prob_set2_solns

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Remaining questions from Problem set #1 and Problem set #2 4. a) -Bgt would block all synaptic transmission that depends on nicotinic ACh receptors. (You will hear more about "nicotinic" ACh receptors soon.) Two major examples are transmission at the neuromuscular junction and transmission between pre-ganglionic and post-ganglionic neurons in the autunomic nervous system. It might block transmission in parts of the central nervous system as well, because at least some synaptic transmission in the CNS appears to be based on nicotinic AChRs and some of these synapses may be sensitive to -Bgt. b) By far the majority of neuronal action potentials in mammals (in most other animals, too) are based on the action of voltage-gated Na + channels. Therefore, TTX will shut down activity in the brain. (Note: A few neurons may carry information via alternative mechanisms, for example, Ca 2+ -based action potentials. These cells would be unaffected by the presence of TTX. In addition, some voltage-gated Na + channels are known to be insensitive to TTX, but not many of them are.) c) Cholinesterase hydrolyzes ACh, limiting the amount of time the concentration of ACh remains high in the synaptic cleft. It therefore shortens the time during which synapses are active. By blocking cholinesterase activity, physostigmine would increase the time during which [ACh] remained high in the synaptic cleft, prolonging synaptic activation. Consequently, physostigmine would increase muscle activity greatly and would, in the absence of synaptic desensitization, produce rigid paralysis. d) By blocking K + channels, TEA would slow down repolarization in neurons. Neurons would remain depolarized longer, causing synaptic transmission and trans-synaptic excitation to be prolonged. As a result, activity in the spinal cord might be expected to increase. It is also possible that all of the neurons in the cord might be stuck in a depolarized state, causing them to fire a barrage of action potentials until they became fatigued, at which time, activity would be reduced. (Note that inhibitory neurons would also remain excited longer, along with the excitatory neurons, so you can't really predict for sure what would happen.) It is clear that several predictions are plausible. You would have to do the experiment to find out what really happens. Most predictions include the disruption of normal activity. In a question like this, the most important part of your answer is to support your prediction with a plausible physiological mechanism. 5. a) In temporal summation, multiple action potentials propagated along a single pre-synaptic neuron arrive in rapid succession at the synaptic terminals. If summation is to occur, each successive action potential must cause the release of transmitter before the post-synaptic effect of transmitter from the previous action potential has disappeared. As a result, the post-synaptic potentials add to one another and produce a PSP that is larger than a single PSP would be. In spatial summation, post-synaptic potentials caused by action potentials in several pre-synaptic
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