Neurons and Glia 3 Flashcards
(159 cards)
1
Q
Which general type of cell do most brain tumours arise from? (1)
A
Glial cells
2
Q
What is the approximate mortality rate for glioblastomas? (1)
A
100%
3
Q
Give three key features of brain tumours. (3)
A
- Do not metastasise outside of CNS
- Located in the cranium
- Limited space for expansion
4
Q
True or false? (1)
Benign brain tumours are able to kill the patient as well as rapidly-growing tumours.
A
True - they can kill depending on size and location
5
Q
Describe why gliomas do not cause a midline shift in the brain. (1)
A
Glioma cells kill the resident neurones as they invade.
6
Q
Describe a key difference between the functioning of glioma cells and normal astrocytes. (1)
A
Normal astrocytes take up glutamate, but glioma cells release glutamate.
7
Q
Name an ion channel usually found in the membrane of an astrocyte which is absent in a glioma cell. (1)
A
GLT1 (EAAT)
8
Q
Describe the general mechanism used by glioma cells to kill neurones. (3)
A
- Glioma cells release glutamate into the extracellular space
- Glutamate binds to neurones
- Neurones increase intracellular calcium (cytotoxicity)
9
Q
What is the most likely method of excess glioma-released glutamate in the extracellular space binding to neurones? (1)
A
Via NMDA receptors
10
Q
Describe the effect of CNQX (an AMPA inhibitor) on glutamate-induced neuronal excitotoxicity due to a glioma. (1)
A
There would be no effect
11
Q
Describe the effect of MK-801 and D-AP5 (both NMDA inhibitors) on glutamate-induced neuronal excitotoxicity due to a glioma. (1)
A
They would both protect neurones from excitotoxicity (less neuonal cell death).
12
Q
What is the predominant clinical presentation for a glioma, and what is the pathophysiology behind this symptom? (2)
A
Seizures
which are caused by increased glutamate.
13
Q
Name the channel/process which is used by glioma cells to release glutamate into the extracellular space.
Describe how this works. (2)
A
Cysteine-glutamate exchanger (Xc)
Cysteine moves into cell and glutamate moves out of cell.
14
Q
What would the effect on glutamate release by glioma cells be if levels of cysteine in the extracellular space were increased? (1)
A
Glutamate release would be enhanced
15
Q
What happens to cysteine once it has been taken up into glioma cells? (2)
A
It is converted to glutathione
which protects the glioma cells from dying.
16
Q
Describe the response of glioma cells to the glutamate that they release into the extracellular space. (3)
A
- Glioma cells express Ca-permeable AMPA receptors
- Glutamate binds to AMPA receptors
- This sets up Ca oscillations in glioma cells
17
Q
Describe a potential benefit of calcium oscillations occuring in glioma cells. (1)
A
Calcium signalling may aid in proliferation, angiogenesis, and invasion of glioma cells.
18
Q
GYK1 and JSTx are both AMPA receptor inhibitors.
What would be the effect on glioma cells of adding these to a cell culture? (1)
A
The glioma cells would not be able to produce calcium oscillations.
19
Q
Name two drugs which are able to inhibit the cysteine-glutamate transporter in glioma cells. (2)
A
Sulfasalazine
S4CPG
20
Q
Describe the mechanism used by glioma cells to infiltrate healthy brain tissue. (
A
- Chloride moves into the cell via the NKCC1 transporter
- Chloride leaves the cell via CIC-2 and CIC-3 channels
- Water follows chloride by osmosis so the cell can shrink and invade
21
Q
Which cells are CIC-2 and CIC-3 chloride channels present on?
A
Glioma cells
22
Q
Describe the role of the Nernst equation in chloride movement out of glioma cells. (4)
A
- Glioma cell has negative Vm due to K channels
- Chloride moves in and makes Ecl less negative
- Vm now wants to rise to get closer to Ecl
- The cell depolarises by moving chloride out against its concentration gradient
23
Q
What is chlorotoxin (in the context of gliomas)? (2)
A
Toxin from scorpion venom (36aa)
which binds to CIC-2 and CIC-3 channels on glioma cells.
