unit 1 Flashcards
1
Q
afferent
A
sensory
2
Q
efferent
A
motor
3
Q
neurons
A
main proccessing cell in NS
4
Q
Ca2+ concentation in cell
A
extremely low
5
Q
Na+ concentration in cell
A
low
6
Q
K+ concentration in cell
A
high
7
Q
Ca2+ concentration outside of cell
A
high
8
Q
Na+ concentration outside of cell
A
high
9
Q
K+ concentration outside of cell
A
low
10
Q
ATPase - Na+/K+ pump
A
3 Na+ out, 2 K+ in
11
Q
ectoderm
A
neural stem cells - neurons and macroglia
12
Q
mesoderm
A
myeloid cells - microglia
13
Q
trilaminar disc
A
includes ectoderm, mesoderm and endoderm
14
Q
histology
A
microscopic study of tissues
15
Q
silver golgi stain
A
stains entire cell but only a fraction of all the cells; stains both neuronal bodies and neurites - inaccurate in cell density
16
Q
cresyl violet nissl stain
A
stains nucleus and rough ER (nucleic acids); gray matter prominent; great for showing cell density; easy to discriminate between glia and neurons because rough ER is more prominent in neurons.
17
Q
Astrocytes
A
regulate levels of chemical and ion balance in environment surrounding neurons - at nodes of ranvier and synapses; can send signals to environment to influence neuron guidance, survival and outgrowth
18
Q
satellite cells
A
glial cells in PNS; analogous to astrocytes in many ways
19
Q
hemotoxylin and eosin
A
hemotoxylin: stains DNA in nucleus purple/blues
eosin: stains proteins and other components in cytosplasm pink/red
20
Q
GFAB
A
glial fibrillary acidic protein; astrocyte specific
21
Q
gene expression
A
dna (gene) –> mRNA –> protein –> expression
22
Q
regulation of extracellular space
A
occures in tripartite synapse; keyrole in regulating synaptic transmission by removing glutamate from synapse through reuptake
23
Q
EAAT 1 and 2
A
protein transport - excitatory amino acid transport (astrocyte reuptake of glutamate)
24
Q
excessive levels of glutamate in synapse
A
post-synaptic neuron dies due to excitotoxicity
25
excitotoxicity
too much Ca2+ in post-synaptic neuron
26
NMDA (ionotropic)
allows for Ca2+ influx
27
K+ buffering regulation
astrocytes regulate K= levels by taking it up via inward rectifying potassium (Kir) channels - if no Kir then resting potential increases
28
less K+ efflux
depolarization
28
tight junction
btw capillary endothelial cells; restricts passage of substances larger than 10nm
29
K+ efflux
hyperpolarization
29
blood-brain barrier
involves endothelial cells, pericates and astrocytes
30
astrocyte endfoot
projection of astrocyte lies adjacent to endothelial cells allowing for interaction in BBB and adds another layer of protection, allows for tight junction
31
neuronal injury
astrocytes become "activated" to injury = upregulation of GFAP; activated microglia secretes molecules that promote such upregulation
32
A1
toxic to neurons
33
A2
neuroprotective
34
microglia
resident immune cells; phagocytosing cells; remove debris after injury, program cell death, intoduce new cells; even in resting state are very active; when activated can be beneficial and detrimental; HAVE LOTS OF FUNCTIONS
35
myelin
lipid (mostly) and protein rich; in WHITE matter
36
oligodendrocytes
CNS; wrap myelin around axons of multiple neurons; multiple neurons affected
37
schwann cells
PNS; wrap myelin around axon of a single neuron: one neuron has multiple schwann cells
38
ependymal cells
line ventricles, produce CSF which provides protection
39
endothelial cells
line BBB
40
light microscopy
uses light to visualize a specimen; lower magnitude (10x - 800x)
41
electron microscopy
uses electrons to visualize specimen; extremely high magnitude (up to 50,000,000x)
42
scanning electron microscopy (SEM)
visualize surface/3D structure
43
transmission electron microscopy (TEM)
visualize intracellular (2D) at extremely high magnitude
44
In TEM CNS has....
no space
45
in TEM PNS has....
