Chapter 24 131. Conditioning of the eyeblink reflex involves a. a distributed memory. b. a specifically localized memory. c. both of the above. d. none of the above. 132. If protein synthesis is required for memory STORAGE, then injection of an inhibitor of protein synthesis just before training should result in a. deficits in long-term, but not short-term memory. b. an inability to learn at all. c. a requirement for longer periods of training. d. deficits in short-term but not long-term memory. 133. If protein synthesis is required for memory FORMATION, then injection of an inhibitor of protein synthesis just before training should result in a. deficits in long-term, but not short-term memory. b. an inability to learn. c. a requirement for longer periods of training. d. deficits in short-term but not long-term memory. 134. If protein synthesis is required for memory RETRIEVAL, then injection of an inhibitor of protein synthesis just before training should result in a. deficits in long-term, but not short-term memory. b. an inability to learn. c. a requirement for longer periods of training. d. deficits in short-term but not long term memory. 135. The purpose of the experiments in which a goldfish was trained to avoid shock when a light flashed on was to show that a. such learning was correlated with an increase in the concentration of a specific biochemical substance. b. memory resided in an electrical "trace" in the brain. c. inhibition of protein synthesis could interfere with memory storage. d. inhibition of protein synthesis had no effect on memory formation. 136. Injection of puromycin, an inhibitor of protein synthesis, into a goldfish two hours after training, resulted in a fish that a. did not learn the task. b. learned the task, but required twice as many trials, and could recall the task three days later. c. was normal with respect to its ability to learn and remember. d. learned the task normally, but had forgotten it three days later. 137. Injection of puromycin, an inhibitor of protein synthesis, into a goldfish just before training, resulted in a fish that a. did not learn the task. b. learned the task, but required twice as many trials, and could recall the task 3 days later. c. was normal with respect to its ability to learn and remember. d. learned the task normally, but had forgotten it 3 days later. 138. A major chemical basis of long-term learning and memory is thought to be a. protein synthesis. b. changes in transmitter release. c. mediated by changes in potassium channels. d. none of the above. 139. Habituation is a. a loss of behavioral response to a stimulus on repetitive presentation of the stimulus. b. a simple, stereotyped response to a stimulus. c. a PERMANENT behavioral change as a consequence of experience. d. the rapid acquisition of a learned response to a stimulus during a brief period in the early life of an organism. 140. The simplest type of learning is thought to be a. habituation. b. conditioning. c. adaptation. d. imprinting. 141. Eric Kandel has contributed important work in the field of a. neuroethology. b. neural development. c. neuroendocrinology. d. neural basis of simple learning. 142. Among other topics, Kandel has worked on a. cellular mechanisms of sensitization. b. specificity of central connections during development. c. the bat/moth prey capture/avoidance system. d. hormonal control of eclosion (molting) behavior in Aplysia . 143. Cellular work on the mechanisms of learning is being done in the laboratory of a. Kandel. b. Roeder. c. Sperry. d. Truman. 144. Habituation of Aplysia 's gill-withdrawal reflex is thought to occur a. at the synapse between sensory and motor neurons. b. at the neuromuscular junction. c. in the siphon skin. d. in the gill muscles. 145. Habituation of Aplysia 's gill withdrawal reflex is though to occur by means of a. a reduction in the amount of transmitter released at the neuromuscular junction. b. a reduction in the amount of transmitter released at the sensory neuron to motor neuron synapse. c. an increase in central inhibition. d. an increase in muscle fatigue. 146. In the study of habituation of the gill withdrawal reflex in Aplysia , the idea that the behavioral change was due to a failure of the sensory neurons to respond to the stimulus was rejected by experiments in which, after habituation a. direct electrical stimulation of the gill motor neurons resulted in contraction of the gill withdrawal muscles. b. direct electrical stimulation of the sensory neurons showed that they could still conduct impulses. c. a strong dishabituating stimulus to the head allowed the withdrawal reflex to be evoked again. d. a decrement in EPSPs in the motor neuron was demonstrated. 147. Dishabituation is the sudden a. loss of a complex learned response upon presentation of a series of strong, novel stimuli. b. reappearance of a reflex that had waned, upon presentation of a series of strong, novel stimuli. c. loss of a complex learned response upon presentation of a single, strong novel stimulus. d. reappearance of a reflex that had waned, upon presentation of a single, strong novel stimulus. 148. In order for a habituated reflex response to be dishabituated, the dishabituating stimulus should be a. weaker than the habituating stimulus, delivered at the same site as the habituating stimulus. b. weaker than the habituating stimulus, delivered at a different site as the habituating stimulus. c. the same strength as the habituating stimulus. d. stronger than the habituating stimulus. 