Explain why two sensations (e.g. first and second) can be elicited by activation of nociceptors? How do these sensations differ?
•Pain is sensed in two phases, the first very fast one is conducted via A-fibers and the second slower one by C-fibers.
•Pain transmitted by C-fibers is unlocalized due to peptidergic transmitters (e.g. Substance P which enhances and prolong action of glutamate).
•Pain transmitted by C-fibers is unlocalized due to peptidergic transmitters (e.g. Substance P which enhances and prolong action of glutamate).
Sliding filament hypothesis: What is the molecular basis of contraction? F-actin, myosin, troponin-tropomyosin, Ca-Ions, ATP. Which of these components represent the trigger for contraction? What happens if ATP is lacking? What’s the role of troponin-tropomyosin?
•The thick and thin filaments comprise the contractile machinery of the muscle.
•In a contracting muscle adjacent thick and thin filaments slide past each other, propelled by cyclical interactions between the myosin heads of the thick filaments and binding sites on the actin of the adjacent thin filaments.
•This mechanism is triggered by Ca2+ influx and uses ATP as energy source.
•The troponin-tropomyosin complex and F actin form the thin filament.
•In a contracting muscle adjacent thick and thin filaments slide past each other, propelled by cyclical interactions between the myosin heads of the thick filaments and binding sites on the actin of the adjacent thin filaments.
•This mechanism is triggered by Ca2+ influx and uses ATP as energy source.
•The troponin-tropomyosin complex and F actin form the thin filament.
In humans, injury of the spinal cord is often followed by a so-called “spinal shock”. What are the symptoms of a “spinal shock” and why does it occur in humans but not in mice?
•Spinal cord injury
•-> Neurons involved in reflex arcs no longer receive basal level of excitatory stimulation from brain.
•-> Become hyperpolarized and thus less responsive.
•Recovery is possible.
•A spinal shock does not occur in mice because reflex circuits are not controlled by the brain.
•-> Neurons involved in reflex arcs no longer receive basal level of excitatory stimulation from brain.
•-> Become hyperpolarized and thus less responsive.
•Recovery is possible.
•A spinal shock does not occur in mice because reflex circuits are not controlled by the brain.
In which organs are Leptin and Ghrelin produced?
•Ghrelin is produced by P/D1 cells lining the fundus of the human stomach that stimulate appetite.
•Ghrelin levels increase before meals and decrease after meals.
•It is considered the counterpart of the hormone leptin, produced by adipose tissue (fat), which induces satiation when present at higher levels.
•Ghrelin levels increase before meals and decrease after meals.
•It is considered the counterpart of the hormone leptin, produced by adipose tissue (fat), which induces satiation when present at higher levels.
What is the effect of leptin and ghrelin on food intake and energy expenditure?
•The ghrelin level is high before food intake and decreases after food intake.
•Thus, ghrelin is a hormone which stimulates appetite.
•On the contrary, leptin reduces appetite.
•The level of leptin in the blood stream is high if the body has much adipose tissue.
•Thus, ghrelin is a hormone which stimulates appetite.
•On the contrary, leptin reduces appetite.
•The level of leptin in the blood stream is high if the body has much adipose tissue.
Which of these is true about the cerebellum?
•Parallel fibers of ganule cells inhibit purkinje cells in all directions and thereby leading to contrast enhancement.
•Neighboring purkinje cells receive input from the same granule cells with increasing delay thereby providing a possibility for temporal segmentation of movement.
•Neurons of the subcortical nuclei are excited by axon collaterals of climbing neurons. Thus, the transmission can only occur if purkinje neurons are inhibited by inhibitory interneurons.
•Parallel fibers of ganule cells inhibit purkinje cells in all directions and thereby leading to contrast enhancement.
•Neighboring purkinje cells receive input from the same granule cells with increasing delay thereby providing a possibility for temporal segmentation of movement.
•Neurons of the subcortical nuclei are excited by axon collaterals of climbing neurons. Thus, the transmission can only occur if purkinje neurons are inhibited by inhibitory interneurons.
•Neighboring purkinje cells receive input from the same granule cells with increasing delay thereby providing a possibility for temporal segmentation of movement.
•Neurons of the subcortical nuclei are excited by axon collaterals of climbing neurons. Thus, the transmission can only occur if purkinje neurons are inhibited by inhibitory interneurons.
•Neurons of the subcortical nuclei are excited by axon collaterals of climbing neurons. Thus, the transmission can only occur if purkinje neurons are inhibited by inhibitory interneurons.
The genetic disease “Chorea Huntington” is characterized by a degeneration of the striatum. Explain the symptoms of the disease.
•The striatum contains GABAergic nerve cells which are affected by “Chorea Huntington”.
•These neurons degenerate which causes uncontrolled muscle movement (tics).
•This is why “Chorea Huntington” is also called “Veitstanz”.