24
Q
Give four uses of chlorotoxin (CTx) in the diagnosis and treatment of glioma. (4)
A
- Identifying / marking gliomas
- Targeting treatment at gliomas
- Conjugated magnetic nanoprobes for use in MRI
- CTx bound siRNA vectors
25
Give an equation to work out the number of cells in a glioma.
What is the clinical meaning of this? (2)
Number of cells = 2^x (x = number of cell divisions)
This means that gliomas grow exponentially (very fast)
26
Describe the log kill method of chemotherapy. (2)
Chemotherapy is able to kill a certain percantage of cells each time
however a certain proportion of cells survive / are resistant.
27
Describe how tumour size changes with a typical 'surgery followed by chemotherapy' treatment plan for glioma. (3)
Surgery kills a chunk of cells
then chemotherapy kills a proportion
but a small percentage of cells remain, gradually increasing tumour size despite repeated chemotherapy.
28
Describe a potential method of overcoming the 'log kill method' of chemotherapy and the survival of a small number of cancer cells.
Why isn't this used clinically? (2)
- Giving chemotherapy more frequently
- However it would cause too much damage to healthy tissue
29
Give two general reasons why, despite using chlorotoxin to target treatment at glioma cells, we are still not able to cure the cancer. (2)
- Exponential growth
- Treatment resistance
30
Describe what is meant by an 'activity-dependent increase in [K]o', and the consequences of this. (4)
- When an action potential occurs, neurones give out potassium into extracellular space
- Results in an activity-dependent increase in [K]o
- Increase in extracellular K increases Ek and therefore Vm
- Neurone becomes more excitable
31
What mechanism is in place in the CNS to counteract the effect of activity dependent [k]o increase? (1)
Astrocytic potassium buffering
32
Describe two effects that an activity-dependent rise in [k]o has on the profile of subsequent action potentials.
Also describe the relative effect sizes. (2)
- Small increase in Vm (small depolarisation)
- Large decrease in size of AHP
33
Describe why activity-dependent rise in [k]o only has a small effect on Vm.
Give an equation that could be used to calculate this effect. (2)
At this point the membrane is also permeable to sodium ions.
Could calculate effect using GHK.
34
Describe why activity-dependent rise in [k]o has a large effect on AHP.
Name an equation which could be used to calculate the effect size. (2)
Membrane is only really permeable to potassium.
Effect could be calculated by Nernst equation.
35
Describe the effect that an activity-dependent rise in [k]o would have on Vm of the astrocyte.
How could this effect be calculated? (2)
- Increased (less negative) Vm of astrocytes
- Can be calculated by the Nernst equation
36
Describe the general effect on the astrocytic membrane potential of changing [k]o from 3mM to 0.3mM. (1)
Hyperpolarisation
37
Describe the general effect on the astrocytic membrane potential of changing [k]o from 3mM to 30mM. (1)
Depolarisation
38
Describe the main method used by astrocytes to buffer potassium (including the name of the channel used). (4)
- Kir4.1 channels (inwardly rectifying potassium channels)
- take potassium into astrocytes
- predominantly at negative membrane potentials
- even if it means moving potassium against its concentration gradient.
39
Use the Nernst equation to describe how astrocytes are able to buffer potassium against its concentration gradient. (3)
- Rise in [k]o means rise in Ek
- Vm needs to rise to meet Ek
- It does this by taking in potassium (against its concentration gradient)
40
Describe the effect of barium ions (Ba) on astrocytic potassium buffering and [k]o. Explain why this effect happens. (3)
- Ba ions block Kir4.1 channels
- This prevents potassium buffering
- So [k]o can increase even more
41
Describe the inwards potassium current in astrocytes...
