1. Why does a neuron have multiple dendrites?

a. So that it can receive signals from many places. They also increase surface
area and contain ribosomes.
2. How do neurons communicate?
a. By changes in their membrane's permeability to ions in two flavors: graded
potentials and action potentials. In most neurons, the electrical signal causes
the release of chemical messengers (neurotransmitters) to communicate with
other cells.
3. What does the axonal region do?
a. It undergoes action potentials to deliver information (typically
neurotransmitters).
4. What is the somatic system
a. The part of our PNS which communicates with SKELETAL muscles (generally
considered to be the voluntary actions but there are exceptions: reflexes).
There is one neuron coming from the CNS per muscle and can ONLY lead to
muscle excitation.
5. What is the autonomic system
a. This is the parasympathetic (rest & digest) and sympathetic (fight or flight)
systems. Both use a two neuron relay between CNS and effector organ.
Innervates smooth & cardiac muscle, glands, and GI neurons. Can be
excitatory or inhibitory.
6. What is the CNS vs. PNS
a. CNS = brain and spinal cord
b. PNS = autonomic and somatic systems
7. What are afferent neurons and their structure?
a. They receive sensory input from tissues and organs, send it to the brain. They
have only a single process (an axon) which divides to form a peripheral
process and a central process (which enters the CNS). The cell body it
outside the CNS.
8. What are efferent neurons and their structure?
a. They receive information from the interneurons of the CNS and use it to
produce motor output, secretion in glands, and signals to nerves. Their cell
bodies and dendrites are inside the CNS but the axons extend into the
periphery. They are bound to afferent neurons with connective tissue to form
nerves.
9. What are interneurons?
a. They are >99% of all neurons. They connect neurons within the CNS. They
are entirely inside the CNS and the number of interneurons interposed
between the aff. and eff. is directly correlated to the complexity of actions.
10. How many neurons do we have and how are they broken down?
a. 10¹¹ total. Relative numbers: afferent (1), efferent (10), interneurons (200k).
11. What is a synapse?
a. It's where two neurons attach to each other. The presynaptic cell's axons are
communicating with the postsynaptic cell's dendrites.
12. What are glia/glial cells?
a. They make up 90% of the cells in the brain. They play a role in directing
which synapses are formed, hold onto neurons, provide food, form myelin,
and play a role in signaling. They do not fire APs.
13. Which cells have resting potential?
a. Pretty much all of them. It does not correlate with ability to fire an AP. ALL
resting potential is negative.
14. What is the axon hillock?
a. It is the trigger zone where the electrical signal is generated.
15. What is the advantage of electrical signaling?
a. It's very fast.
16. When does chemical signaling occur?
a. Electrical signaling is in the neuron only. Chemical signaling is between
neurons.
17. What are the possible outcomes?
a. Muscle contraction or relaxation
b. Hormone secretion
18. What are myelin sheaths?
a. 20-200 layers of highly modified plasma membrane that help signals to move
more quickly and conserves energy.
19. What are nodes of Ranvier?
a. Spaces between myelin sheaths where the electrical signal is generated as it
propagates down the axon.
20. How do ions move across the membrane?
a. 1. Channels (ligand and voltage gated)
b. 2. Pumps (eg Na+ and K+)
21. What are the relative ion concentrations inside vs outside the cell?
a. K+ is the ONLY one that is higher inside the cell!
22. Why is the Na+/K+ an electrogenic pump?
a. We get 2 K+ in for each 3Na+ out. Builds up the negative charge inside the
cell.
23. What causes the resting potential in a cell?
a. An unequal distribution of charge between the interior and exterior of the cell.
There is a fixed anion on the inside of the cell.
24. What are K+ leak channels?
a. They allow K+ to leak out of the cell until the driving force due to
concentration gradient is equal and opposite to the driving force due to K+
electrical gradient. (remember: from concentration point of view, K+ wants to
flow out but from electrical gradient POV, it wants to move in). The end result
of this is that it makes the inside of the cell MORE negative that we'd have
just from the Na+/K+ pump.
25. What is the Nernst Equation?
a. It allows you to calculate the equilibrium resting potential for an individual ion
only. It does not give the resting potential of the cell overall because more
than one ion contributes.
26. What is the resting potential of a normal cell and what would it be if it was only K+?
a. It is generally -70 but if just K+ was contributing, the Nernst equation would
give us a value of -90.