•These neurons degenerate which causes uncontrolled muscle movement (tics).
•This is why “Chorea Huntington” is also called “Veitstanz”.
What is the function of the hippocampus with respect to memory formation?
•Although the hippocampus is involved in memory formation, it actually does not store any declarative memory.
•However, it reveives input from the cortex via the entorhinal cortex and sends a modified signal back to the cortex.
•However, it reveives input from the cortex via the entorhinal cortex and sends a modified signal back to the cortex.
Would you expect that the mice (with lesioned hippocampus) develop a retrograde amnesia? Explain.
•Retrograde amnesia is a form of amnesia where someone will be unable to recall events that occurred before the onset of amnesia.
•Since the hippocampus is not needed for memory recall a retrograde amnesia will not develop.
•Since the hippocampus is not needed for memory recall a retrograde amnesia will not develop.
Why does PKA inactivation affect LTP?
•PKA plays an essential role in LTP in both the mossy fiber pathway and the Schaffer collateral.
•It is part of second-messenger cascades leading either to more transmitter release in presynaptic cells or to recruitement of non-NMDA receptors in postsynaptic cells, respectively.
•It is part of second-messenger cascades leading either to more transmitter release in presynaptic cells or to recruitement of non-NMDA receptors in postsynaptic cells, respectively.
Which of these is correct about the amygdala?
•The amygdala is part of the limbic system which is a phylogenetically old system of the brain.
•The amygdala is one of the few brain regions that lack peptidergic neurons.
•The amygdala consists of several nuclei which show a topical organization.
•Although the amygdala is also involved in learning processes, LTP is restricted to the hippocampus.
•Valium acts on GABAergic interneurons in the amygdala and decreases anxiety by increasing hyperpolarization.
•The amygdala is part of the limbic system which is a phylogenetically old system of the brain.
•The amygdala is one of the few brain regions that lack peptidergic neurons.
•The amygdala consists of several nuclei which show a topical organization.
•Although the amygdala is also involved in learning processes, LTP is restricted to the hippocampus.
•Valium acts on GABAergic interneurons in the amygdala and decreases anxiety by increasing hyperpolarization.
•The amygdala is part of the limbic system which is a phylogenetically old system of the brain.
•The amygdala consists of several nuclei which show a topical organization.
•Valium acts on GABAergic interneurons in the amygdala and decreases anxiety by increasing hyperpolarization.
•The amygdala consists of several nuclei which show a topical organization.
•Valium acts on GABAergic interneurons in the amygdala and decreases anxiety by increasing hyperpolarization.
Neurons in the CNS do not regenerate whereas neurons in the PNS may regenerate. What is thought to be the cause for this difference?
•Neurons in the CNS are in principle able to regenerate but this ability is suppressed by central myelin (this may be why myelination occurs late in development).
•The suppression can be abolished by antibodies against NI-35 (“nogo”) which seems to be the main factor.
•In the PNS myelin is not generated by oligodendrocytes but by Schwann cells.
•The suppression can be abolished by antibodies against NI-35 (“nogo”) which seems to be the main factor.
•In the PNS myelin is not generated by oligodendrocytes but by Schwann cells.
What happens during Myasthenia gravis? What are the typical symptoms?
•During Myasthenia gravis acetylcholine receptors at motor end plates are blocked by antibodies.
•This leads to fluctuating weakness and fatiguability of muscle movement.
•The muscle weakness increases during periods of activity and improves after periods of rest.
•This leads to fluctuating weakness and fatiguability of muscle movement.
•The muscle weakness increases during periods of activity and improves after periods of rest.
Why are ACh-esterase inhibitors like neostigmine helpful?
•Muscle function is improved by cholinesterase inhibitors, such as neostigmine and pyridostigmine.
•These slow the natural enzyme cholinesterase that degrades acetylcholine in the motor end plate;
•The neurotransmitter is therefore around longer to stimulate its receptors (which there are less of in this disease).
•These slow the natural enzyme cholinesterase that degrades acetylcholine in the motor end plate;
•The neurotransmitter is therefore around longer to stimulate its receptors (which there are less of in this disease).
Give an example of another autoimmune disease.
•Multiple Sclerosis is an example for another autoimmune disease.
•Symptoms include changes in sensation, visual problems, muscle weakness, depression, difficulties with coordination and speech, severe fatigue, cognitive impairment and problems with balance caused by demyelination of axons due to a malfunction of the autoimmune system.
•Symptoms include changes in sensation, visual problems, muscle weakness, depression, difficulties with coordination and speech, severe fatigue, cognitive impairment and problems with balance caused by demyelination of axons due to a malfunction of the autoimmune system.
Flashcard set info:
Author: szara
Main topic: Biology
Topic: Neurobiology
Published: 06.04.2010
Tags: Functional Neuroanatomy
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