a) in the absence of Kir4.1 channels
b) in the presence of Kir4.1 channels
c) in the presence of Kir4.1 channels AND barium ions
(3)
a) very little potassium current
b) moderate potassium current
c) moderate potassium current is reduced (but not as low as a))
42
Describe the effect on [k]o and subsequent action potentials over time if a neurone continues to fire for an extended period. (2)
- [k]o reaches a maxmimum ('ceiling') level and will cease rising further despite more action potentials occurring
- AHP will continue to change
43
Describe two roles of ATP in astrocytic buffering of potassium. (2)
- Assists in potassium uptake via Na/K pumps
- Equivalates inward potassium current with outward Na current via Na/K pumps
44
In the astrocyte, what is the stimulus which activates the Na/K pump to give out Na and take up K after an action potential has occurred? (1)
Increase in extracellular potassium
45
In the neurone, what is the stimulus which activates the Na/K pump to give out Na and take up K after an action potential has occurred?
How does the Na/K pump get the energy to do its job? (2)
- Increased Na in axon cytoplasm
- Increased Na also recruits mitochondria, which move towards site of AP to produce ATP for the pump
46
Name the process by which potassium is dissipated one it has been taken up into an astrocyte. (1)
Spatial buffering
47
Give two potential reasons why inward potassium current in astrocytes may have to be equivalated with outward sodium current. (2)
- Maintain osmolarity
- Maintain Vm of astrocyte
48
Name a method (apart from spatial buffering) by which potassium is buffered in the CNS.
Which cells carry out this other method? (2)
- Potassium siphoning
- Carried out by Muller cells in the retina
49
What is a muller cell and where is it found?
Describe its shape and position within its 'parent' structure. (4)
A Muller cell is a specialised astrocyte
found in the retina.
It is a long cell
which spans the length of the retina.
50
Why does the middle portion of a Muller cell show very little response to a rise in [k]o?
Why is this not an issue for the CNS, given that a rise in [K]o is bad? (3)
There are not many potassium channels towards the middle of the Muller cell.
It is not an issue because potassium does not tend to accumulate in this area, due to a relative lack of synapses.
Neurones in the retina synapse towards either end of the Muller cell.
51
Describe simply the process of potassium siphoning by Muller cells, including which ion channels are involved. (3)
- Kir2.1 takes in potassium
- Potassium spreads throughout cell
- Kir4.1 gets rid of potassium into vitreous humor, subretinal space, and blood vessels
52
Describe the type/s of potassium current (inward or outward) which can be mediated by Kir4.1 channels in the Muller cell of the retina. (2)
Inward and outward current of similar amplitudes.
53
Describe the type/s of potassium current (inward or outward) which can be mediated by Kir2.1 channels in the Muller cell of the retina. (2)
Mediates inward currents but almost no outward currents.
54
Describe the type/s of potassium current (inward or outward) which can be mediated by TASK channels in the Muller cell of the retina. (2)
Weak inward currents but strong outward currents
55
Describe the rough distribution of Kir4.1 channels on the Muller cell membrane. (1)
Found in membranes which have contact with the vitreous body, subretinal space, and blood vessels.
56
Describe the rough distribution of Kir2.1 channels on the Muller cell membrane. (1)
Expressed in membrane which has contact with neurones and synapses
57
Once potassium has been taken up into Muller cells in the retina, give three places where it can be 'dumped' to get rid of it. (3)
Blood vessels
Subretinal space
Vitreous humor
58
Describe the method of inheritance of Huntington's disease. (1)
Autosomal dominant
59
Name the protein which is mutated and dysfunctional in Huntington's disease. (1)
Huntingtin
60
Why do researchers think that astroctyes are involved in Huntington's disease? What evidence do they have? (1)
Striatal astrocytes express mutant Huntingtin protein
61
Summarise the role of striatal astrocytes in the pathophysiology of Huntington's disease. (4)
- Striatal astrocytes have a lower expression of Kir4.1
- Reduced ability to buffer activity-dependent release of K
- Increased [k]o
- Increased neuronal excitability
62
A mouse model of early onset Huntington's disease was produced, which was called R6/2. Signs and symptoms of Huntington's disease typically appeared by P60-P80.
