1.A. For questions 1–5 see Y pp. 4614–4616, 4818.

2.B.

3.A.

4.B.

5.C.

6.B. Hall p. 93.

7.A. Hall pp. 92–95. The binding site is located on the α subunit, the transmembrane segment is the most highly conserved, and the cytoplasmic loop connecting M3 and M4 is the least highly conserved. Both the N- and the C-terminals are extracellular. Response A is correct.

8.B. Hall p. 95.

9.C. For questions 9–10 see Hall p. 97.

10.A.

11.B. For questions 11–16 see Hall pp. 97–99. The N-methyl-D-aspartate (NMDA)

12.C. receptor is voltage regulated in that the open channel is occluded at normal

13.C. resting potential by Mg²⁺. Depolarization drives Mg²⁺ out of the cell, allowing

14.A. other ions to pass.

15.B.

16.B.

17.B. For questions 17–21 see Hall p. 99.

18.E.

19.E.

20.B.

21.B.

23.E. Hall p. 138. Pro-opiomelanocortin gives rise to adrenocorticotropic hormone (ACTH) and (β-lipotropin. ACTH then gives rise to α-melanocyte-stimulating hormone (α-MSH) and corticotropin-like intermediate lobe peptide (CLIP), and β-lipotropin gives rise to γ-lipotropin and β-endorphin.

24.A. Hall p. 164. Reversal of flow through voltage-gated channels is not a mechanism of removal of Ca²⁺ from the cytosol.

25.E. Hall p. 195. The decreased concentration of cyclic guanosine monophosphate (cGMP) results in decreased current through the Na⁺ channel and consequent hyperpolarization.

26.A. Hall pp. 186, 201. Each G protein may be regulated by separate receptors.

27.C. For questions 27–33 see Hall pp. 214, 219, 225, 235, 239.

28.D.

29.E.

30.B.

31.A.

32.D.

33.E.

34.E. Hall p. 46. The Na⁺/K⁺ pump uses one molecule of adenosine triphosphate (ATP) for every three Na⁺ ions transported.

35.B. Hall pp. 49–51. Chloride permeability does not change during the action potential.

36.B. Hall p. 67.

37.D. Hall p. 67.

38.A. For questions 38–40 see Hall pp. 70–74. Miniature end-plate potentials result

39.B. from random release of quanta of acetylcholine but do not produce an action

40.D. potential.

41.B. Hall p. 79.

42.A. Hall pp. 258–259. Dynamin uses GTP as an energy source. Dynein is the motor protein for retrograde fast axonal transport. Slow axonal transport occurs at several millimeters per day; fast axonal transport occurs at 200 to 400 mm/day and utilizes microtubules.

44.A.

45.A.

46.B.

47.B.

48.B.

49.C.

50.B.

51.D.

52.B.

53.C. K&S pp. 654, 817, 821. Destruction of the anterior lobe of the cerebellum releases the cells of origin of the lateral vestibular tract from inhibition by Purkinje’s cells, thereby facilitating extensor motor neurons.

54.C. For questions 54–59 see V&A pp. 56–58; K&S pp. 716–717, 730.

55.F.

56.B.

57.D.

58.E.

59.A.

60.B. K&S pp. 968–969.

61.C. K&S p. 1108. Chromatolysis is associated with increased protein synthesis. Retraction bulbs, from the buildup of transported materials, occur at both the proximal and the distal ends of the cut nerve. Wallerian degeneration begins in the distal end of the axon about 1 week after initial degenerative changes begin in the axon terminal.

62.B. Carp p. 14. Carbon dioxide and volatile anesthetic agents increase cerebrospinal fluid (CSF) production, whereas carbonic anhydrase inhibitors and norepinephrine inhibit CSF production.

63.D. K&S p. 78.

64.A. For questions 64–68 see V&A pp. 36–37.

65.B.

66.E.

67.D.

68.C.

69.B. For questions 69–72 see V&A pp. 38–39.

70.A.

71.C.

72.A.

74.E. a cerebral blood flow of 8 and 23 mL/100 g/min is known as the ischemic

75.B. penumbra. The biochemical abnormalities, including depletion of ATP and creatine phosphate and increase of K⁺ level (from injured cells), can be reversed if adequate blood flow is restored in a timely fashion.

76.C. For questions 76–83 see K&S pp. 835–840. The cerebellar cortex consists

77.B. of three layers that contain five cell types. The molecular layer (outermost)

78.C. is composed of the axons of the granule cells (parallel fibers), stellate and

79.C. basket cells (interneurons), and dendrites of the underlying Purkinje’s cells.

80.D. The Purkinje’s cell layer (middle) contains the cell bodies of the Purkinje’s

81.D. neurons. They are the sole output of the cerebellar cortex and are inhibitory.

82.A. The granular (innermost) layer contains numerous granule cells (excitatory;

83.C. utilize glutamate), a few Golgi’s cells, and glomeruli (where cells in the granular layer form complex synaptic contacts with the incoming mossy fibers). Afferents to the cortex terminate either in the granule cell layer as mossy fibers or on the dendrites of Purkinje’s cells as climbing fibers. Both mossy and climbing fiber inputs are excitatory to both the deep cerebellar nuclei and the cortex. Stellate and basket cells directly inhibit Purkinje’s and Golgi’s cells, and Golgi’s cells inhibit granule cells.

84.A. K&S pp. 804–805.

85.D. K&S p. 432.