space
46
ion flow
dependent upon electrostatic forces, chemical forces (concentration gradient) and permeability
47
driving forces are
electrostatic forces and chemical forces; tells which way and how powerfully an ion would flow if open ion channels selectable for it
48
driving force equation
voltage of the cell - voltage of the equilibrium potential of the ion
49
ion flow equation
driving force * permeability
50
equilibrium potential
membrane potential at which a particular ion is at electrochemical equilibrium
51
nerst equation
Ex = RT/zF ln [x]out/[x]in
52
the membrane
phospholipid bi-layer; capacitor (can store charge)
53
voltage of membrane potential
voltage in - v out = ~-70mV
54
membrane potential is dependent on 3 factors
Na/K pump, K+ efflux through leak channels, intracellular organic anions
55
resting membrane isnt Ek because
there are other ions (Na+ and Ca2+) but they don't have the same permeability as K+
56
goldman equation
accounts for several ions contributing to membrane potential and membrane permeability (Pion)
57
EPSPs and IPSPs
are graded, can be summed (at axon hillock), and spread by passive propagation
58
EPSP
depolarization; makes cell more likely to AP (cation)
59
IPSP
hyperpolarization; less likely to AP (anion)
60
length constant equation
length constant: sq*(rm/ri)
61
length constant
distance at which a change in V has decayed by 37%
62
length constant is directly related to
membrane resistance (rm)
63
length constant is indirectly related to
axial/internal resistance (ri)
64
long length constant =
potential can spread further before decaying
65
longer diameter =
lower ri
66
more myelin sheath =
higher rm
67
time constant equation
T = rm cm
68
cm
capacitance of neuron membrane
69
velocity is related
directly to length constant and inversly to T
70
if sum of EPSPs and IPSPs
reaches threshold potential then AP
71
spatial summation
excitatory potential from MANY neurons to trigger threshold potential
72
temporal summation
many excitatory potentials from one neuron triggers threshold potential
73
voltage-gated channels
form an aqueous pore in membrane, between s5 & 6 and contains 4 transmembrane domain with 65 repeating segment
74
VG channels
+ charge amino acids in S4 segments act as Voltage-sensors
75
VG K+ and VG Na+ channels are
structurally similar just deal with different ions
76
VG Na+ CHannels
depolarization activates and are very fast; after they are opened and then close, they are inactivatable --- need repolarization to become activatable again (refractory period)
77
myelination on APs
drastically increases the velocity of AP propagation and allows for saltatory conduction
78
saltatory conduction
depolarization travels form node to node via passive propagation (at myelin sheaths)
79
in multiple sclerosis
rm decreases and length constant decreases
80
after AP travels all the way down the axon
activation of VG-Ca2+, Ca2+ influx (causes NT fusion), fusion of synaptic vesicles with pre-synpatic membrane, QUANTAL release of NT vesicles
81
SNARE proteins
catalyze fusion of vesicles with plasma membrane
82
synaptotagim
Ca2+ sensor
83
V-SNARE
synaptobrevin (detect Ca2+ levels)
84
T-SNARE
syntaxin and SNAP-25
85
during vesicle fusion
V and T-SNARE interact allow NT release
86
NT release
CA2+ elevated in localized manner (Ca2+ microdomains)
87
release of synaptic vesicles is extremely rapid THUS
release sites must be closed to Ca2+ channels
88
why must synaptic vesicles be recycled and NT re-loaded into vesicles?
