Neurophysiology Flashcards
1
Q
What is the CNS composed of?
A
Brain and spinal cord.
2
Q
What is the peripheral nervous system composed of?
A
Cranial and spinal nerves.
3
Q
What are the 4 specialized sub-regions of all neurons?
A
Input, integration, conduction, output.
- Input: neurons.
- Integration: Cell body
- Conduction: Axon
- Output: terminals.
4
Q
Inward current
A
Cations flow INTO the cell (negative) or anions flow OUT
5
Q
Outward current
A
Cations flow OUT of the cell (positive) or anions flow IN
6
Q
What is the cellular Vr?
A
Negative due to differences in ion concentrations and permeability.
7
Q
What ion is permeable to the cell at rest? How does this ion move through the cell?
A
Potassium K (via leakage channels)
8
Q
How are concentration gradients maintained at Vr?
A
Active transport of potassium and sodium.
9
Q
What do electrical signals result from? (in terms of the cell)
A
Ion fluxes through channels, which change the Vm.
10
Q
What two ways are channels activated?
A
- Ligand binding.
2. Changes in Vm (voltage induced)
11
Q
How are channels deactivated?
A
Maintained depolarization (prolonged)
12
Q
Describe the channel inactivation and activation of sodium voltage channels?
A
- at Vr, the channel is closed, but the inactivation gate is open (as the channel has not been inactivated).
- The cell depolarizes and the change in Vm causes the channel to open; both gates are open so sodium flows into the cell.
- After prolonged depolarization, the inactivation gate closes; the activation gate is open but no ions can pass through.
To reset, the activation gate closes, allowing the inactivation gate to open once Vm reaches Vr.
13
Q
Channelopathies (what are examples of consequences?)
A
Diseases arise from mutations in genes that code for ion channel subunits.
ie)
Channel remains open too long (slow inactivation)
Cell becomes hyperexcitable
Uncontrolled excitation can cause brain seizures
14
Q
Dravet’s syndrome
A
Mutation of the alpha-subunit gene for sodium channel; severe myoclonic epilepsy of infancy.
15
Q
What is the electrical driving force on ions provided by?
A
The membrane potential.
16
Q
Conductance
A
The ease with which ions flow across the membrane (siemens), Always positive.
17
Q
Resistance
A
Inverse of conductance (how difficult it is for ions to flow) in Ohms.
18
Q
What is equilibrium potential?
A
The membrane potential such that the current of a specific ion is 0.
19
Q
When is the net current zero for a specific ion? (I=0)
A
When membrane potential is equal to equilibrium potential.
Both forces are equal and opposite (conc vs electrical)
20
Q
What is the Ohm’s law we will use to find ionic current?
A
If I = V/R, then I = g(V), such that V is the net sum of (Vm-E)
21
Q
What will the membrane voltage always move towards?
A
The E of the ion with the increasing conductance (much like electrons on a wire, they will take the path of the least resistance)
22
Q
What is Nernst Equation?
A
E = 58/z log(X0/Xi)
z= valence of ion X0= concentration outside cell Xi= concentration inside cell.
23
Q
What does the Nernst equation determine?
A
Which ion is contributing to a measured membrane current.
24
Q
At resting potential, what is the membrane potential closest to? why?
A
Ek, the equilibrium potential of potassium because the membrane is highly permeable to potassium, not sodium.
25
Which scientists worked with squid axons? What did they discover?
Hodgkin and Huxley, defined the ionic basis of action potentials.
26
What is a graded potential? (Or Passive potential)
Can be depolarizing or polarizing and varies with strength of stimulus. It is initiated by a sensory or chemical stimulus.
27
Describe passive current flow
Passive conductance decays over time as ion flow reaches greater resistance. The resistance depends on the shape and size of the vessel. (smaller axons and dendrites have more resistance, like drinking a milkshake out of a coffee stir-stick.)
28
What is nerve action potential (AP)?
Rapid, short-lasting (transient) change in membrane potential that results in a brief reversal of polarity. Vi moves from a negative value to a positive value.
