neuronal structure and signaling Flashcards
1
Q
neurons make up what % of CNS cells
A
10%
2
Q
do neurons divide or differentiate?
A
no…terminally differentiated/non dividing
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)
4
Q
the soma contains…
A
the nucleus (where protein synthesis occurs)
5
Q
dendrite is the…
A
major INPUT process. graded potentials occur here.
6
Q
the axon is the…
A
OUTPUT process for signalling
7
Q
axon hillock is where
A
a.ps start…also called the initial segment
8
Q
axon terminals are where
A
vesicles are stored
9
Q
afferent neurons
A
are sensory/input neurons that send info to the CNS
10
Q
afferent neuron cell bodies are located
A
OUTSIDE the CNS and are called GANGLIA
11
Q
efferent neurons
A
are motor/output neurons that send infor to effector cells in the periphery
12
Q
efferent neuron cell bodies are located
A
WITHIN the CNS (and project to outside of it)
13
Q
interneurons
A
are located WITHIN the CNS and fn as integrators/switches
14
Q
glial cells make up what % of cells in the CNS
A
90%
15
Q
can glial cells undergo cell division
A
yes
16
Q
glial cells in the CNS are called
A
oligodendrocytes
17
Q
glial cells in the PNS are called
A
schwann cells
18
Q
microglia are
A
phagocytic cells that are in the CNS
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)
20
Q
schwann cells provide myelin to
A
one axon (many schwann cells per axon though)
21
Q
oligodendrocytes provide myelin to
A
many axons
22
Q
guillain-barre syndrome
A
demyelination of peripheral motor axons
23
Q
unreactive state of microglia
A
neurons release glycoprotein CD200 to keep microglia (phagocytic cells) unreactive
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)
25
movement of materials through axons occur through what component
microtubules w/in the axon
26
anterograde transport
from cell body to terminal via KINESINS
27
kinesins are
motor proteins that transport during anterograde transport
28
retrograde transport
from axon terminal to cell body via DYNEINS
29
retrograde transport can include the movement of...
growth factors or VIRUSES
30
herpes virus type I
- 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
31
in infants virus can...
go beyond the trigeminal ganglion and cause encephalitis
32
damaged CNS neurons
do not regenerate...they "sprout" but never reach their targets
33
why do sprouted CNS neurons never reach their targets
scar formation
34
what role do astrocytes have in nerve regeneration
they inhibit it by making chondroitin sulfate proteoglycans
35
in the PNS, is nerve regeneration possible
yes! some functional recovery can occur which is clinically significant in dental procedures in which nerve injury takes place.
36
what is the first response (in a timeline) of a nerve to a SEVERE nerve injury
1. anterograde degeneration
2. terminal degeneration
(peripheral process of neuron lost...approaching the ganglia)
37
what is wallerian degeneration
anterograde degeneration (from terminal towards the ganglion)
38
what is transganglionic degeneration
central process of the neuron is lost (plus the ganglia and peripheral process)...this occurs later on in the severe nerve injury
39
what is transynaptic degeneration
some signal crosses the synapse (where another nerve is synapsing on the one that was injured) to degenerate the adjacent neuron
40
what is the nerve response to a LESS SEVERE injury
you get both terminal degeneration and anterograde degeneration but also get CHROMATOLYSIS
41
what is chromatolysis
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?)
42
what is a schwann cell's response to regeneration
the cells proliferate and produce LAMININ and NGF
43
what is the role of laminin in regeneration
schwann cells produce this as a substrate for regenerating axons to grow on
44
what is the role of NGF
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
45
NGF regulates the gene expression of what
- microtubules/microfilaments (for nerve axon structure)
- n.t
- ion channels
- n.t receptors
46
collateral sprouting
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
47
the older the patient (of nerve injury) the...
less transmedian regeneration/sprouting. negative correlation of age and recovery of function
48
synaptotagmin
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)
49
4 ways what n.t can diffused
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
50
synaptic integration
interactions b/w inputs on a neuron influence whether or not there will be an output/a.p by that neuron
51
temporal summation
adding together of PSP's from one synaptic contact over time
52
spacial summation
adding together of PSP's produced by different synpases
53
what is a classical neurotransmitter
used for rapid communication (msec)...they act on the postsynaptic cell to produce an excitatory or inhibitory effect
54
what are neuromodulators
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
acetylcholine is synthesized by
choline and acetyl co-A
56
what enzyme makes acetylcholine
choline acetyletransferase
57
what enzyme stops the action of Ach
acetylcholinesterase diffuses/degrades Ach
58
what is another way for Ach action to stop
reuptake of choline by presynaptic neuron
59
what neurons release ACh
- all motor neurons
- those in nucleus basalis and pons
- pregang symp and psymp
- all postgang psymp
60
what is the ACh receptor type in the CNS
muscarinic receptor...EXCEPT postgang psymp (PNS)
61
muscarinic ACh mechanism
ACh binds and (INDIRECTLY) causes g protein activation to open or close ion channels
62
muscarinic receptors are blocked by
atropine
63
what is the ACh receptor type in the PNS
nicotinic receptors (not many in the CNS)
64
nicotinic ACh mechanism
ACh binds and DIRECTLY opens the ion channels (channel located in the ACh receptor)
65
ACh nicotinic receptors are blocked by
curare (like at the neuromuscular jn)
66
ACh neurons in the nucleus basalis/basal forebrain are for
cognitive fn
67
ACh neurons in the pontine nuclei are for
sleep regulation
68
myasthenia gravis
autoimmune disorder. ab made that target nicotinic receptors (ACh receptors). muscle weakness (neuromuscular jn).
