1. REVIEW SLIDES

2. NOTE:
Disclaimer: students may find typos/mistakes in these reviews. If you spot them, please feel free to make a change and then the instructor the corrected Power Point.
Disclaimer: these slides are not intended to substitute for exam preparation. Finding a mistake does not exempt students from knowing the material.

3. Chapter 7
The Nervous System

4. Which of the following best describes the function of the nervous system? a. protection, thermoregulation b. regulation of other body systems c. secretion of regulatory molecules called hormones d. movements of the skeleton

5. Which of the following best describes the function of the nervous system? a. protection, thermoregulation b. regulation of other body systems c. secretion of regulatory molecules called hormones d. movements of the skeleton

6. _______________ disease is caused by a degeneration of the dopaminergic neurons of the substantia nigra.

7. _Parkinson’s__ disease is caused by a degeneration of the dopaminergic neurons of the substantia nigra.

8. Which division of the nervous system innervates involuntary effectors?

9. Which division of the nervous system innervates involuntary effectors
Which division of the nervous system innervates involuntary effectors? Autonomic nervous system

10. The membrane of resting nerve cells is more permeable to ____________ ions than __________ ions. a. sodium, potassium b. calcium, potassium c. potassium, sodium d. chloride, potassium

11. The membrane of resting nerve cells is more permeable to ____________ ions than __________ ions. a. sodium, potassium b. calcium, potassium c. potassium, sodium d. chloride, potassium

12. The average cell has a resting potential of ___________________ (provide a range of mV)

13. The average cell has a resting potential of __-65 to -85 mV_____ (provide a range of mV)

14. Injured CNS axons do not regenerate, whereas injured PNS axons do.
True
False

15. Injured CNS axons do not regenerate, whereas injured PNS axons do.
True
False

16. ______________ cells form the myelin sheath in the PNS, whereas __________________ form the myelin sheath in the CNS.

17. Schwann cells form the myelin sheath in the PNS, whereas oligodendrocytes form the myelin sheath in the CNS.

18. Somatic motor neurons are responsible for both __________ and voluntary control of skeletal muscles.

19. Somatic motor neurons are responsible for both _reflex__ and voluntary control of skeletal muscles.

20. ____________________ is produced by autoimmune attack mediated by T cells on the myelin sheaths in the CNS.

21. Multiple sclerosis__ is produced by autoimmune attack mediated by T cells on the myelin sheaths in the CNS.

22. ____________________ is produced by autoimmune attack, mediated by T-cells, on the myelin sheaths of the PNS. This produces rapid onset of symptoms that include muscle weakness (which can dangerously affect the muscles of breathing) due to dysfunction of somatic motor axons, and cardiac and blood pressure problems due to dysfunction of autonomic axons.

23. Guillain-Barre syndrome is produced by autoimmune attack, mediated by T-cells, on the myelin sheaths of the PNS. This produces rapid onset of symptoms that include muscle weakness (which can dangerously affect the muscles of breathing) due to dysfunction of somatic motor axons, and cardiac and blood pressure problems due to dysfunction of autonomic axons.

24. Ion channels that open in response to depolarization are called

25. Ion channels that open in response to depolarization are called voltage-gated.

26. What is the difference between an action potential and an EPSP?

27. What is the difference between an action potential and an EPSP?
Action potentials are not summed; EPSPs are summed
Action potentials occur on Axons and EPSPs occur on dendrites and cell bodies (see table in book p. 187)

29. Describe an action potential

30. Depolarization of an Axon

31. Describe the all-or-none law

32. Describe the all-or-none law
The amplitude (size) of action potentials is always the same, regardless of the strength of the depolarization stimulus (beyond threshold)

33. Because action potentials look like spikes, they are often called _____________ potentials.

34. Because action potentials look like spikes, they are often called _____spike___ potentials.

35. Because of the all-or-none characteristic of action potentials, stronger stimuli do NOT result in signals of __________________ amplitude.

36. Because of the all-or-none characteristic of action potentials, stronger stimuli do NOT result in signals of ____greater____ amplitude.

37. Stronger stimuli affect action potentials by increasing their __________________.

38. Stronger stimuli affect action potentials by increasing their _frequency__.

39. As the intensity of stimulation increases, more and more axons will become activated. This process is called ___________________.

40. As the intensity of stimulation increases, more and more axons will become activated. This process is called recruitment.