29
What is a spiking neuron?
A neuron that is firing APs
30
Threshold
Vm at which the AP is initiated, which is always more positive than Vrest.
31
Describe depolarization
Vrest reaches Vm, passing the threshold and opening voltage-dependant sodium channels.
Sodium channels then begin to all slowly close, and potassium channels begin to open to re-polarize.
32
What drug blocks sodium current?
TTX: Tetrodoxin
33
What drug blocks voltage-gated potassium channels?
TEA: Tetraethylammonium
34
How does conductance change during AP?
Conductance is greater for sodium, then greater for potassium.
35
What are leakage channels?
The basis of passive current flow; the pathway with the least resistance is through leakage channels once resistance increases down the length of an ion.
36
Refractory period
The time during which an axon is resistant to depolarization. Sodium channels are inactivated.
37
Where are sodium channels concentrated?
At the nodes of Ranvier.
38
What is the function of the myelin sheath?
To reduce current loss across the membrane (no leakage channels), acting as an electrical insulator.
39
Why is scorpion toxin relevant to APs?
This toxin binds to sodium channels to slow inactivation and produce a longer AP, causing paralysis and delayed response.
40
How do anesthetics work?
Block voltage-dependant sodium channels or hyperpolarize membranes using chlorine (Vm is SO negative that it would take god himself to reach threshold)
41
Multiple sclerosis
Loss of myelin sheath, slow spike conduction.
42
Bi-directional synapse
Electrical
43
Unidirectional synapse
Chemical
44
What is the first way of knowing that a synapse is chemical?
Vesicles.
45
Briefly describe the sequence of events that occur in transmission at a typical chemical synapse.
1. NT is synthesized and packaged into vesicles.
2. AP invades the terminal, causing calcium gates to open.
3. Influx of calcium activates protein that drags vesicles to docking sites. Vesicles then fuse with membrane and dump NT into synapse.
4. NT binds to post-cell receptor, which will open or close, causing an inhibitory or excitatory effect.
5. NT are removed via glial cells or enzymatic degradation or diffusion
46
What occurs when glutamate is released from the PreSC?
Glutamate binds to receptors on PostSC, which activate a sodium channel and cause an EPSP.
47
What occurs when GABA is released from the PreSC?
GABA binds to PostSC, activating chlorine channels that cause the hyperpolarization of the post synaptic cell. (IPSP).
48
What was discovered about calcium current in an AP? How was this discovered?
Hodg and Hux used the squid axons to record calcium current with and without the use of a Calcium channel blocker. They found PSP present when the calcium channels were not blocked.
49
What are calcium chelators? How were they used in research?
Chelators do not impact the PreCS membrane potential, but bind to calcium to prevent them from activating the carrying proteins. Therefore NTs are not released and no PSP is present.
50
EPSPs _______ over long distances.
Decay.
51
"End-Plate"
Synapse between nerve and muscle: neuromuscular joint nmj
52
End-plate potential (EPP)
an EPSP at the nmj
53
Miniature endplate potential (MEPP)
Results from the release of a single vesicle.
54
Each quantum is _______ vesicle(s).
One.
55
Synaptic delay
Time between onset of of presynaptic spike and onset of EPSP.
56
What NT is released at the nmj? What does it do?
Acetylcholine, open channels that conduct both Na and K.
57
What breaks down Acetylcholine?
Acetylcholinesterase
58
What is the name for the receptor that acetylcholine binds to?
Nicotinic cholinergic receptor.
59
How do transmitter-gated channels and voltage-gated channels work together?
Acetylcholine receptors depolarize cell, which causes voltage-gated channels to open and further depolarize the cell (cause AP)
60
Synaptic Transmission Disorders
Myasthenia gravis: loss of voltage gated Ca channels; muscle weakness.
Botulism: impairs NT release at end-plate, muscle paralysis.