69
myasthenia gravis is treated with
acetylcholinesterase inhibitors to prolong the effect of ACh
70
alzheimers disease and ACh
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
biogenic amines are synthesized from
a.a...they include the catecholamines, serotonin, and histamine
72
catecholamines include
dopamine, norepinephrine, and epinephrine
73
catecholamines are synthesized from
a.a, tyrosine
74
catecholamine release is dependent on
Ca2+
75
termination of catecholamine action is through
1. presyntaptic reuptake
| 2. degradation by MAO (monoamine oxidase)
76
neurons for biogenic amines are found
in very limited locations
77
receptors for biogenic amines are found
extensively in the CNS
78
receptors for biogenic amines are
exclusively G-protein couples receptors
79
dopamine neurons are found in the
1. ventral tegmental area
| 2. substantia nigra
80
in the VTA, dopamine is associated with
reward and addiction
81
cocaine and amphetamine do what
prolong dopamine action at the synapse in the VTA
82
in the substantia nigra, dopamine is associated with
the motor system
83
loss of dopamine in the S.N results in
parkinson's disease
84
D1 vs D2 dopamine receptors
D1: activate adenylate cyclase-->a.p
D2: inhibit a.c--> hyperpolarization
85
tardive dyskinesia
drugs that block D2 receptors can cause this.. presented as rhythmic oral movements.
86
norepinephrine neurons are found
1. locus ceruleus
| 2. brainstem
87
norepinephrine neurons in the locus ceruleus are responsible for
attention and sleep
88
norepinephrine neurons in the brainstem are responsible for
autonomic/homeostatic fns
89
norepinephrine neurons include
postgang symp
90
noepinephrine receptor type
noradrenergic (alpha and beta types)....g-protein coupled
91
alpha NE receptors
type 1: release Ca=excitatory
| type 2: open K channels/block Ca=inhibitory
92
beta NE receptors
open Ca channels
93
depending on receptor, NE effects are
very different
94
serotonin is synthesized from
tryptophan
95
serotonin neurons are located in
1. rostral raphe nuclei
| 2. caudal raphe nuclei
96
serotonin neurons in the rostal raphe nuclei are responsible for
sleep, mood, homeostasis
97
serotonin neurons in the caudal raphe nuclei are responsible for
sensori-motor fn
98
histamine is synthesized from
histadine (a.a)
99
histamine neurons are found
small pop. of hypothalamic neurons
100
histamine is responsible for
sleep-wakefullness
101
histamine receptors are
g-protein coupled (H1-H4)
102
what are the EXCITATORY amino acid n.ts
glutamate and aspartate
103
excitatory a.a n.ts bind to what kind of receptors
ionotropic receptors and metabotropic receptors
104
ionotropic receptors for the excitatory a.a n.ts have channels that....
are permeable to cations (which allow for a depolarizing/excitatory effect): Na, K, Ca
105
metatropic receptors are
g-protein coupled
106
the NMDA receptor is what kind of receptor
ionotropic
107
properties of NMDA receptors
- involved in fns that last
| - can be responsible for excitotoxicity (excessive excitation)
108
the NMDA receptor is the synaptic mechanism for
long term potentiation
109
what is long term potentiation (LTP)
- 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
describe NMDA receptor mediated potentiation
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
how does phosphorylation of the NMDA receptor influence LTP
phosphorylation permanently removes the Mg block on the NMDA receptor....which allows Ca to flow into the post synaptic cell
112
how does Ca entry into the post synaptic cell (through the NMDA receptor) effect LTP
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
what is the astrocytes role in the glutamate pathway
reuptake
114
what is the glutamate reuptake pathway
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
what are the inhibitory a.a n.ts
GABA (modified form of glutamate...in the CNS) and glycine
116
what are the 2 receptors for GABA
1. ionotropic receptor (GABA-a)
| 2. metabotropic receptor (GABA-b)
117
what channel does the GABA-a receptor open
Cl-...which HYPERPOLARIZES THE CELL
118
what channel does the GABA-b receptor open
K+....causing K+ to flow out of the cell (down its [ ] gradient) which will HYPERPOLARIZE the cell
119
huntinton chorea is linked to what deficiency
GABA...since this is an inhibitory n.t, have trouble suppressing inhibitory effects on muscles (uncontrolled excitability) which= motor spasticity
120
glycine (inhibitory n.t) opens what type of channels
Cl-
121
the effects of glycine are inhibited by what
strychnine
122
peptide neuromodulators are typically
released with other n.ts
123
properties of peptide neuromodulators
- 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
actions of peptide neuromodulators are terminated by
1. proteolysis
| 2. diffusion
125
by what is NO synthesized
L-arginine--> NO by nitric oxide synthase
126
is NO stored in vesicles
nope! its a gas so it freely diffuses across the membrane (doesn't require a synapse)
127
NO acts to
modulate other n.t release
| -also plays a role in brain fns like LTP
128
how does ATP act as an n.t
usually excitatory and co-released with other classic n.ts