Describe three astrocytic changes which you expect to observe in the striatum of R6/2 mice at day P60. (3)
- Mutant Huntingtin protein inclusions
- Depolarised Vm
- Lower membrane conductance (increased resistance)
63
Using V=IR, describe why applying a small depolarisation to a healthy astrocyte and a striatal astrocyte in Huntington's disease would produce different amplitudes of response. (3)
A Huntington's astrocyte would produce a smaller response.
Because R increases
So current response to the same size voltage change would be smaller.
64
Describe a reason why striatal astrocytes in Huntington's disease might have an increased Vm. (2)
Increased [k]o due to less buffering
so Ek and therefore Vm is increased.
65
A mouse model of early onset Huntington's disease was produced, which was called R6/2. Signs and symptoms of Huntington's disease typically appeared by P60-P80.
Describe the Ba-sensitive Kir4.1 currents that you would expect to see in R6/2 striatal astrocytes at P60-P80 compared to wild type. (1)
Current would be reduced
66
What is meant by the term 'rheobase'. (1)
The minimum current needed to cause an action potential in a neurone.
67
Describe the rheobase you would expect to see in striatal neurones from a patient who has Huntington's disease. (1)
Reduced
68
A mouse model of early onset Huntington's disease was produced, which was called R6/2. Signs and symptoms of Huntington's disease typically appeared by P60-P80.
Which one of the following options would not happen as a result of forcing R6/2 mice to express the Kir4.1 gene? (1)
a) Reduced [k]o in the striatum
b) Improved motor deficits
c) Improved survival
d) Increased astrocytic membrane potential
d) increased astrocytic membrane potential - this occurs in mice where the Kir4.1 gene is not expressed
69
Describe/define multiple sclerosis. (4)
An AUTOIMMUNE disease which exclusively affects the CNS, although symptoms may be seen in the periphery.
It is characterised by INFLAMMATORY DEMYELINATION and AXONAL PATHOLOGY.
70
Give four risk factors for multiple sclerosis. (4)
- Female
- Northern latitudes
- Exposure to epstein barr virus
- Genetic predisposition
71
Give two major protective factors for multiple sclerosis. (2)
- EBV negative
- Live near equator
72
Give the three most common presenting symptoms of multiple sclerosis. (3)
- Unilateral optic neuritis
- Partial myelitis
- Focal sensory disturbance
73
Describe 'unilateral optic neuritis'. (1)
Blurred vision and pain in one eye
74
Describe 'partial myelitis'. (1)
Inflammation of the spinal cord, usually causing torso impaired sensation, weakness, and ataxia.
75
Describe what is meant by 'focal sensory disturbance'. (1)
Limb paraesthesias
76
Name a type of imaging that would be useful in diagnosing multiple sclerosis. (1)
T2 weighted MRI
77
Give the criteria needed for a diagnosis of multiple sclerosis to be made.
Describe how this criteria would be met. (2)
Lesions/attacks disseminated in both space and time.
This would be met by having multiple lesions identified by MRI, and two or more temporally isolated attacks.
78
Name the diagnostic criteria used for MS. (1)
McDonald criteria
79
Name two types of multiple sclerosis. (2)
- Remitting relapsing
- Primary progressive
80
Describe the progression of remitting relapsing MS. (2)
Periods of relapse and remission.
New baseline function after each relapse.
81
True or false? (1)
If a patient presents with unilateral optic neuritis, and says that they also had left arm weakness three years ago, they are likely to have RRMS.
False - lesions are disseminated in time and space, however in RRMS the 2nd attack usually occurs within 2 years of the first
82
Describe the progression of primary progressive MS. (1)
Condition and function continually decline.
83
Describe why RRMS and PPMS cannot be treated at distinct illnesses. (1)
After about 15 years, RRMS may develop into PPMS.
84
If two patients are both diagnosed with MS at the same time, one with PPMS and one with RRMS, who is likely to need a walking aid first? (1)
PPMS
85
Describe how geographical location affects a person's chances of developing MS.
How do age and geographical location interact? (3)
Incidence of MS increases moving further away from the equator.
A child (<20) who moves country will adopt risk of new country.
An adult who moves country will retain risk of original country.
