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Neurobio > unit 1 > Flashcards

unit 1 Flashcards

1
Q

afferent

A

sensory

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2
Q

efferent

A

motor

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3
Q

neurons

A

main proccessing cell in NS

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4
Q

Ca2+ concentation in cell

A

extremely low

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5
Q

Na+ concentration in cell

A

low

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6
Q

K+ concentration in cell

A

high

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7
Q

Ca2+ concentration outside of cell

A

high

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8
Q

Na+ concentration outside of cell

A

high

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9
Q

K+ concentration outside of cell

A

low

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10
Q

ATPase - Na+/K+ pump

A

3 Na+ out, 2 K+ in

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11
Q

ectoderm

A

neural stem cells - neurons and macroglia

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12
Q

mesoderm

A

myeloid cells - microglia

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13
Q

trilaminar disc

A

includes ectoderm, mesoderm and endoderm

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14
Q

histology

A

microscopic study of tissues

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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

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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.

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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

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18
Q

satellite cells

A

glial cells in PNS; analogous to astrocytes in many ways

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19
Q

hemotoxylin and eosin

A

hemotoxylin: stains DNA in nucleus purple/blues
eosin: stains proteins and other components in cytosplasm pink/red

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20
Q

GFAB

A

glial fibrillary acidic protein; astrocyte specific

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21
Q

gene expression

A

dna (gene) –> mRNA –> protein –> expression

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22
Q

regulation of extracellular space

A

occures in tripartite synapse; keyrole in regulating synaptic transmission by removing glutamate from synapse through reuptake

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23
Q

EAAT 1 and 2

A

protein transport - excitatory amino acid transport (astrocyte reuptake of glutamate)

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24
Q

excessive levels of glutamate in synapse

A

post-synaptic neuron dies due to excitotoxicity

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25
Q

excitotoxicity

A

too much Ca2+ in post-synaptic neuron

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26
Q

NMDA (ionotropic)

A

allows for Ca2+ influx

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27
Q

K+ buffering regulation

A

astrocytes regulate K= levels by taking it up via inward rectifying potassium (Kir) channels - if no Kir then resting potential increases

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28
Q

less K+ efflux

A

depolarization

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28
Q

tight junction

A

btw capillary endothelial cells; restricts passage of substances larger than 10nm

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29
Q

K+ efflux

A

hyperpolarization

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29
Q

blood-brain barrier

A

involves endothelial cells, pericates and astrocytes

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30
Q

astrocyte endfoot

A

projection of astrocyte lies adjacent to endothelial cells allowing for interaction in BBB and adds another layer of protection, allows for tight junction

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31
Q

neuronal injury

A

astrocytes become “activated” to injury = upregulation of GFAP; activated microglia secretes molecules that promote such upregulation

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32
Q

A1

A

toxic to neurons

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33
Q

A2

A

neuroprotective

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34
Q

microglia

A

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

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35
Q

myelin

A

lipid (mostly) and protein rich; in WHITE matter

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36
Q

oligodendrocytes

A

CNS; wrap myelin around axons of multiple neurons; multiple neurons affected

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37
Q

schwann cells

A

PNS; wrap myelin around axon of a single neuron: one neuron has multiple schwann cells

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38
Q

ependymal cells

A

line ventricles, produce CSF which provides protection

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39
Q

endothelial cells

A

line BBB

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40
Q

light microscopy

A

uses light to visualize a specimen; lower magnitude (10x - 800x)

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41
Q

electron microscopy

A

uses electrons to visualize specimen; extremely high magnitude (up to 50,000,000x)

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42
Q

scanning electron microscopy (SEM)

A

visualize surface/3D structure

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43
Q

transmission electron microscopy (TEM)

A

visualize intracellular (2D) at extremely high magnitude

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44
Q

In TEM CNS has….

A

no space

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45
Q

in TEM PNS has….

