Chapter 6 Section C: Synapses
revised 29 September 2009
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?
In what form are neurotransmitters (NT) stored in the presynaptic terminal?
What triggers the release of NT?
How is calcium involved in the release of NT?
What types of ion channels are found in the postsynaptic membrane?
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 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?
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 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?
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?
In what way can an axonaxonic synapse lead to presynaptic facilitation or presynaptic inhibition?
What is an agonist?
What is an antagonist?
According to figure 6-34, what are the steps involved in the synthesis, release, and recycling of NT?
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?
Which type of acetycholine receptor is coupled to G-proteins and thus is metabotropic?
What do neurotransmitters in the family of biogenic amines have in common?
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?
What is the difference between metabotropic and ionotropic receptors? (Not clearly stated in the text.)
Which NT is associated with appetite disorders, mood disorders, and sleep?
How does the synthesis of neuropeptide neurotransmitters differ from that of the other NTs?
What two gases can serve as neurotransmitters?