86
When in the lifespan does geographical location appear to have the most affect on changing risk of developing MS? (1)
Below 20yrs
87
Why does geographical location have an affect on chances of developing MS? (1)
Don't know - no environmental agent has been found
88
Are genetic or environmental factors more likely to be more important when determining risk of developing MS?
Give a reason for this. (2)
Environmental
If a family moves country, parents retain original risk but children adopt new risk. Therefore members of the same family have different risks.
89
Give two pieces of evidence that support the argument that the effect of latitude on MS may be due to sun exposure and vitamin D. (2)
- Risk of developing MS is associated with low vit D levels
- SOLAR study showed that vit D reduced MS relapses in pts by 32%
90
Describe the typical (most common) demographic for a patient being newly diagnosed with MS. (2)
Female
in their 20s.
91
Describe how the incidence of MS changes with age. (1)
Increasing age = lower incidence
92
Describe how the prevalence of MS changes with age. (1)
Prevalence rises with age, but then drops off as older people die due to other ailments.
93
Which allele is the most frequent genetic factor associated with increased MS risk? (1)
HLA-DRB1
94
Give the concordance of MS between female monozygotic twins. (1)
30%
95
Describe how demyelination affects length constant in MS. (2)
Demyelination = decreased rm
Length constant too small to allow sufficient voltage spread to excite subsequent node.
96
Describe how the dysfunctional propagation of action potential in MS results in symptoms. (1)
Signals don't reach the target, or signals reach the target at different times.
97
Describe the expected action potential propagation between nodes, if the area inbetween is demyelinated. (1)
Delay in action potential propagation, and in some cases AP may be blocked completely.
98
Why aren't stem cell transplants a widely-used treatment for MS, despite the fact that they are highly effective? (2)
- Very expensive
- High infection risk for pt
99
Describe how stem cell treatments may be used to treat MS. (3)
- Stem cells harvested
- Bisulfan used to wipe out immune system
- Autologous stem cells infused to 'create new immune system' which should not attack myelin
100
How effective are stem cell treatments in treating MS? (1)
Very - patients cease to have relapses
101
Name two viruses which are related to Epstein Barr virus. (2)
- Herpes virus
- Cytomegalo virus
102
Describe the illness associated with Epstein Barr virus. (1)
Often asymptomatic but may cause mononucleosis
103
True or false? (1)
Epstein Barr virus directly causes multiple sclerosis.
False - EBV is part of a chain of events leading to MS, but is not sufficient to lead to MS by itself
104
Give three potential ways that the link between EBV and MS may potentially be exploited in treatment/prevention of multiple sclerosis. (3)
- EBV vaccine acting as MS prophylaxis
- Antivirals for EBV in early MS
- Kill CNS B cells where EBV lies dormant (currently no technique to do this)
105
A study was carried out in soldiers. 801 developed MS. How many were EBV positive at the time of MS onset? (1)
All of them
106
If CMV is related to EBV, can we assume that it is also linked to MS? (1)
No
107
How common is EBV? (1)
Extremely common - most people will develop it
108
What is NfL, and why is it measured in studies on multiple sclerosis? (2)
NfL (neurofilament light chain) is a molecule found in high levels in myelinated neurones.
Increased NfL in serum is used as an indicator of neuronal damage.
109
Describe the relationship between EBV infection, MS, and serum NfL levels. (1)
Serum NfL levels may increase after EBV infection in patients who go on to develop MS.
110
The ampunt of glucose reaching the brain depends on which two physiological factors? (2)
- Blood glucose concentration
- Blood supply to the brain
111
Describe the effects of insulin on blood glucose levels. (1)
Decreases blood glucose levels
112
Describe the effect of glucagon on blood glucose levels. (1)
Increases blood glucose levels
113
Give two advantages of insulin being able to decrease blood glucose levels. (2)
- Blood sugar does not get too high
- Glucose can enter cells
114
What is the general effect on the brain if insulin levels are too high? (1)
Brain is prevented from receiving enough glucose.