A

space

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46
Q

ion flow

A

dependent upon electrostatic forces, chemical forces (concentration gradient) and permeability

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47
Q

driving forces are

A

electrostatic forces and chemical forces; tells which way and how powerfully an ion would flow if open ion channels selectable for it

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48
Q

driving force equation

A

voltage of the cell - voltage of the equilibrium potential of the ion

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49
Q

ion flow equation

A

driving force * permeability

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50
Q

equilibrium potential

A

membrane potential at which a particular ion is at electrochemical equilibrium

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51
Q

nerst equation

A

Ex = RT/zF ln [x]out/[x]in

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52
Q

the membrane

A

phospholipid bi-layer; capacitor (can store charge)

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53
Q

voltage of membrane potential

A

voltage in - v out = ~-70mV

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54
Q

membrane potential is dependent on 3 factors

A

Na/K pump, K+ efflux through leak channels, intracellular organic anions

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55
Q

resting membrane isnt Ek because

A

there are other ions (Na+ and Ca2+) but they don’t have the same permeability as K+

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56
Q

goldman equation

A

accounts for several ions contributing to membrane potential and membrane permeability (Pion)

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57
Q

EPSPs and IPSPs

A

are graded, can be summed (at axon hillock), and spread by passive propagation

58
Q

EPSP

A

depolarization; makes cell more likely to AP (cation)

59
Q

IPSP

A

hyperpolarization; less likely to AP (anion)

60
Q

length constant equation

A

length constant: sq*(rm/ri)

61
Q

length constant

A

distance at which a change in V has decayed by 37%

62
Q

length constant is directly related to

A

membrane resistance (rm)

63
Q

length constant is indirectly related to

A

axial/internal resistance (ri)

64
Q

long length constant =

A

potential can spread further before decaying

65
Q

longer diameter =

A

lower ri

66
Q

more myelin sheath =

A

higher rm

67
Q

time constant equation

A

T = rm cm

68
Q

cm

A

capacitance of neuron membrane

69
Q

velocity is related

A

directly to length constant and inversly to T

70
Q

if sum of EPSPs and IPSPs

A

reaches threshold potential then AP

71
Q

spatial summation

A

excitatory potential from MANY neurons to trigger threshold potential

72
Q

temporal summation

A

many excitatory potentials from one neuron triggers threshold potential

73
Q

voltage-gated channels

A

form an aqueous pore in membrane, between s5 & 6 and contains 4 transmembrane domain with 65 repeating segment

74
Q

VG channels

A

+ charge amino acids in S4 segments act as Voltage-sensors

75
Q

VG K+ and VG Na+ channels are

A

structurally similar just deal with different ions

76
Q

VG Na+ CHannels

A

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
Q

myelination on APs

A

drastically increases the velocity of AP propagation and allows for saltatory conduction

78
Q

saltatory conduction

A

depolarization travels form node to node via passive propagation (at myelin sheaths)

79
Q

in multiple sclerosis

A

rm decreases and length constant decreases

80
Q

after AP travels all the way down the axon

A

activation of VG-Ca2+, Ca2+ influx (causes NT fusion), fusion of synaptic vesicles with pre-synpatic membrane, QUANTAL release of NT vesicles

81
Q

SNARE proteins

A

catalyze fusion of vesicles with plasma membrane

82
Q

synaptotagim

A

Ca2+ sensor

83
Q

V-SNARE

A

synaptobrevin (detect Ca2+ levels)

84
Q

T-SNARE

A

syntaxin and SNAP-25

85
Q

during vesicle fusion

A

V and T-SNARE interact allow NT release

86
Q

NT release

A

CA2+ elevated in localized manner (Ca2+ microdomains)

87
Q

release of synaptic vesicles is extremely rapid THUS

A

release sites must be closed to Ca2+ channels

88
Q

why must synaptic vesicles be recycled and NT re-loaded into vesicles?

A

continuous stim of NT junction causes release of NT that far exceeds the readily available pool

89
Q

where are NTs re-synthesized

A

axon terminal

90
Q

axosecretory

A

terminal secretes directly into bloodstream

91
Q

axoaxonic

A

axon terminal secretes into another axon

92
Q

axodendritic

A

terminal ends on dendrite spine

93
Q

axocellular

A

axon with no connection secretes into extracellular fluid

94
Q

axosomatic

A

terminal ends on soma

95
Q

axosynaptic

A

terminal ends on another axon terminal

96
Q

small molecule NT

A

glutamate, GABA, dopamine, etc; small clear-core vesicles; synthesized at axon terminal

97
Q

neuropeptides

A

dense-core vesicles; made in cell body and transported (anterograde) to distal axon

98
Q

neurons typically produce

A

ONE small NT and maybe one peptide transmitter

99
Q

the NT a neuron produces depends on

A

expression of synthetic enzymes

100
Q

in neurons that release both sm and neuropeptides

A

low level activity leads to release of SM transmitters but high frequency still causes neuropeptides to release