61
Reversal potentials
Membrane potential at which there is zero net current through a transmitter-gated channel
Equilibrum potential for a transmitter-gated channel permeant to more than one ion.
62
Describe how reversal potential is analogous to equilibrium potential at a synapse.
Equilibrium at a synapse is the equilibrium potential of sodium. The reversal potential is between sodium and potassium because both ions are present.
63
What is the relevance of the Goldman-Hodgkin-Katz equations?
States that the reversal potential is dependant on the relative conductances of the synaptic channel to the ions (also equilibrium potential for these ions).
64
What is the rule about Membrane voltage and reversal potential?
Vm will always move towards the reversal potential when the conductance increases.
65
How is synaptic strength measured?
Amplitude of EPSP
66
How is synaptic plasticity measured?
Changes in EPSP
67
What is Long-term Potentiation?
Form of synaptic plasticity that involves strengthening the synapse.
68
What is an example of synaptic plasticity at a mammalian central synapse?
LTP in the hippocampus.
69
What is different about the potentiated state compared to the basal state?
Potentiated states have larger EPSPs
70
Why does the hippocampus show plasticity so easily?
It is full of synapses.
71
What is Consolidation?
Turns short-term memory into long-term memory through rehearsal.
72
What does the tri-synaptic circuit of the hippocampus contain?
dentate gyrus, CA3, CA1.
73
In humans, damage to this area in the Schaffer collateral pathway is sufficient enough to cause severe memory impairment.
CA1
74
Tetanus
Intense stimulation at a high frequency
75
How does memory processing transition through the hippocampal pathway?
Dentate gyrus receives signals from the internal cortex via axons on the perforin pathway.
Granule neurons in the d.g synapse with pyramidal neurons of the CA3 region.
CA3 neurons connect their axons (Schaffer collateral) to the CA1 pyrimadal cells. The signal that reach the CA1 are passed to the subiculum, then processed back out to the internal cortex.
76
What structures are present on the postsynaptic CA1 cell?
NMDA and AMPA receptors.
77
How are AMPA and NMDA activated? What is each receptor permeable to?
Binding of glutamate.
AMPA: sodium.
NMDA: calcium.
78
Why is the NMDA receptor blocked at Vm? What is it blocked by? How does it become unblocked?
The receptor is blocked by magnesium. It is blocked to prevent small frequency potentials from causing LTP. The magnesium is repelled when a large influx of sodium causes depolarization (Magnesium is positive).
79
What are coincidence receptors?
Require a pre-synaptic and post-synaptic event to open the channel.
80
What does calcium act as in the CA1 cell?
A second messenger in the early and late phase of LTP.
81
Describe the early phase of LTP
Calcium binds to CaMK2 and causes the phosphorylation and insertion of AMPA receptors.
82
What happens when you give tetanus to only one axon of the Schaffer collateral and test for LTP on both neural pathways one and 2?
Generally, what conclusion will this experiment draw?
Only the neural pathway given tetanus will exhibit LTP. This shows that LTP is pathway-specific.
83
How long does LTP last in intact animals?
More than a year.
84
How long does LTP last in slices?
Several hours.
85
What is a silent synapse?
A synapse in which the CA1 neuron contains only NMDARs.
86
What is a functional synapse?
A synapse in which the CA1 neuron contains both NMDAR and AMPAR.
87
What will adding more postsynaptic receptors do?
Increase synaptic strength (more Na can flow in)
88
Describe the late phase of LTP
A prolonged influx of calcium causes an increase in TF that results in new gene expression.
Results in new and more proteins being produced. Also causes an increase in growth factors: produces more synapses.
89
In general, what is the outcome of LTP?
More synaptic connections and AMPA receptors: lower frequency potentials cause depolarization.
90
What is CREB?
Cyclic AMP response element-binding protein; a TF activated by the second messenger cAMP in late-phase LTP.
91
What is PKA?
cyclic AMP-dependent protein kinase, which phosphorylates CREB.
92
What does low-frequency stimulation induce in CA1-CA3 synapse? How does this happen?