27. What are oligodendrocytes and how do they differ from Schwann cells?
a. They produce myelin in the brain + spinal cord. Each can branch to make
myelin for 40 axons. Schwann cells are only found in the PNS and produce
individual myelin sheaths.
28. What is the Goldman-Hodgkin-Katz equation?
a. It is an expanded version of the Nernst equation which takes into account the
permeabilities of multiple ions in the cell. Note, resting potential = Vm
29. Why is it a problem to lack Na+ outside the cell?
a. You could move away from resting potential and/or lose water.
30. What is depolarization?
a. When ion movement reduces the charge imbalance of the membrane's
resting potential
31. What is overshoot?
a. The development of a charge reversal (into + territory) during the firing of an
AP
32. What is repolarization?
a. Movement back toward the resting potential
33. What is hyperpolarization?
a. the development of even more negative charge inside a cell (past resting
potential) at the end of an AP.
34. Why does Na+ want to move SO much?
a. It wants to flow into the cell because of both its chemical gradient and its
electrical gradient.
35. How do ligand/chemical gated channels work?
a. 1. Ligand gated which open after receiving a stimulus
b. 2. Voltage gated which open when membrane potential changes.
c. 3. Mechanical (ex touch or channels in ear)
36. What are the types of ion channels?
a. 1. Open = leak channels (have gates, but usually open).
b. 2. Gated.
37. In which direction do electrical signals travel and how do we know it won't go
backwards?
a. From the dendrites to the axons. They don't go backwards due to refractory
periods.
38. The firing of an Action Potential (AP): step by step
a. 1. Steady resting potential is near Ek because Pk>Pna due to K+ leak
channels.
b. 2. Axon sends a chemical neurotransmitter (such as acetylcholine) to the
ligand gated Na+ channel of our dendrite.
c. 3. The ligand gated sodium channel opens and Na+ flows in, bringing the
membrane to threshold by the depolarizing stimulus.
d. 4. The voltage gated channels located at the axon hillock experience the
change in voltage and open, rapidly depolarizing the membrane and allowing
more Na+ to rush in.
e. 5. Inactivation of Na+ channels and delayed opening of K+ voltage gated
channels halts depolarization
f. 6. K+ flows out along electrical gradient, repolarizing the membrane back to
negative.
g. 7. Persistent current through slowly closing K+ channels hyperpolarizes the
the membrane. The Na+ channels are closing.
h. 8. Voltage gated K+ channels close and K+ returns to its equilibrium, the cell
returns to resting potential.
39. What is threshold?
a. The membrane potential at which voltage gated Na+ channels are going to
open.
40. What controls how long the voltage gated channels are open?
a. It is a FIXED time.
41. What does conduction velocity depend on?
a. 1. Axon diameter (bigger = faster due to decreased internal resistance)
b. 2. Level of myelin sheath insulation => because the nodes are the only places
where the AP are generated
c. (where the ions cross the membrane).
42. What is the interaction between the myelin and the nodes?
a. Where myelin is, there is only a flow of current. The nodes keep the signal
fresh and of the same amplitude.
43. What is an inactivation gate?
a. It inactivates the Na+ channel after a certain period of time (while it is still
OPEN) and prevents it from responding to further changes in membrane
potential. It prevents the AP from flowing backward toward the cell body
44. What is the absolute refractory period?
a. The time when most Na+ channels are inactivated, most K+ channels are
open. At the peak of of the polarization chart. New signals won't cause any
affect.
45. What is the relative refractory period?
a. As we cross back down below threshold and into hyperpolarization. Another
AP is possible but we need a larger signal than we did during resting potential
bc we have further to go to reach hyperpolarization. Typically lasts 1-15ms.
46. How do neurotransmitters pass the signal to the postsynaptic cell?
a. They bind with specific proton receptors on the receiving neuron
47. What is axonal transport?
a. Moves organelles and materials up to 1meter along the axon to help maintain
structure and function. The microtubule rails run the length of the axons. The
kinesins (away from body) and dyneins (toward body) bind to cargo and one
end and use energy from hydrolysis of ATP to walk along the microtubules.