86.D. For questions 84–86 see K&S pp. 969–970. Unlike the ACh receptors at the neuromuscular junction, the ACh receptors in autonomic ganglia contain only two types of subunits. The fast excitatory postsynaptic potential (EPSP) is mediated by nicotinic ACh receptors, the slow EPSP is mediated by muscarinic receptors opening Na⁺ and Ca²⁺ channels and closing K⁺ channels, and the slow inhibitory postsynaptic potential (IPSP) is mediated by muscarinic receptors that open K⁺ channels. A variety of peptides that appear to be modulatory in action may be co-released with ACh.

87.A. K&S pp. 968–969. Increased sympathetic activity results in bladder wall relaxation.

88.B. Carp pp. 171–172.

89.B. Carp p. 393.

90.C. K&S p. 210.

91.B. K&S pp. 78, 720–721. Renshaw cells inhibit Ia inhibitory interneurons that act on antagonist motor neurons.

93.D. nucleus (Deiters’ nucleus) receives direct inhibitory input from Purkinje’s

94.B. cells in the cerebellar vermis. Decerebrate rigidity is exacerbated if the portion

95.A. of the cerebellum connected to Deiters’ nucleus is interrupted because of

96.B. removal of this inhibitory action. The lateral vestibulospinal tract has a facilitatory effect on both alpha and gamma neurons that innervate muscles in the limbs; this tonic excitation of the extensors of the leg and the flexors of the arm helps in the maintenance of posture.

97.C. Hall pp. 10, 135. The initial steps of N-linked glycosylation take place in the endoplasmic reticulum.

98.A. For questions 98–104 see Hall p. 200; K&S pp. 114, 153, 270, 286, 307–308.

99.G.

100.F.

101.B.

102.E.

103.C.

104.D.

105.A. Hall p. 35. At the equilibrium potential, the chemical and electrical forces are equal. There is no net movement of K ions across the membrane.

106.D. Hall p. 189. The β subunit inhibits activation by both stabilizing the binding of GDP and inhibiting the binding of GTP.

107.C. G&G pp. 199–203. Succinylcholine and decamethonium cause depolarizing neuromuscular blockade. The effect is not reversed by anticholinesterase agents and is amplified by decreased muscle temperature.

108.C. For questions 108–111 see K&S pp. 457–458.

109.B.

110.D.

111.A.

112.A. K&S pp. 446–448. Proprioception from the leg is relayed in the lateral column by axons of neurons in Clarke’s column. In addition to sending axons to the primary somatic sensory cortex (SI), thalamic neurons send a sparse projection to the secondary somatic sensory cortex (SII).

113.D. For questions 113–121 see K&S pp. 849–850.

114.A.

115.B.

116.C.

117.D.

118.E.

119.D.

120.B.

121.B.

123.E. Carp p. 253. The pineal gland synthesizes melatonin from serotonin by the action of two enzymes sensitive to variations of diurnal light. The rhythmic fluctuations in melatonin synthesis are directly related to the daily light cycle.

124.C. For questions 124–128 see K&S pp. 187–189, 241–242. The nicotinic and

125.B. muscarinic receptors both bind acetylcholine and are found in sympathetic

126.C. neurons, whereas the directly gated receptors in skeletal muscle are muscarinic.

127.B. Hexamethonium selectively blocks nicotinic ACh receptors. Muscarinic receptors

128.A. activate a second messenger system that closes a K⁺ channel (called the M channel).

129.D. K&S p. 210.

130.E. K&S p. 967.

131.B. For questions 131–137 see K&S pp. 676–679.

132.A.

133.B.

134.B.

135.A.

136.C.

137.B.

138.B. K&S pp. 678–679. During skeletal muscle contraction, calcium binds to troponin. Both the association and detachment of cross bridges require ATP (not GTP). During relaxation, Ca²⁺ is actively pumped out of the intracellular space and back into the sarcoplasmic reticulum.

139.B. K&S p. 217.

140.A. K&S pp. 1006–1007. Alcohol decreases the release of ADH.

141.D. K&S pp. 280–281. The enzymes that catalyze the synthesis of the low molecular weight transmitters are usually cytoplasmic (dopamine-β-hydroxylase is an exception), but this is not a criterion that must be fulfilled for a chemical to be considered a transmitter.

142.E. K&S pp. 281, 290. VIP is considered a neuroactive peptide, not a neurotransmitter.

143.E. K&S p. 964. The sweat glands are innervated by the sympathetic system only.

144.B. K&S pp. 718–719. The activity of γ motor neurons is profoundly reduced by lesions in the cerebellum.

146.B. K&S pp.529, 533–534. Cells of the retina and lateral geniculate nucleus have concentric receptive fields that fall into two classes: on-center or off-center. Simple cells of the visual cortex have rectangular receptive fields. The receptive field of a complex cell in the primary visual cortex has no clearly distinct excitatory or inhibitory zones. Orientation but not position of the light stimulus is important.

147.E. For questions 147–151 see K&S pp. 432–435. Meissner’s corpuscles and

148.B. Merkel’s receptors are both found superficially in the dermal papillae and

149.C. have small receptive fields. Pacinian and Ruffini’s corpuscles are found in the

150.D. deeper subcutaneous tissue and have large receptive fields. Both Merkel’s

151.A. receptors and Ruffini’s corpuscles are slowly adapting and subserve pressure sensation. Pacinian corpuscles are more sensitive to low- than high-frequency stimuli and transmit flutter. Pain sensation is transmitted by free nerve endings.