101
Q

glutamate synthesis

A

glutamine catalyzed by glutaminase

102
Q

vesicular uptake

A

vATPase generates proton gradient (acidification) and works with VGLUT to pump glutamate into the vesicle from the cytoplasm

103
Q

VGLUT

A

H+/glutamate antiporter; glutamatergic neuron marker

104
Q

glutamate ionotropic receptor (iGluR)

A

AMPA and NMDA; fast excitator

105
Q

AMPA

A

Na+ influx/K+ efflux

106
Q

NMDA

A

Na+ and Ca2+ influx/K+ efflux; have to kick off Mg so glutamate can bind

107
Q

glutamate metabotropic receptor (mGluR)

A

group I: slow excitatory; group II and III: slow inhibitory; based on nature of g-protein - pathway will be different

108
Q

Gas pathway

A

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
Q

Gai pathway

A

g-protein disassembles; ai will inhibit AC the cAMP decreases leading for hyperpolarization because cAMP-gated cation channels (anion will depolarize)

110
Q

glutamate is

A

primary excitatory NT in CNS; excitation/inhabitation imbalance in epilepsy; excitotoxicity; ketamine: NMDA antagonist

111
Q

GABA synthesis

A

glutamine –> glutamate –> GAD —> GABA

112
Q

GABA and glutamate recycle

A

GABA and glutamate are recycled into glutamine in astrocyte and the cycles go through

113
Q

GABA vesicle uptake

A

VGAT

114
Q

GABA ionotropic receptor

A

GABAa

115
Q

GABAa

A

hyperpolarize via Cl influx

116
Q

GABA metabotropic receptor

A

GABAb

117
Q

GABAb

A

inhibits adenylylcyclase; couple to Gai

118
Q

GABA is

A

primary inhibitory NT in the CNS; excitation/inhibition imbalance in epilepsy; mutations in genes encoding GABAa subunits are implicated in epilepsy

119
Q

GABAa targeted by many drugs

A

benzodiazepines, alcohol (both agonist)

120
Q

acetylcholine synthesis

A

made from choline and acetyl CoA; ACh is rapidly broken down by AChE

121
Q

ChAT

A

makes ACh

122
Q

vChAT

A

vesicle ACh is packaged in

123
Q

ACh Esterase

A

on postsynpatic cell; breaking down ACh once in synapse

124
Q

ACh receptor ionotropic

A

nicotinic

125
Q

nACh

A

non-specific so other ions can flow in but mostly Na+ so EPSP

126
Q

why is nACh have mostly Na+ efflux

A

driving flow is increased for Na+ more than K+ and Ca2+ because of equilibrium potential, nACh is more permeable to Na+

127
Q

ACh metabotropic receptor

A

muscarinic (just know it has subtypes)

128
Q

ACh Alzeheimers drugs

A

increase levels of ACh in synapse by inhibiting AChE

129
Q

how is sarin gas different than alzheimers drugs?

A

the overstimulation is irreversible

130
Q

catecholamines

A

dopamine, norepinephrine, epinephrine - derives from tyrosine

131
Q

indolamines

A

serotonin - derived from trytophan

132
Q

tyrosine pathway

A

tyrosine – (tyrosine hydroxylase)–> L-DOPA –(AADC)–> dopamine –(DBH)–> norepinephrine –(PNMT)–> epinephrine

133
Q

tryptophan pathway

A

tryptophan –(tryptophan hydroxylase)–> 5-HTP –(AADC)–> serotonin

134
Q

vesicle uptake of monoamines

A

VMAT loads all into vesicles

135
Q

monoamine removal from synapse

A

reuptake, diffusion and enzymatic degradation

136
Q

dopamine transporter

A

DAT

137
Q

norepinephrine transport

A

NET

138
Q

serotonin transporter

A

SERT

139
Q

enzymatic degradation via…

A

MAO and COMT

140
Q

dopamine receptors

A

DI (Gs - stimulatory) and D2 (Gi - inhibitory)

141
Q

epinephrine and norepinephrine receptors

A

adrenergic receptors - metabotropic

142
Q

serotonin receptors

A

mostly metabotropic but 5-HT3 is ionotropic

143
Q

dopamine pathway

A

mesolimbic: from ventral tegmental area (VTA) to nucleas accumbens (Nac) – reward

144
Q

norepinephrine location

A

sympathetic post-ganglionic neurons

145
Q

treatment of Parkinson’s with…

A

L-DOPA (dopamine precursor)

Neurobio (6 decks)

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