Chapter 10: Hormonal Control Systems
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Chapter 6 Section C: Synapses revised 4 October 2011
In what way does the postsynaptic membrane potential change at an excitatory synapse?
In what way does the postsynaptic membrane potential change at an inhibitory synapse?
In neurophysiology, what is meant by convergence?
In neurophysiology, what is meant by divergence?
What are the differences between electrical and chemical synapses? Which is faster? Which is bi- directional? Which is more common in the nervous system of humans?
What are electrical synapses particularly well suited to do?
In what structures are neurotransmitters (NT) stored in the presynaptic terminal?
How is calcium involved in the release of NT? Where does this Ca++ come from and how does it get into the cytoplasm near the axon terminal?
What two classes of ion channels may be found in the postsynaptic membrane? Which of these is associated directly with an ion channel and which influences ion channels by way of an second messenger system?
Approximately how long is “synaptic delay” and what event are occurring during “synaptic delay?”
What are the various fates of NT in the synaptic cleft that prevents the NT from affecting the postsynaptic receptors over and over and over?
What role may astrocytes play in synaptic transmission at chemical synapses?
What determines whether a chemical synapse is excitatory or inhibitory: the NT or the nature of the receptors in the postsynaptic membrane?
What ions move in which directions through the postsynaptic membrane at a typical excitatory synapse?
Explain why an ion channel that is permeable to both Na+ and K+ causes a depolarization in the postsynaptic membrane.
What is an EPSP? What makes EPSPs graded potentials?
Some IPSPs are not accompanied by a change in membrane potential in the postsynaptic cell. Why is this still considered an IPSP?
How is Cl- involved in IPSPs at some synapses?
What is the equilibrium potential for Cl-?
Which cations (positively charged ions) are moving in which direction through the postsynaptic membrane is responsible for an IPSP? What is the main driving force for this movement? What is the amplitude (in millivolts) of a typical EPSP?
Why doesn’t a single EPSP lead to an action potential?
How can temporal summation lead to an action potential?
How can spatial summation lead to an action potential?
Which region of a neuron has the lowest threshold for producing an action potential?
How is the proximity of an excitatory synapse to the axon hillock related to that synapse’s likelihood of producing an action potential? How is this related to the decremental conduction of graded potentials?
Which lasts longer: an action potential or graded potential?
Based on the relative durations of action potentials and synaptic potentials, explain why action potentials are often produced in rapid succession.
How is calcium involved in boosting the release of NT when the presynaptic terminal is experiencing a rapid sequence of action potentials? How would the amplitude of the postsynaptic potential be affected over time?
In what way can an axo-axonic synapse lead to presynaptic facilitation or presynaptic inhibition?
What is an agonist?
What is an antagonist?
What is the mode of action of Botox and for what purposes is it employed?
According to figure 6-34, what are the steps involved in the synthesis, release, and recycling of NT?
Also according to figure 6-34, by what means might drugs interfere with synaptic transmission?
Based on the timing of their effects, how are neurotransmitters distinguished from neuromodulators?
What enzyme, located where, terminates the action of acetylcholine by breaking it down?
How does Sarin nerve gas paralyze its victims?
What are the names for the two types of acetylcholine receptors and why are they so named?
Why is nicotine considered a very addictive substance?
Which type of acetylcholine receptor is coupled to G-proteins and thus is metabotropic?
What is the name of a common antagonist for muscarinic receptors?
Which neurotransmitter is used by neurons that are involved with Alzheimer’s disease?
What do neurotransmitters in the family of biogenic amines have in common structurally? Which biogenic amines are subclassified as catecholamines?
What is the fate of catecholamines once released from the presynaptic terminal?
Name the enzyme involved in the inactivation of catecholamines.
Do drugs that inhibit MAO boost or suppress synaptic transmission at adrenergic synapses?
Which category of NT is associated with appetite disorders, mood disorders, and sleep?
What NTs act via adrenergic receptors? What is synonym for serotonin?
Which amino acids are commonly used at NT in the CNS?
Why is an understanding of serotonergic synapses useful for behavioral scientists?
How does the synthesis of neuropeptide neurotransmitters differ from that of the other NTs?
What term is given to a substance that relieves pain without a loss in consciousness?
How does nitric oxide qualify as a neurotransmitter? Can NO be stored and released from synaptic vesicles? Does NO bind to receptors embedded in the post-synaptic membrane? If not, how does it act?