Kinesins move anterograde with enzymes, mitochondria,
neurotransmitter-filled vesicles, and organelles. Dyneins move retrograde and
bring recycled vesicles, growth factors, and chemical signals. Retrograde
transport is also how harmful agents can attack the CNS.
48. What determines the magnitude of the resting membrane potential?
a. 1. differences in specific ion concentrations
b. 2. differences in membrane permeability to different ions (depending on # of
channels).
49. In a neuron at rest, was is the order of K+, Cl-, and Na+ channels?
a. Pk>Pcl>Pna.
50. What causes Cl- to be lower in concentration inside of cell?
a. The Na+ and K+ generate a negative membrane potential. The Cl- wants to
flow down its electrical gradient OUT of the cell.
51. What's the difference between grading and action potentials?
a. Grading potentials are for short distance signaling
 b. Action potentials are for long distance signals of neuronal and muscle
membranes.
52. How do we measure the intensity of a graded potential?
a. 1. The degree of depolarization
b. 2. The scope to which depolarization spreads to adjacent regions. (The flow
of charge is decremental).
53. What distinguishes GP and AP? (Graded potential vs action potential)
a. 1. GP can have summation, AP is all or nothing.
b. 2. All AP reach the same amplitude.
c. 3. GP can be depolarizing or hyperpolarizing
d. 4. GP has no threshold.
e. 5. GP is decremental, AP is not.
f. 6. The duration of a GP can vary but is fixed for an AP.
g. 7. GP is caused by environmental stimulus. AP is caused by GP
54. What is excitability?
a. The ability to produce an AP
55. What are the timespans and changes of the AP
a. 1-4 milliseconds and changes of up to 100mV.
56. How far is threshold from resting?
a. About 15mV, so at about -55mV.
57. What is saltatorial conduction?
a. What occurs in myelinated neurons in which action potentials jump from one
node to the next as they propagate along.
58. Why do all AP reach the same amplitude and what is the implication?
a. Because past threshold, the membrane events are caused by the positive
feedback look, not the stimulus itself. As a result, an AP conveys no
information about the size of the signal. So the size of the signal has to be
communicated by the frequencies of APs fired.
59. How do local anesthetics work?
a. They block Na+ voltage gated channels from opening.
60. What effects can drugs have on synapses?
a. 1. Increase leakage of neurotransmitter from vesicle to cytoplasm, exposing it
to enzyme breakdown.
b. 2. Increase transmitter release into cleft
c. 3. Block transmitter release
d. 4. Inhibit transmitter synthesis
e. 5. Block transmitter reuptake
f. 6. Block cleft enzymes that metabolize the transmitter
g. 7. Bind to receptor on postsynaptic cell as antagonist or agonist (most
common)
h. 8. Inhibit or stimulate 2nd messenger activity.
61. What is the effect of synapses?
a. The influence the likelihood that a neuron will fire an AP through excitatory or
inhibitory graded potentials.
62. What is convergence?
a. The idea that information from many cells influences a single cell's activity
63. What is divergence?
a. Allows one information source to affect many pathways
64. What determines the level of excitability in a postsynaptic cell?
a. The number of synapses that are active and the number that are excitatory
vs. inhibitory.
65. What are the two types of synapses?
a. 1. Electrical - rely on gap junctions to directly share electrical signals
b. 2. Chemical - the presynaptic cells has an axon terminal which holds
neurotransmitters in vesicles. The post synaptic cell has density of receptor
proteins. The synaptic cleft prevents direct electrical conduction
66. How is neurotransmitter released?
a. Neuron terminals have voltage-gated Ca2+ channels which open upon
depolarization. These allow Ca2+ to rush into the cell. They bind to a protein
which causes SNARE to undergo a conformational change, either fusing the
vesicle to the presynaptic membrane permanently or in a kiss-and-run fusion.
67. Why don't GPs have refractory periods?
a. Because it does not involved voltage-gated channels.
68. How is a postsynaptic cell activated?
a. The neurotransmitter binds to a ligand gated channel and the membrane
potential changes.
69. What happens to neurotransmitters when they unbind? How do we get remove them
from the cleft?
a. 1. reuptake - active transport back into presynaptic cell
b. 2. diffuse away from receptor site
c. 3. enzymatically transformed into inactive substances.
70. What are EPSPs? (excitatory postsynaptic potential)
a. They open Na+ and K+ channels. They are always in the depolarization
direction.
