Neuro physio Flashcards
1
Q
After resolution of HSV-1 (herpes labialis), where virus stays?
A
virus enters a latent phase - viral particles lay dormant in neural SENSORY ganglia (most commonly trigeminal)
2
Q
What induces HSV-1 reactivation?
A
Stress, illness
3
Q
How is called transport when HSV-1 goes from skin to neurons?
A
virus enters nerve terminals –> dynein-dependent (retrograde) trasnsport in neuron.
4
Q
How is called transport when HSV-1 goes up from neurons to skin?
A
kinesin-dependent (anterograde) transport
5
Q
In which part of the neuron stays HSV-1?
A
Latent virus integrated in DNA
6
Q
The function of kinesin?
A
motor protein, that moves intracellular cargo (organelles, viral particles) away from nucleus, down to the axon and toward the nerve terminal.
7
Q
Kinesin-mediated movement is powered by …………….. and guided by …………………….
A
ATP hydrolysis;
guided by microtubule filaments
8
Q
Direction of cargo in dynein and kinesin transport?
A
Dynein - toward the nucleus;
Kinesin - away from the nucleus.
9
Q
What protein is respondible for herpes labialis recurrence?
A
kinesin - it moves viral particles away from nucleus. Dynein - is not responsible, because it moves particles to neural sensory ganglia - important in establishing the latent phase following primary HSV infection
10
Q
What do lamins?
A
It helps to form the fibrillar network that lines the inside of the nuclear envelope.
11
Q
Lamins provide structural support. What other 2 functions related to cell genetics?
A
Help to organize genome and regulate gene transcription
12
Q
Where is located spectrin?
A
intracellularly along the plasma membrane
13
Q
For which cell is important spectrin?
A
RBCs - maintains distinct shape. When defect - hereditary elliptocytosis and spherocytosis
14
Q
In which cells is expressed vimentin?
A
In mesenchymal
15
Q
What is the function of vimentin?
A
Securing organelles inside the cytosol and provides resistance to mechanical stress
16
Q
What is the role of second messengers in release of ACh in synapsis in NMJ?
A
None. It does not play any role in synapsis in NMJ
17
Q
What stains Nissl stains in neuron?
A
RER
18
Q
Kinesin is …………………….. protein
A
microtubule assoc motor protein
19
Q
What is direction of transport in kinesin in relation to microtubules?
A
Away from nucleus - toward the plus ends of microtubules
20
Q
What is the result of toxic insult to kinesin?
A
impaired anterograde transport –> results in deficiency of synaptic vesicles at the nerve terminal
21
Q
Microvilli and microtubules?
A
Microvilli do not contain microtubules or microtubule associated proteins. It contains actin thin filaments.
22
Q
Function of desmosomes?
A
mediate cell-cell adhesion between epithelial cells.
23
Q
Location of T-tubules?
A
junction of the A and I brands of striated myocytes
24
Q
Function of T-tubules?
A
they are open to extracellular space and facilitate the spread of the depolarization to the inside of the cell.
25
What is the primary excitatory neurotrasmiter in the brain?
Glutamate
26
The glutamate NMDA receptor is a .................... and .................... ion channel
Potential-dependent and ligand-gated ion channel
27
What ion form a plug in glutamate NMDA receptor?
magnesium
28
What are two events that opens glutamate NMDA receptors?
Displacement of magnesium and binding of glutamate
29
What initiates displacement of magnesium in glutamate NMDA receptor?
initial depolarization impuls (non-NMDA mediated) --> loss of negative potential --> displaced magnesiujm
30
Why in dying neurons can occur displacement of magnesium in glutamate NMDA?
loss of the ATP-dependent sodium-potassium gradient
31
glutamate bind glutamate NMDA receptors along with ......................
glycine
32
What allow unrestricted flow of calcium, sodium and potassium via glutamate NMDA receptors?
conformational changes that occurs after glutamate binding
33
Why there is depolarization in glutamate NMDA receptors if there is also potassium efflux?
influx of Sodium + calcium (depolaryzation) > efflux of potassium (hyperpolarize) --> NET = depolarization overcome hyperpolarization
34
What and where changes of magnesium concentration induces glutamate mediated neuron depolarization?
Higher extracellular magnesium levels block the NMDA channes --> decr. influx of calcium and sodium --> inhibited glutamate-mediated neruon depolarization
35
During acute ischemic stroke, a sudden, massive rise in .................................. occurs within the infarct zone.
extracellular glutamate
36
High extracellular glutamate levels in acute ischemic stroke leads to .................
glutamate NMDA receptor excessive activation --> increased calcium influx --> intracellular calcium overload.
