145
action of D2
Inhibit adenylate cyclase (leading to hyperpolarization)
146
what do prescribed antidepressents and antiemetics bind to
Block D2 receptors
147
what can prescribed D2 blockers cause
Tardive Dyskinesia
148
how often do people get Targive Dysinesia
20-50% in patients receiving dopamine blocking drugs
149
what does Targive reflec
Delayed onset
150
is Tardive Dyskinesia more common in old
yes
151
symptoms of Tardive dyskinesia
PResented as rhythmic oral movements (oral-buccal-lingual stereotopy)
152
How is Norepinephrine synthesized
Dopamine acted on by Dopamine decarboxylase
153
where is NE synthesized
In the synaptic terminal
154
how is NE action stopped
MAO
Diffusion
re-uptake
155
location of NE in the nervous system
NE neuron include sympathetic postgnaglionic neurons
| Some CNS neurons with lost of projections
156
Recptors for NE
G protein coupled receptors (alpha and BEta)
157
Function/disease of NE
many autonomic and homeostatic function
158
nucleus for NE
Locus Ceruleus
| other brainstem
159
Affect of NE depends partly on
what receptor type it binds to
160
action of locus ceruleus for NE
attention/sleep
161
action of brainstem groups of NE
autonomic and homeostatic fucntion
162
action of alpha 1 NE receptor
Intracellular release Ca++ (excitation)
163
action of alpha 2 NE receptor
Opening K+ channels or blocking Ca++ (inhibitor
164
action of beta NE receptor
opens Ca++ channels
165
why is epinephrine combined with local anesthetics
restrict diffusion of anesthetic
166
what NE receptor does Smooth muscle have
Lots of Alpha 1, little beta 2
167
NE action on smooth muscle alpha 1 and beta 2 leads to
alpha 1: contraction
| beta 2: dilation
168
NE action of BEta 1 of heart leads to
contraction
169
what is Serotonin synthesized from
typtophan
170
where is serotonin found
raphe nuclei in brinastem
171
recetpors for serotonin
G-protein coupled recetpros (16 subtypes
172
what serotonin synapse is the target of mood-altering drugs
5-HT
173
functions of serotonin
Range from sensorimotor system to cognitive function (mood)
174
what is Histamine derived from
Amino acid Histidine
175
where is Histamine found
In small population of hypothalamic neurons
176
what recetpors respond to Histamine
G-protein coupled
177
roll of Histamine
Sleep-wakefulness
178
How common are the neurons that synthesizecatecholamine ligands
very limited in location
179
where are receptors for catecholamines generally found
Throughout the CNS
180
What type of receptor is normal for Catecholamines
G-protein coupled with many subtypes to open and close ion channels
181
general function of Catecholamines
Arousal/attention, feeding, movement, cognitive function (many)
182
dissorders of catecholamines leads to
Motor Dysfunction: Parkinson's, tardive dyskinesia
| Cognitive disorders: depression, schizophrenia, addiction
183
what are the excitable amino acid neurotransmitters
Glutamate and aspartate
184
the most common excitatory neurotransmitter
Glutamate
185
what receptrors do amino acid neurotransmitters bind
Ionotropic : AMPA, Kainate, NMDA
- premeable to Na, K, and Ca++
also metabotropic receptors (G-protein)
186
full name for the NMDA REceptor
N-methyl-D-Asparate
187
what is the roll of the NMDA receptor
involved in functions that loast: memory formation, chronic pain
188
what type of cell death is the NMDA REceptor associated with
Excitotoxicity
189
what causes excitotoxicity
```
excessive activation (epilepsy, trauma, stroke)
Intracellular Ca++ reaching toxic levels (Excited to death)
```
190
what is the synaptic mechansism of long term potentiaion
the NMDA Receptor
191
the most common excitatory neurotransmitter
Glutamate
192
are amino-acids excitatory or inhibitory
both
193
tetanic stimulation
rapid stimulus on pre-synaptic side
194
how does long term potentiation occure
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
How does NMDA mediated Potentiation occur
- 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
Depolarization via AMPA/Kainate receptors leads to what
Removal of Mg+ black (LTP_
197
Calcium enrey into cell via NMDA receptor leads to
Phosphorylation of NMDA receptor
Phosphorylation of AMPA receptors
INCreased AMPA
Synth of retrograde messenger NO
198
what does NO do for LTP
facilitates glutamate synth/release pre-synaptically
199
how long is LTP
variable time duration
200
Glutamate REuptake PAthway
```
Glutamate release
Postsynaptic binding
Uptake by astrocyte (glutamate transporter)
Conversion to glutamine
Glutamine release
Neuronal glutamine uptake
Conversion to glutamate
```
201
Inhibitory amino acid
GABA (gamm-amminobutyric acid) - main
| Glycine
202
what is GABA made from
modified form of glutamate
203
receptors for GABA
GABA A
| GABA B
204
what type of receptor if GABA A
ionotropic that opens Cl- channel
205
what type of receptor is GABA B
metabotropic to open K channels
206
disease of GABA deficit
Huntington Chorea
207
what is Huntington chorea
form of motor spasticity from GABA deficit
208
where does Glycine normally inhibit
in the spinal cord
209
action of Glycine
opens Cl- channels
210
what blocks Glycine
by strychnine
211
stychnine leads to
Convulsions
212
how are peptides form
by a peptide link between 2+ amino acids
213
how many peptide neurotransmitters are there
80ish
214
examples of PEptides neurotransmitters
endogenous opioids
Substance P
neuropeptide Y
215
roll of endogenous opoids
pain
216
roll ofsubstance P
Pain
217
roll of Neuropeptide Y
Feding
218
when are peptides released
co-released with other neurotransmitters
219
where are peptides synthesized
Synth in soma (must be transported)
220
function of peptides
neuromodulator
221
action length of peptides
lasts a long time
222
how are peptide actions terminated
Proteolysis and diffusion
223
how does Presynpatic modulation of opoids occur
opiods bind to a Mu opioid receptor on the presynaptic cell.
| This leads to more inhibition of the postsynaptic cell
224
how is NO synthesized
L-arginine to NO by nitric oxide synthase
225
how is NO stored
Not in vesicles
226
how is NO transmitted
free diffusible across membranes (no synapse)
227
Roll of NO gas
modulates neurotransmitter release (glutamate and gaba)
| plays a roll in numberous brain fucntion (LTP)
228
is ATP excitatory or inhibitor
Usually excitatory (taste)
229
how is ATP released
Usually co-released with classical neurotransmitters
230
how is ATP stored
not always stored in vesicles (Taste)
231
how is ATP released
from hemichannels (like gap channels
232
what creceptors does ATP act on
Family of P2 receprots
- P2X: ionotropic
- P2Y: metabotropic