71. What are IPSPs? (Inhibitory Postsynaptic Potential)
a. They open Cl- and K+ channels. Can be for hyperpolarization or stabilization.
72. What is temporal summation?
a. Input signals occur from the same presynaptic cell but separated by time. The
second occurs before the first has completely died down.
73. What is spatial summation
a. Two inputs occur from two separate synapses.
74. How do we limit the amount of neurotransmitter released?
a. 1. Only a few vesicles undergo exocytosis
b. 2. We can remove the ligand from the synapse
75. Who can neurons talk to?
a. muscle cells, glands, other neurons.
76. What are the two series neurons of the autonomic nervous system called and what
are the functions of each?
a. 1. Preganglionic has cell body in the CNS. → autonomic ganglion→
b. 2. Postganglionic fibers extend from the ganglion cell body to the smooth or
cardiac muscles, glands, or GI neurons. the POSTGANGLIONIC
SYMPATHETIC fibers are the ONLY neurons which secrete
NOREPINEPHRINE.
77. What neurotransmitters do we know?
a. 1. Acetylcholine = all neurons in somatic nervous system and the
preganglionic fiber
 b. 2. norepinepherine = the postganglionic sympathetic fiber only.
78. What kind of receptor is the acetylcholine receptor?
a. It is a ligand-gated channel.
79. How is acetylcholine removed?
a. It is broken down by acetylcholinesterase (closing the channel) and then the
choline is re-uptaken into presynaptic neuron for reassembly.
80. When would we want to inhibit ache
a. If we want to treat symptoms of demyelinating disorders - inhibiting AChE
could help signals to persist longer.
81. What is GABA (gamma-Aminobutyric acid)
a. the main inhibitory neurotransmitter. is amino acid derived
82. What is glutamate
a. excitatory amino acid
83. What are NE and Epi?
a. Catecholamine neurotransmitters. Catecholamines are form from tyrosine.
They share similar structures. Epi has a single methyl group that NE does
not. They can be interconverted in the body by enzyme catalyzed reactions.
84. What is the cerebrum?
a. Forebrain, responsible for reasoning and cognition.
85. What is the cerebellum?
a. Hindbrain, responsible for coordination and movement.
86. What does the brainstem do?
a. Responsible for basic physiological functions such as breathing.
87. How many neurons are there per muscle coming from CNS?
a. 1 neuron per muscle. They can get very long :)
88. Where are receptors for NE and Epi?
a. 1. Smooth muscle
b. 2. Cardiac muscle
c. 3. Gland cells
d. 4. on some CNS neurons
89. Dendrotoxin
a. Blocks voltage gated K⁺ channels in neurons -- effectively blocks
repolarization of cells.
90. Lead
a. Lead competes with calcium for common binding sites and is incorporated
into calcium transport systems in the nervous system, where calcium
regulates neurotransmitter release. Since lead often has a higher affinity for
binding sites on proteins than calcium does, it competitively inhibits the
binding of Ca2+ to neuronal receptors.
91. Tetrodotoxin
a. Blocks voltage gated Na+ toxins.
92. Sarin
a. Irreversible inhibitor of acetylcholinesterase leading to muscle spasms,
respiratory failure
93. Rohypnol
a. increases affinity for GABA, which in turn, allows Cl⁻ ions to flow in and make
it harder/impossible to fire an AP.
94. Caffeine
 a. competitive nonselective cAMP phosphodiesterase inhibitor
95. monosynaptic reflex arc
a. single neuron between sensory neuron and motor neuron. eg, knee jerk
protective mechanism.
96. polysynaptic reflex arc
a. includes at least one interneuron between sensory and motor neuron. eg
when you step on a tack and know to put your OTHER foot down as your
affect foot withdraws.
97. vagus nerve
a. one of 12 cranial nerves, is responsible for many parasympathetic effects in
thoracic and abdominal cavities
98. Interoreceptors
a. sensory neurons that monitor internal environment parameters (blood volume,
blood pH, pCO2 in blood.
99. Proprioceptors
a. sensory neurons important for position sense (ie how we maneuver in our
houses in the dark)
100. Exteroreceptors
a. sensory neurons that monitor external environment ie touch, light, sound,
taste, pain, temperature
101. Nociceptors
a. sensory neurons for pain that relay that into to the brain.