41. Name two ways that neurons respond to stimuli of greater and greater strength.

42. Name two ways that neurons respond to stimuli of greater and greater strength.
1) Action potentials fire with increasing frequency
2) More and more axons are activated. (recruitment)

43. Name the two types of refractory period of an action potential

44. Name the two types of refractory period of an action potential
Absolute refractory period
Relative refractory period

45. The __________________ refractory period can be overcome by a second strong stimulus.

46. The ______relative_ refractory period can be overcome by a second strong stimulus.

47. Where on a neuron is an action potential first produced?  

48. Where on a neuron is an action potential first produced?
Action potentials are produced at the initial segment of the axon. (Axon hillock)

49. Where on a neuron is an EPSP or IPSP first produced?

50. Where on a neuron is an EPSP or IPSP first produced?
Dendrites and cell bodies

51. How long is an axon?

52. How long is an axon?
Axons vary in length from a few millimeters to a meter!

53. Axons can form many branches called _____________________.

54. Axons can form many branches called collaterals___.

55. Axons are covered in myelin with open spots called ___________________.

56. Axons are covered in myelin with open spots called Nodes of Ranvier.

57. EPSPs and IPSPs can be “summed,” which means that their relative strengths can be added up to determine whether they will reach the threshold required to trigger a(n) ___________________.

58. EPSPs and IPSPs can be “summed,” which means that their relative strengths can be added up to determine whether they will reach the threshold required to trigger a(n) action potential.

59. When we say that EPSPs are “graded,” we mean that they can be of varying _____________, unlike action potentials, which are all-or-none.

60. When we say that EPSPs are “graded,” we mean that they can be of varying magnitude, unlike action potentials, which are all-or-none.

61. Because EPSPs have no refractory period, they are capable of ________________; therefore, another stimulation can result in an increased amount of depolarization.

62. Because EPSPs have no refractory period, they are capable of summation; therefore, another stimulation can result in an increased amount of depolarization.

63. This graph shows the _______ nature of EPSPs.

64. This graph shows the graded nature of EPSPs.

65. FOR YOUR INFORMATION

66. Describe events at the synapse that lead to the release of a neurotransmitter.

67. Release of Neurotransmitter
See notes for this slide
Docking involves a SNARE complex of proteins that bridge the vesicle membrane and the plasma membrane. The SNARE proteins include one in the vesicle membrane (synaptobrevin-2) and two anchored in the plasma membrane (syntaxin and SNAP-25). When an action potential arrives at the presynaptic axon terminal, depolarization opens the Ca+2 channels. When Ca2+ enters the cell, it binds to a protein called synaptotagmin that serves as a Ca2+ sensor
Vesicles containing neurotransmitter are docked at the plasma membrane by three SNARE proteins.
The Ca2+ synaptotagmin complex displaces part of SNARE, and the vesicle fuses.
Forms a pore to release the NT
Neurotransmitter diffuses across the synapse, where it binds to a specific receptor protein.
The neurotransmitter is referred to as the ligand.
This results in the opening of chemically regulated ion channels (also called ligand-gated ion channels).
The neurotransmitter (ligand) binds to a receptor in the postsynaptic membrane

68. Summary of Neurotransmitter Action

69. Drugs that bind to and thereby activate receptor proteins are called __________________, whereas drugs that bind to and thereby reduce the activity of receptor proteins are ________________.

70. Drugs that bind to and thereby activate receptor proteins are called agonists, whereas drugs that bind to and thereby reduce the activity of receptor proteins are antagonists.

71. Muscarinic acetylcholine receptors are NOT found on the surfaces of skeletal muscle. They are found on _______________, ______________ and ______________ cells.

72. Muscarinic acetylcholine receptors are NOT found on the surfaces of skeletal muscle. They are found on cardiac muscle, smooth muscle and glandular cells.

73. Describe the action of ACh at a muscarinic receptor

74. Describe the action of ACh at a muscarinic receptor
Muscarinic (5 subtypes of receptor) (blocked by atropine)
Heart
Beta gamma complex binds to K+ channels, opens them, K+ diffuses out  IPSP
Smooth muscle of stomach
Alpha subunit dissociates, binds to K+ channels, closes them, K+ stays inside cells  depolarization  stomach contractions

75. MUSCARINIC Ach Receptors Require G-Proteins
In the heart, K+ channels are opened by the beta-gamma complex, creating IPSPs (hyperpolarization) that slow the heart rate.
In the smooth muscles of the stomach, K+ channels are closed by the alpha subunit, producing EPSPs (depolarization) and the contraction of these muscles.
Binding of acetylcholine opens K+ channels in some tissues (IPSP) or closes K+ channels in others (EPSP).
Heart: K+ channels open, creating IPSPs  heart rate slowed
Smooth muscle: K+ channels close, creating EPSPs  smooth muscles contract

76. Describe the action of ACh at a nicotinic receptor

77. Describe the action of ACh at a nicotinic receptor
Nicotinic (blocked by curare) (see next slide)
Somatic motor neurons
Nicotinic  excitatory

78. BINDING OF ACETYLCHOLINE (LIGAND) TO ITS RECEPTOR
ACETYLCHOLINE CAN BIND TO ITS RECEPTOR, WHICH IS ALSO AN ION CHANNEL
Notice that 2 acetylcholines must bind

79. Table 9.6

80. CH 7
Describe the action of epinephrine at a beta-adrenergic receptor

81. Monoamines use G-protein Coupled Channels
THIS IS A SECOND MESSENGER SYSTEM
Norepinephrine, like Acetylcholine, is used as a neurotransmitter in the CNS and PNS. Sympathetic neurons of the PNS use norepinephrine as their neurotransmitter at their synapse with smooth muscle, cardiac muscle, glands.
. This is a BETA ADRENERGIC receptor.