115
Describe in general terms how insulin allows glucose to enter cells in the body. (3)
- Insulin binds to membrane receptor
- More GLUT-4 channels move to membrane
- Glucose enters through GLUT-4 channels
116
True or false? (1)
Cells in the brain rely on the activity of insulin for glucose to be able to enter cells.
False - the majority of cells in the brain can take up glucose without using insulin
117
Which cells in the body release insulin? (1)
B cells
(in the islets of Langerhans in the pancreas)
118
Describe how the Em of b cells in the islets of Langerhans changes in the presence of glucose. (2)
- At low glucose concentrations Em is negative (-60mV)
- At high glucose concentrations the cell depolarises
119
Describe how glucose triggers the release of insulin from pancreatic b cells. (6)
- Glucose transported into cell by GLUT transporter
- Glucose metabolised to ATP
- ATP closes K channels
- Cell depolarises
- Calcium channels open
- Insulin released by exocytosis
120
Describe simply how insulin levels respond to a change in blood glucose. (1)
Increased blood glucose results in increased blood insulin.
121
Describe type 1 diabetes. (1)
Autoimmune-mediated death of pancreatic B cells.
122
Describe how type 1 diabetes affects the brain. (2)
- Treatment for T1DM is exogenous insulin
- Taking too much insulin leads to hypoglycaemia
- Hypoglycaemia has severe negative consequences for the brain
123
Give six pieces of evidence which may support the fact that glucose is the brain's main energy support. (6)
- Complex homeostatic mechanisms to control glucose concentration
- Gluconeogenesis
- The brain has glucose-sensing neurones
- Arteries and veins going to/from brain show differences in glucose concentration
- NMR is able to show presence of glucose metabolites in the brain
- Increased insulin can induce coma
124
Describe the difference in glucose concentration between arteries entering and veins leaving the brain.
What conclusion can be drawn from this? (2)
Arteries have higher levels of glucose.
So glucose must be being used up in the brain.
125
True or false? (1)
Glucose is the only energy source for the brain.
False - glutamate is able to indirectly contribute to energy production, but is not a main source of energy for the brain
126
Describe how glutamate is able to contribute to energy production in the brain. (2)
- Glutamate converted to alpha-ketoglutarate
- Which participates in the TCA cycle
127
Insulin used to be used as a treatment for which mental illness?
How was this thought to work? (2)
Insulin was used to treat schizophrenia,
because it induced seizures and it was thought that epilepsy and schizophrenia could not occur together.
128
Describe how the brain and skeletal muscle may work together so that they can both get enough energy. (2)
- Skeletal muscle may provide brain with lactate
- Resulting in increased availability of glucose for the muscle
129
True or false? (1)
There are no energy reserves in the brain.
False - there is glycogen in the brain
130
Describe a piece of evidence that supported the hypothesis that there were no energy reserves in the brain. (1)
Occluding the blood supply to the brain results in rapid loss of consciousness and death.
131
Where are glycogen stores found in the brain? (1)
Astrocytes
132
Describe the levels of glycogen in the brain compared to liver and skeletal muscle. (1)
Glycogen levels are much lower in the brain, but it is still present.
133
Which receptors allow glucose to enter neurones in the brain? (1)
GLUT3
134
Which receptors allow glucose to enter astrocytes in the brain? (1)
GLUT1
135
Describe the effects of insulin on GLUT1 and GLUT3 receptors in the brain. (1)
These glucose transporters are not dependent on insulin.
136
Describe the structure of glycogen, and why its structure makes it ideal to store in cells. (3)
Branched molecule
which does not dissolve in water.
It is ideal for storage because it has no effect on osmotic pressure when stored in cells.
137
Give two ways that neurones may signal to astrocytes that they want to use the stored glycogen. (2)
- Glutamate release
- K release
(These are related to APs so indicate increased activity)
138
Describe how glycogen in astrocytes provides energy to neurones. (4)
Which receptors/transporters on astrocyes and neurones are involved?
Glycogen broken down to form lactate.
Lactate leaves astrocytes via MCT1.
Lactate enters neurones via MCT2.
Lactate used as an energy source via incorporation into TCA cycle.