37
What happens when there is increased intracellular calcium concentration in neuron? eg in acute ischemic stroke?
It accumulates in mitochondria --> triggered apoptotic neuronal death (excitotoxicity)
38
What and where release dying neurons?
they release more glutamate into the extacellular space --> increased excitation in neighboring neurons.
39
Calcium overload (cytotoxicity) leads to 3 outcomes in CNS.
Mitochondrial dysfunction;
inc. ROS;
protease activation
40
modulation of the ............ receptor is an emerging frontier in neuroprotection
NMDA
41
What cases loss of membrane potential in CNS injury?
decreased ATP
42
WHat initiates depolarization in damaged CNS?
initial nonspecific depolarization
43
What ion is used therapeutically to block depolarization in CNS?
Magensium. It blocks glutamate NMDA receptors --> prevent passage of calcium and sodium.
Magnesium itself does not pass through the NMDA receptors!!!
44
Excessive activation of the glutamate NMDA receptor causes ..................
Excitotoxic neuronal death through uncontrolled calcium influx
45
By what depolarization is released magnesium from glutamate NMDA?
by non-NMDA-mediated depolarization
46
at what stage of the cell NMDA receptors are blocked by magnesium?
at the hyperpolarized resting membrane potential
47
NMDA channels are impermeable to .....................
anions
48
NMDA channels are .................. to anions
impermeable
49
The influx of chloride and bicarbonate anions induces ..................
hyperpolarization
50
Influx of chloride and bicarbonate mediates ...................... ............ potential, generated by .............. channels.
inhibitory postsynaptic; GABA-A channels.
51
Neurons can also be hyperpolarized by ......................... ................., mediating inhibitory potentials generated by GABA-B channels.
potassium efflux
52
Influx of chloride and bicarbone ---> ................. channels.
Efflux of potasium --> ............... channels.
GABA-A;
| GABA-B
53
Excitatory postsynaptic potential (EPSP) is a small ............................................. that moves the ..................... neuron closer to the threshold for full action potential firing
depolarization;
| postsynaptic
54
The EPSP occurs with rising .......................
Intracellular calcium
55
EPSP and calcium conductance relation?
The EPSP occurs with rising intracellular calcium (bottom panel), indicating that the involved postsynaptic receptor acts, at least in part, by increasing calcium conductance.
56
What receptors participate at least in part in EPSP by increasing calcium conductance?
postsynaptic receptors
57
What regulates synaptic plasticity?
increased calcium influx --> second-messenged signaling cascades --> regulation of synaptic plasticity
58
repetitive excitation of postsynaptic neurons renders them more ....................., producing ................... ...................... over time
responsive; stronger EPSPs
59
repetitive excitation of postsynaptic neurons renders them more responsive, producing stronger EPSPs over time. How is called this process?
long-term potentiation (LTP) - dictates synaptic strength between hippocampal neurons
60
Long-term potentiation is important in hippocampal neurons. LTP function in these neurons?
plays a critical role in the molecular basis of memory, learning, and addiction.
61
Acute blockade of glutamate NMDA receptors confers the ....................... of certain medications (eg, ketamine) and some drugs of illicit use
amnestic property
62
Chronic blockade (eg, memantine) can exert ....................................... effects by dampening glutamate-induced excitotoxicity
neuroprotective
63
What is process of exitotoxicity?
neuron apoptosis due to calcium overload
64
Dopamine can be either ............ or ................. depending on the receptor subtype
excitatory or inhibitory
65
Dopamine can be either excitatory or inhibitory depending on the ................
receptor subtype
66
D2 receptors are generally coupled to Gi proteins that inhibit protein kinase A, leading to the opening of potassium channels that ............... neuronal depolarization.
inhibit
67
D2 receptors are generally coupled to ......... proteins.
Gi
68
Gi proteins inhibits .............
protein kinase A
69
Inhibition of protein kinase A leads to ..................
opening of potassium channels --> inhibited neuronal depolarization
70
GABA is the chief ....................... neurotransmitter
inhibitory
71
GABA causes postsynaptic hyperpolarization via ....................................
Increased chloride and bicarbonate influx (ie, ionotropic GABA-A ion channel) or increased potassium efflux (ie, metabotropic GABA-B receptor.
72
increased potassium efflux (ie, .............................. GABA-B receptor
metabotropic
73
increased chloride and bicarbonate influx (...................... GABA-A ion channel)
ionotropic
74
The glycine receptor causes inhibitory ........................ via increasing membrane permeability to chloride.
postsynaptic hyperpolarization
75
The glycine receptor causes inhibitory postsynaptic hyperpolarization via increasing membrane permeability to ...............