Long-term depression (LTD).
LTD activates phosphatases that dephosphorylate proteins in early/late-phase LTP. As a result, AMPARs are removed from the membrane.
93
What are the 3 general rules of LTD/LTP?
1. Factors that activate protein kinases or inactivate phosphatases will promote LTP and reduce LTD.
2. Opposite of above.
3. Insertion of AMPARs = LTP.
Removal of AMPARs = LTD.
94
What are the six major divisions of the CNS?
1) Cerebral hemisphere
2) Diencephalon
3) Midbrain
4) Pons and cerebellum
5) Medulla
6) Spinal cord.
95
Structures in the cerebral hemisphere:
Basal ganglia, cerebral cortex, amygdala, hippocampal formation.
96
The function of cerebral hemisphere:
Cognitive function, perception and motor function (planning)
97
Structures in the diencephalon:
Thalamus and hypothalamus.
98
Function of diencephalon:
Thalamus acts as a relay station that processes sensory signals going to the cerebral cortex. Hypothalamus regulates body hormonal levels by controlling the secretion of hormones.
99
Function of midbrain:
Controls eye movement and is involved in skeletal muscles.
| Contains relay nuclei of visual and auditory systems (superior and inferior colliculus)
100
Functions of pons
Relays signals from the cerebral cortex to the cerebellum.
101
Function of the cerebellum
Receives sensory input from the spinal cord and semicircular canals as well as motor info from the cerebral cortex.
Coordinates the timing of skeletal muscle contractions and eye movements.
Involved in maintaining posture.
102
Function of medulla:
Regulates respiration and blood pressure.
103
Dorsal roots contain axons of ______ neurons
Sensory
104
Ventral roots contain axons of _______ neurons
Motor
105
What are the two most prominent sulci?
Central sulcus, Lateral sulcus
106
Where is the primary motor cortex?
Precentral gyrus
107
Where is the primary somatosensory cortex?
Postcentral gyrus.
108
Function of frontal lobe:
STM, planning and sequencing behavior.
109
Function of parietal lobe:
Somatosensory information processing, recognizing spatial locations of objects.
110
Function of occipital lobe:
Processing visual information
111
Function of temporal lobe:
Contains hippocampus and amygdala
112
Hippocampus function:
Learning ability and memory
113
Function of amygdala:
Emotional expression, associations between emotions and events.
114
Where are the Caudate Putamen and Globulus pallidus located?
Basal ganglia
115
What is the combined function of the caudate nucleus, globulus pallidus, and putamen?
Regulates movements.
116
What does the internal capsule contain?
Thalamocortical fibers.
117
Corpus callosum function:
Connects two hemispheres
118
Function of the optic chiasm:
Crosses optic nerves from eyes.
119
How many layers make up the cortex?
7
120
What is layer IV specialized to?
Afferent sensory information (from thalamus)
121
Explain the topographical organization of the cortex:
Spacially adjacent parts of the body are represented in adjacent cortical areas.
122
What is the corticospinal tract?
Controls muscles required for precise movements (hands and fingers)
123
Most neural pathways are _______ symmetrical
Bilaterally
124
Crossing axons are called:
Commissures
125
Association cortices
Make up 80% of the human brain, involved in cognition, attention, identification of relevant features of stimuli, recognition of objects, planning behavior, memory storage.
126
What do the association cortices do?
Integrate information from multiple brain regions, link sensory to motor.
127
Prefrontal cortex function:
Temporal organization of behavior.
Remembering sensory cues linked to motor actions.
Temporary memory store.
128
Prefrontal neurons encode ________ of visual cues.
Spatial location.
129
Where is the majority of visual integration and information processing?
Primary visual cortex (V1) or striate cortex.
130
What is the extrastriate cortex?
Visual cortex V3, V4, V5.
131
What does the striate cortex contain? What do these structures respond to?
Neurons that respond to specific colors, motion, and orientation.
132
How would you describe the process by which information is integrated through the extrastriate cortex?