149. One mechanism proposed to underlie dishabituation of the gill withdrawal reflex of Aplysia is a. long lasting synaptic depression. b. post-tetanic potentiation. c. heterosynaptic facilitation. d. none of the above. 150. Dishabituation and sensitization in Aplysia are both though to involve a. presynaptic inhibition. b. non-inhibitory presynaptic mechanisms. c. REDUCTION in the amount of transmitter release. d. only changes in motor neuron excitability. 151. Sensitization in Aplysia is thought to involve the following sequence of events a. increase in cAMP ---> release of serotonin ---> blocking K+ channels ---> more transmitter release. b. spike broadening ---> more transmitter release ---> increase in cAMP ---> blocking K+ channels. c. release of serotonin ---> increase in cAMP ---> blocking K+ channels ---> spike broadening. d. blocking K+ channels ---> spike broadening ---> more transmitter release ---> increase in cAMP. 152. In the study of the cellular mechanisms underlying sensitization, one step in the series that leads to the increased synaptic efficacy is partial blocking of a a. potassium channel, leading to a quicker (narrower) action potential that releases more transmitter. b. sodium channel, leading to a quicker (narrower) action potential that releases more transmitter. c. potassium channel, leading to a broader action potential that releases more transmitter. d. sodium channel, leading to a broader action potential that releases more transmitter. 153. The role of adenylyl cyclase in sensitization in Aplysia neurons is a. to activate the membrane-bound G protein, which in turn promotes protein phosphorylation. b. to act as a receptor for serotonin, the transmitter substance that initiates the process. c. to promote the phosphorylation of proteins via synthesis of cAMP. d. to promote the synthesis of cAMP, which in turn directly closes certain potassium channels. 154. Recent work has shown that in tissue cultures of Aplysia sensory and motor neurons, a. brief pulses of acetylcholine will produce short term but not long term potentiation. b. electrical stimulation of the motor neurons will prevent the expression of sensitization. c. application of a protein inhibitor just before a brief pulse of serotonin is applied prevents long term but not short term potentiation at the synapse. d. protein inhibitors have no effect on the synapses formed between neurons in tissue culture. 155. Protein synthesis may be involved in the development of long-term sensitization in Aplysia . This was shown by experiments in which a. Aplysia could not remember being trained to avoid an electrical shock after the administration of an inhibitor of protein synthesis. b. exposure of the nervous system to an enzyme that speeded breakdown of cAMP (an enzyme that required synthesis to be present in the normal animal) resulted in an animal that withdrew its gill to any stimulus anywhere on the body. c. an inhibitor of protein synthesis was added to a tissue culture dish containing sensory and motor neurons, and serotonin pulsed at the neurons just after the inhibitor was added could cause short-term but not long-term sensitization. d. serotonin squirted at sensory and motor neurons in tissue culture would not cause any effect at all after the neurons had been exposed to an inhibitor of protein synthesis. 156. NMDA receptors appear to be involved in a. sensitization. b. habituation. c. imprinting. d. long term potentiation. 157. NMDA channels in the vertebrate brain differ from K or Q channels in that only NMDA channels a. are activated (opened) by glutamate. b. allow K+ to leave the cell when they are open. c. allow Na+ to enter the cell when they are open. d. are normally blocked by Mg++ ions. 158. Depolarization immediately prior to synaptic activation of an NMDA-bearing neuron seems to be important in the development of long-term potentiation. This is because the depolarization a. is necessary for direct activation of protein kinases that mediate the long-term effects. b. causes a conformational change in K or Q channels that alters their response to the presence of transmitter substance. c. alters the equilibrium potential of certain ions, thereby affecting their flow into or out of the cell, and consequently altering the cell's response. d. moves Mg++ away from the NMDA-associated channel, thereby allowing ions to flow through it when it is opened by the transmitter substance. 159. In the vertebrate hippocampal brain slice preparation, a. learning-like changes in synaptic action have never been shown to occur. b. cAMP levels in specific target cells have been shown to rise when long term potentiation is evoked in those cells, but not when it is evoked in other cells. c. serotonin has been shown to be the transmitter that causes sensitization at selected synapses. d. the detailed neural circuitry underlying a complex learned behavior has been identified. 160. Long term potentiation (LTP) in the vertebrate brain may require the action of a retrograde messenger. The evidence for this is that a. more transmitter seems to be released from the presynaptic terminal after LTP than before. b. there is an increased size of the postsynaptic potential after LTP. c. the presynaptic neuron is much more likely to fire action potentials after LTP. d. Calcium cannot enter the postsynaptic terminal in sufficient quantity to bring about LTP without the action of some additional substance released from the presynaptic terminal that helps remove Mg++ ions from the NMDA receptor.