Chloride
76
What receptor mediates inhibitory interneuron transmission in the spinal cord?
glycine receptor
77
Glycine receptor mediates inhibitory interneuron transmission in the ...............
spinal cord
78
The norepinephrine alpha2 receptor is located predominantly on .............................................. in neuron
presinaptic nerve temrinals
79
In what systems is located alpha 2 receptor?
CNS and PNS
80
Activation of alpha2 receptors inhibits ............................. from the nerve terminal, inducing sympatholytic effects (eg, reduced heart rate, vasodilation).
norepinephrine release
81
What is the main excitatory neurotransmiter of the CNS?
glutamate
82
Calcium entry programs the neuron to depolarize more robustly to ....................
repeated stimulations
83
The resting membrane potential shown in the graph is negative, indicating that at rest, the membrane is permeable to an ion with a ..........................
negative equilibrium potential (potassium or chloride)
84
Opening of ligand-gated ion channels in response to ..................................... binding, causes an increase in membrane potential to above zero.
neurotransmiter
85
Membrane potential increases to above zero. This indicates that the membrane has become permeable for an ion with a .........................
positive equilibrium potential (sodium or calcium)
86
Opening of voltage-gated ion channels in response to the change in membrane potential, causes a drop in membrane potential, indicating that the membrane becomes permeable to an ion with a ............................
negative equilibrium potential (potassium or chloride
87
If the membrane were permeable for sodium at rest, the resting membrane potential would be......................
positive as the equilibrium potential of sodium is +60 mV.
88
Membrane become more permeable for calcium or sodium following the opening of the voltage-gated ion channels. membrane potential would be .................
positive as both ions have positive equilibrium potentials.
89
Permeability to ion and total membrane potential relation?
The more permeable the membrane becomes for a cellular ion, the more that ion's equilibrium potential contributes to the total membrane potential.
90
Glutamate binding leads to opening of ................ in postsynaptic neurons and leads to ............................. influx
ligand-gated sodium channels;
| leads to sodium influx --> membrane depolarization
91
What part merges neuron body and axon?
axon hillock
92
What substances are contained in axon hillock?
large number of voltage-gated sodium channels.
93
When an action potential is triggered and propagates along the axon via a steady influx of sodium ions?
Once the axon hillock becomes sufficiently depolarized
94
Once the axon hillock becomes sufficiently depolarized .......................
an action potential is triggered and propagates along the axon via a steady influx of sodium ions
95
What happens when action potential reaches the axonal terminal?
voltage gated calcium channels opens --> influx of calcium --> leads to fusion of vesicles containing neurotrasmitter and release of this neurotrasmiter
96
Seizures occur due to .............., ....................... firing of ....................... neurons in the brain
Seizures occur due to abnormal, synchronized firing of hyperexcitable neurons in the brain
97
RER contains calcium. How it participates in vesicles fusion in neuron?
It doesn't play any role. Calcium that is in RER and is released, is more important for skeletal muscle contraction
98
What 4 changes are collectively known as action potential?
depolarization, repolarization, hyperpolarization and resting potential
99
The action potential occurs due to changes in the membrane permeability to ...................... (2) ions.
Na+ and K+ ions
100
Resting potential is maintained at -70mV bys high permeability to ........ and low permeability to .............
potassium and sodium
101
While at the resting potential, the inner side of the membrane is ................... charged with respect to the outer surface of the membrane
negatively
102
K efflux at resting potential occurs via ...................... channels.
non-gated K+ channels (leak channels)
103
is there potassium efflux or influx at resting potential?
efflux
104
Depolarization occurs due to opening of .................... channels with rapid influx of ............into the cell.
voltage-gated Na+ channels with rapid influx of Na+ into the cell.
105
The large influx of Na+ leads to an ....................... charge inside the membrane known as depolarization.
increased positive
106
What is the maximum value of action potential?
+35mV
107
Repolarization results from closure ............. channels and simultaneous opening of .............. channels
Na+; K+
108
What process is responsible for returning the membrane potential back to the resting potential?
Potassium efflux during repolarization
109
Why occurs hyperpolarization?
Because the VOLTAGE-gated K+ channels remain open for a short time after repolarization is completed.
110
What is mV when hyperpolarization?
-85mV
111
What channels cause maintains hyperpolarization and what maintains resting potential?
hyper - voltage gated;
when they close - hyperpolarized MP returns to normal resting MP - and is maintained by NON-GATED POTASSIUM CHANNELS (leak channels)
112
K+ ion permeance is highest during the .................... phase of the action potential.
repolarization
113
What is overshoot in MP?
voltage above 0. eg maximum MP is around +35mv. So overshoot is from 0 to 35.