82. Table 9.4

83. What is meant by the term “retrograde neurotransmitter”?

84. What is meant by the term “retrograde neurotransmitter”?
“retrograde” means that the neurotransmitter is released from the postsynaptic neuron and diffuses back to the presynaptic neuron.

85. Explain the steps at the synaptic bulb (terminal bouton) that result from an action potential and lead to the release of a neurotransmitter. Start with 1) Action potential sent to the axon terminus. End with 6) release of neurotransmitter into synaptic cleft.
1-Action potential sent to the axon terminus. 2 3 4 5
6-Release of a neurotransmitter into synaptic cleft

86. Explain the steps at the synaptic bulb (terminal bouton) that result from an action potential and lead to the release of a neurotransmitter. Start with 1) Action potential sent to the axon terminus. End with 6) release of neurotransmitter into synaptic cleft.
1 - Action potential sent to the axon terminus.
2 - Opening of voltage-gated Ca2+ channels.
3 - Entry of Ca2+ and binding to sensor protein (forming synaptotagmin-Ca2+ complex)
4 - Interaction between complex and synaptic vesicles containing neurotransmitter
5 - Exocytosis of synaptic vesicles
6 - Release of a neurotransmitter into synaptic cleft

87. CH 7
Describe endocannabinoids

88. Describe endocannabinoids
CH 7
Describe endocannabinoids
Compounds with effects similar to those of the active ingredient in marijuana (THC)
Bind to the same receptors as THC
Lipids, which are acting as neurotransmitters
Not stored in vesicles, but rather are released from membrane
May be retrograde neurotransmitters

89. Epinephrine, dopamine, norepinephrine, acetylcholine are known as excitatory neurotransmitters because they ___________ the likelihood that the post-synaptic cell will fire an action potential.

90. Epinephrine, dopamine, norepinephrine, acetylcholine are known as excitatory neurotransmitters because they _increase___ the likelihood that the post-synaptic cell will fire an action potential.

91. GABA and glycine are known as inhibitory neurotransmitters because they __________________ the likelihood that the post-synaptic cell will fire an action potential.

92. GABA and glycine are known as inhibitory neurotransmitters because they __decrease____ the likelihood that the post-synaptic cell will fire an action potential.

93. The disease multiple sclerosis is characterized by destruction of CNS myelin sheaths and the formation of hardened scars.

94. The disease __________________is characterized by destruction of CNS myelin sheaths and the formation of hardened scars.

95. In contrast to the all-or-none amplitude of an action potential, excitatory post-synaptic potentials (EPSPs) are

96. In contrast to the all-or-none amplitude of an action potential, excitatory post-synaptic potentials (EPSPs) are graded.

97. Some drugs are called Monoamine oxidase (MAO) inhibitors.
MAO inhibitors have proven useful in the treatment of depression, as well as of panic disorder, anxiety and others.
Which of the following is the best description of their mechanism of action? MAO inhibitors block the _________________________ of neurotransmitters such as dopamine, epinephrine and norepinephrine.

98. Some drugs are called Monoamine oxidase (MAO) inhibitors
Some drugs are called Monoamine oxidase (MAO) inhibitors. MAO inhibitors have proven useful in the treatment of depression, as well as of panic disorder, anxiety and others. Which of the following is the best description of their mechanism of action? MAO inhibitors block the ____breakdown___ of neurotransmitters such as dopamine, epinephrine and norepinephrine.

99. GABA is a neurotransmitter which has _________________ effects on postsynaptic neurons due to its opening of ______________ channels.

100. GABA is a neurotransmitter which has __inhibitory___ effects on postsynaptic neurons due to its opening of chloride ion (Cl-) channels.

101. _________________________ is caused by degeneration of dopaminergic neurons in the substantia nigra.

102. Parkinson’s disease is caused by degeneration of dopaminergic neurons in the substantia nigra.

103. The binding of norepinephrine to its beta-receptors causes the dissociation of G-proteins. In some cases, the alpha G-protein subunit then binds to ____________________, leading to the production of ___________________.

104. The binding of norepinephrine to its beta-receptor causes the dissociation of G-proteins. In some cases, alpha G-protein subunit then binds to _adenylate cyclase_, leading to the production of _cAMP___.
cAMP then activates a protein kinase, which opens ion channels.

105. CHAPTER 3
Describe Huntington’s disease

106. CHAPTER 3
Huntington’s disease is a neurodegenerative disorder. Results in a deficiency of GABA-releasing neurons, which results in uncontrolled movements.
Inherited as a dominant gene
Caused by CAG repeats in the huntingtin gene
GABA is an inhibitory neurotransmitter.