(MCT = monocarboxylate transporters)
139
True or false? (1)
Lactate release by astrocytes only occurs in response to hypoglycaemia or increased neuronal activity.
False - Lactate is tonically released by astrocytes, which may supplement 'standard' glucose metabolism in neurones
140
When looking at 13C NMR spectra from the brain, would you expect to see just a peak for glucose, or would you also expect to see a peak for glycogen? (1)
Also see glycogen peak.
141
How can radioactive/labelled glucose (or 13C glucose) be used to demonstrate glycogen storage in the brain? (2)
Inject marked glucose,
and it will become incorporated into brain glycogen.
142
Following a 13C infusion, 13C begins to get incorporated into brain glycogen.
Would you expect this to be a fast or slow process? (1)
Slow in the presence of glucose.
143
Describe the expected change in the levels of glycogen in the brain of someone with insulin-induced hypoglycaemia.
Why would you expect this? (2)
Brain glycogen decreased in hypoglycaemic people,
because it is used as an energy source in the relative absence of glucose.
144
A study showed that glycogen levels in the visual cortex remained unchanged after visual stimulation, and concluded that this meant that glycogen was not stored in the brain.
Describe the drawbacks of this study and why it not be reliable.
The brain is constantly responding to visual stimuli, so a visual stimulus is not the most reliable way to stimulate the CNS.
This method is very difficult to accurately control.
145
You want to carry out a study on the effects of brain glycogen on LTP.
Which part of the brain would you use for this experiment? (1)
CA1 of the hippocampus
146
Give a process in the brain which appears to rely on lactate released by astrocytes. (1)
LTP
147
DAB is a compound which prevents the breakdown of glycogen.
How might DAB affect the function of the hippocampus? (1)
DAB causes memory deficits.
148
DAB is a compound which prevents the breakdown of glycogen.
DAB causes memory impairment.
Describe a way that memory deficits may be overcome in mice who have been injected with DAB. (1)
Also inject lactate
149
DAB is a compound which prevents the breakdown of glycogen.
Describe the levels of lactate you would expect to find in animals who had DAB injected compared to animals who did not have DAB injected. (1)
Levels in DAB group would have lower lactate.
150
DAB is a compound which prevents the breakdown of glycogen.
Describe the EPSP slope in rats who have had DAB injected vs rats who have not had DAB injected. (1)
Rats with DAB could not maintain increased slope.
151
Give two pieces of evidence proving that glycogen in the brain does not act as a conventional energy store. (2)
- Low levels compared to liver and muscle, which cannot sustain neuronal function for long in absence of glucose
- Glycogen also appears to be important for learning and memory
152
Give an (unproven) theory as to how lactate may be involved in LTP. (1)
Lactate may provide the extra energy needed to make more glutamate.
153
Describe how:
a) systemically administered insulin
b) exhaustive exercise
affect blood glucose levels. (2)
Insulin decreases blood glucose
Exercise decreases blood glucose
154
Describe how:
a) systemically administered insulin
b) exhaustive exercise
affect blood lactate levels. (2)
Insulin increases blood lactate
Exercise increases blood lactate
155
Describe how:
a) systemically administered insulin
b) exhaustive exercise
affect glycogen levels in skeletal muscle. (2)
Insulin increases glycogen levels in muscle.
Exercise decreases glycogen levels in muscle.
156
Describe how:
a) systemically administered insulin
b) exhaustive exercise
affect lactate in the brain. (2)
Insulin increases lactate in the brain.
Exercise increases lactate in the brain.
157
Describe how:
a) systemically administered insulin
b) exhaustive exercise
affect glycogen in the brain. (2)
They both decrease brain glycogen.
158
Give two Bryony theories as to why insulin may increase blood lactate. (2)
Insulin lets glucose into cells which can be metabolised to lactate.
Insulin stimulates formation of glycogen, which can then form lactate by glycogenolysis.
159
Describe how the brain may allow long periods of exercise, even if running on low glucose. (2)
In low glucose the brain can continue to function using lactate derived from glycogen.
This may allow for exercise to continue.