In a hierarchy, starting with V1.
133
Where does the combination of visual perception and visual information procession take place?
Visual association cortices.
134
What is the flow of the DORSAL visuospatial stream?
Striate cortex, extrastriate cortex, posterior parietal cortex.
135
What is the function of the dorsal visual stream?
Determines where an object is located.
136
What is the flow of the VENTRAL visual stream?
Striate cortex, extrastriate cortex, inferior temporal lobe.
137
The function of the VENTRAL visual stream?
Processes info to assess what an object is.
138
What is agnosia?
Damage to inferior temporal lobe, impairs recognition.
139
Do populations of cells or only single cells encode for the perception of objects
Populations
140
Neurons in IT cortex are arranged in _______ columns
Vertical
141
How do IT cortex columns react to slightly different images of the same object?
Neighboring clusters are recruited.
142
What are Grandmother Cells?
Neurons that are specified to recognizing faces.
143
FFA and function
Fusiform face area, identification of a person.
144
OFA and function
Occipital face area, perception of specific facial features.
145
STS and function
Superior temporal sulcus, perception of facial expression.
146
What is prosopagnosia
Defective facial recognition in humans. Results from damage to FFA
147
What is declarative memory? (Explicit)
Concerned with facts and events, requires conscious recall, unlimited capacity.
148
What is nondeclarative memory? (Implicit)
Deals with skills and behavior, recall is automatic, does not need conscious recollection.
149
Short term memory:
Short, limited in capacity, needs continual rehearsal.
150
Long term memory:
Long, large capacity, does not require rehearsal once consolidated.
151
Where is long-term explicit memory stored?
Wernicke's area (meaning of words), temporal cortex (memories of objects).
152
Where is short-term explicit memory stored?
Hippocampus.
153
Where is long-term implicit memory stored?
Cerebellum, basal ganglia, premotor cortex.
154
Widespread projections from _________ converge on the hippocampal region.
Where is the output of the hippocampus directed to?
Association neocortex, directed back to the same neocortical areas.
155
Retrograde Amnesia
Memory loss for events preceding the trauma. Very old memories remain intact.
156
Anterograde Amnesia
Inability to form new memories after trauma.
157
What happened to patient H.M, what did his case unravel about implicit/explicit memory?
H.M had his temporal lobe surgically removed, resulted in severe anterograde amnesia. Had intact procedural memory.
Shows implicit and explicit memory are integrated and stored in different regions.
158
What region is activated during spatial learning?
Right hippocampus
159
What region is activated during verbal memory-word recall?
Left hippocampus
160
What tests are used to probe hippocampus functions?
Imaging studies, various mazes, place cell recordings.
161
What are place cell recordings
Hippocampal neurons can act as place cells. Some neurons will fire when an animal is in a specific location (place fields).
162
How is the mutant CaMK2 blocked in transgenic mice?
Doxycycline binds to tTA, prevents tTA from binding to tetO (which activated CaMK2)
163
What is the phenotype of transgenic mice with mutant CaMK2?
LTD, unstable place fields(impaired spatial learning) in CA1, (hyperactive CaMK2).
164
Angelman's Syndrome
Severe mental impairment and epileptic seizure, dysfunction of CaMK2.
165
Goldilock's CaMK2 phenomenon
Activity of CaMK2 must be perfect.
166
What brain areas are associated with explicit memory disorders?
Fornix, thalamus, amygdala, hippocampus, mammillary body.
167
Dementia
Amnesia and intellectual dysfunctions
168
Alzheimer's Disease (AD)
```
Most common form of dementia.
Memory loss (short-term), failure of language, spatial, judgement skills.
```
Accumulation of neurofibrillary tangles, amyloid plaques, loss of neuron density.
169
What are the possible causes of Alzheimers?
Mutation of amyloid precursor protein (APP), presenilin 1,2 and inheritance of apolipoprotein-E.
170
What neural area is most affected by Alzheimers? What does this show?
Temporal cortex, which stores/integrates explicit memory.