continuous stim of NT junction causes release of NT that far exceeds the readily available pool
89
where are NTs re-synthesized
axon terminal
90
axosecretory
terminal secretes directly into bloodstream
91
axoaxonic
axon terminal secretes into another axon
92
axodendritic
terminal ends on dendrite spine
93
axocellular
axon with no connection secretes into extracellular fluid
94
axosomatic
terminal ends on soma
95
axosynaptic
terminal ends on another axon terminal
96
small molecule NT
glutamate, GABA, dopamine, etc; small clear-core vesicles; synthesized at axon terminal
97
neuropeptides
dense-core vesicles; made in cell body and transported (anterograde) to distal axon
98
neurons typically produce
ONE small NT and maybe one peptide transmitter
99
the NT a neuron produces depends on
expression of synthetic enzymes
100
in neurons that release both sm and neuropeptides
low level activity leads to release of SM transmitters but high frequency still causes neuropeptides to release
101
glutamate synthesis
glutamine catalyzed by glutaminase
102
vesicular uptake
vATPase generates proton gradient (acidification) and works with VGLUT to pump glutamate into the vesicle from the cytoplasm
103
VGLUT
H+/glutamate antiporter; glutamatergic neuron marker
104
glutamate ionotropic receptor (iGluR)
AMPA and NMDA; fast excitator
105
AMPA
Na+ influx/K+ efflux
106
NMDA
Na+ and Ca2+ influx/K+ efflux; have to kick off Mg so glutamate can bind
107
glutamate metabotropic receptor (mGluR)
group I: slow excitatory; group II and III: slow inhibitory; based on nature of g-protein - pathway will be different
108
Gas pathway
g-protein disassembles, as will stimulate adenlylcylase (AC) which produces ATP and cAMP; cAMP-gated ion channel lets Na+ in which can give EPSP
109
Gai pathway
g-protein disassembles; ai will inhibit AC the cAMP decreases leading for hyperpolarization because cAMP-gated cation channels (anion will depolarize)
110
glutamate is
primary excitatory NT in CNS; excitation/inhabitation imbalance in epilepsy; excitotoxicity; ketamine: NMDA antagonist
111
GABA synthesis
glutamine --> glutamate --> GAD ---> GABA
112
GABA and glutamate recycle
GABA and glutamate are recycled into glutamine in astrocyte and the cycles go through
113
GABA vesicle uptake
VGAT
114
GABA ionotropic receptor
GABAa
115
GABAa
hyperpolarize via Cl influx
116
GABA metabotropic receptor
GABAb
117
GABAb
inhibits adenylylcyclase; couple to Gai
118
GABA is
primary inhibitory NT in the CNS; excitation/inhibition imbalance in epilepsy; mutations in genes encoding GABAa subunits are implicated in epilepsy
119
GABAa targeted by many drugs
benzodiazepines, alcohol (both agonist)
120
acetylcholine synthesis
made from choline and acetyl CoA; ACh is rapidly broken down by AChE
121
ChAT
makes ACh
122
vChAT
vesicle ACh is packaged in
123
ACh Esterase
on postsynpatic cell; breaking down ACh once in synapse
124
ACh receptor ionotropic
nicotinic
125
nACh
non-specific so other ions can flow in but mostly Na+ so EPSP
126
why is nACh have mostly Na+ efflux
driving flow is increased for Na+ more than K+ and Ca2+ because of equilibrium potential, nACh is more permeable to Na+
127
ACh metabotropic receptor
muscarinic (just know it has subtypes)
128
ACh Alzeheimers drugs
increase levels of ACh in synapse by inhibiting AChE
129
how is sarin gas different than alzheimers drugs?
the overstimulation is irreversible
130
catecholamines
dopamine, norepinephrine, epinephrine - derives from tyrosine
131
indolamines
serotonin - derived from trytophan
132
tyrosine pathway
tyrosine -- (tyrosine hydroxylase)--> L-DOPA --(AADC)--> dopamine --(DBH)--> norepinephrine --(PNMT)--> epinephrine
133
tryptophan pathway
tryptophan --(tryptophan hydroxylase)--> 5-HTP --(AADC)--> serotonin
134
vesicle uptake of monoamines
VMAT loads all into vesicles
135
monoamine removal from synapse
reuptake, diffusion and enzymatic degradation
136
dopamine transporter
DAT
137
norepinephrine transport
NET
138
serotonin transporter
SERT
139
enzymatic degradation via...
MAO and COMT
140
dopamine receptors
DI (Gs - stimulatory) and D2 (Gi - inhibitory)
141
epinephrine and norepinephrine receptors
adrenergic receptors - metabotropic
142
serotonin receptors
mostly metabotropic but 5-HT3 is ionotropic
143
dopamine pathway
mesolimbic: from ventral tegmental area (VTA) to nucleas accumbens (Nac) -- reward
144
norepinephrine location
sympathetic post-ganglionic neurons
145
treatment of Parkinson's with...
L-DOPA (dopamine precursor)
