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Neurotransmitter Flashcards
1. Where are dendrites located?
2. What does this allow them to do?
3. When do dendrites transmit signals?
Dendrites transmit signals after the opening of
4. When do LGC (Ligand-gated channels) open?
5. What do LGC’s have receptors for?
These open when a ligand (neurotransmitter) binds
to them. They do not need an action potential to
open them.
6. Where are LGC’s located?
7. Why is it important to understand ion
8. What do positive amino acids repel against?
9. What do negative amino acids repel?
10. What do amino acids on ligand gated channels
11. What ions have their own ligand gated
12. What would happen to the resting membrane
potential (RMP) if the sodium channel opened?
13. What would happen to the resting membrane
potential (RMP) if the potassium channel
14. What would happen to the resting membrane
potential (RMP) if the chloride channel
15. What is the Excitatory Postsynaptic Potential
• dendrites only
Many human diseases are from dysfunction of ion
Ions with a positive charge
Ions with a negative charge
Ion selectivity (what ions pass)
16. What does “postsynaptic” refer to?
17. What happens when a NT binds to a LGC?
It opens a sodium channel, so Na+ rushes into the cell.
That makes the inside of the cell more positive.
Approximately Minus 70 mV
We need to get to +30mV to have an action potential
excitatory postsynaptic potentials (EPSP)
Dendrites are spaced in all directions from
neuronal soma.
This allows signal reception from a large spatial
area providing the opportunity for summation of
signals from many presynaptic neurons
Sodium, Potassium, and Chloride
Na+ has a positive charge, so the RMP would become
less negative and go closer to threshold.
K+ would leave with its positive charge, so the RMP
would become more negative and go farther from
Cl- has a negative, so the RMP would become more
negative and go farther from threshold.
The increase in voltage above the normal resting
potential (to a less negative value) is called the
excitatory postsynaptic potential.
Postsynaptic refers to the dendrite of the neuron
receiving the signal.
18. What mV is the resting membrane potential?
19. How many mV do we need to reach threshold?
20. What type of action potential opens sodium
channels, EPSP or IPSP?
21. What type of action potential opens K+ and Cl- Inhibitory postsynaptic potentials (IPSP)
channels, EPSP or IPSP?
Neurotransmitter Flashcards
22. When a K+ channel opens, which direction
does K+ move, and what happens to the inside
of the cell membrane?
It rushes out of the cell, and the inside of the cell
membrane becomes more negative, farther from
starting an action potential.
23. When a Cl- channel opens, which direction
does Cl- move and what happens to the inside
of the cell membrane?
24. What determines whether a neuron “responds”
or not?
It rushes into the cell, and the inside of the cell
membrane becomes more negative, farther from
starting an action potential.
It depends on temporal (how fast) and spatial (how
many) summation of EPSPs and IPSPs
25. Do EPSP’s fire at the same time as IPSP’s?
There might be EPSP’s firing at the same time as
26. If Excitatory and inhibitory postsynaptic
potentials are firing at the same time, how do
you know which one wins?
Add up all the charges from the excitatory and
inhibitory potentials to see which one wins!
27. What is Temporal Summation?
When the same presynaptic neuron fires repeatedly
28. What is Spatial Summation?
When additional presynaptic neurons fire
29. What can cause changes in the voltage of an
excitable cell?
30. When a cell membrane is depolarizing, is it
going closer to threshold or farther away?
31. What neurons fire in people with Parkinson’s
disease: excitatory, inhibitory, or both?
32. What general effect does this cause?
33. What are the symptoms of people with
Parkinson’s disease?
Electrical or mechanical stimulation
34. At threshold, what happens to sodium
35. What 2 types of channels allow sodium
channels to open?
36. When do LGC’s open so sodium can enter the
Closer to threshold
Problems with coordinating movement
They have trouble starting and stopping any motion
and shake at rest
They open, and sodium rushes into the cell
LGC, when a neurotransmitter binds to it
VGC, when the cell membrane charges change
When a neurotransmitter (a ligand) binds to them.
Neurotransmitter Flashcards
37. When do VGC’s open so sodium can enter the
38. What other ions use VGC’s?
When the charge of the inside of the cell membrane
goes from negative to positive.
Potassium, chloride, and calcium
39. What type of VGC is it when it is selective for
potassium or chloride instead of sodium?
It is an inhibitory VGC. If K+ leaves the cell or if Clenters the cell, the inside becomes more negative,
farther from an AP
It is an excitatory VGC. If Na+ or Ca++ enters the
cell, the inside becomes more positive, making it
closer to an AP
Dendrites only
On the axon, from the hillock to synaptic knobs.
They open.
40. What type of VGC is it when it is selective for
41. On what part of a neuron are LGC’s located?
42. On what part of a neuron are VGC’s located?
43. What happens to Na+ channels during
44. Does the amplitude of the action potential
change? (how strong the AP is)
45. Does the frequency of the action potential
46. What is the frequency pattern?
47. The speed of the Action Potential depends on
what two things?
48. How does the action potential event occur?
No, the amplitude of the action potential does not
Yes, the frequency of the action potential does change.
The frequency pattern is a code (like Morse Code) that
transmits information about the stimulus (light, sound,
taste, smell, touch) to the brain.
The size of the neuron fiber (larger is faster) and
whether or not its axon is myelinated (myelinated are
The AP is a passive event: ions diffuse down their EC
gradients when gated channels open. A “wave of
depolarization” occurs along the neighboring areas.
Occurs in one direction along the axon
There is a refractory period (Na+ channels become
49. Why does the action potential regenerate over
and over at each point of diffusion of incoming
50. What are the attributes of saltatory conduction? Saltatory conduction occurs in myelinated axons.
-AP’s only occur at the nodes (Na channels
concentrated here!)
-increased velocity
-energy conservation
51. Why should a child under 3not be on a low fat Children under 3 should not be on a low fat diet
because a lot of the myelin has not yet been produced.
52. Why is a neuron with myelin more efficient
than one without?
Neurons that have myelin are more efficient because
they use less ATP.
53. What autoimmune disorder destroys the body’s Multiple Sclerosis
myelin sheaths?
Neurotransmitter Flashcards
54. How many people have MS in the United
55. What is the female to male ratio?
56. Who has the highest incidents?
57. What are the symptoms of MS?
58. Why don’t patients report these symptoms to
their doctors?
59. How does the diagnostic of MS begin?
60. What 2 structures are important to the function
of the synapse?
61. What structure in a neuron contains
neurotransmitter substances to excite or inhibit
postsynaptic neurons?
62. What organelle provides most of the energy to
synthesize a neurotransmitter?
63. What does membrane depolarization by an
action potential cause?
64. What structure do presynaptic membranes
65. Depolarization of the presynaptic membrane
by an action potential opens what channels?
66. When calcium floods into the neuron, what
67. Where does the neurotransmitter go when it is
68. What happens when the LGC opens?
69. As the neurotransmitter binds to the receptor
(LGC) on the postsynaptic membrane, what 2
kinds of electrical signals can the
neurotransmitter generate?
70. How is the NT removed from the LGC?
71. Where are Voltage- gated calcium channels
72. Where are receptor proteins for the released
neurotransmitter located?
73. What makes the energy for neurotransmitter
74. What types of channels are in the axon of the
presynaptic neuron, and what ion crosses that
1 in 1000
2 to 1
Whites of Northern European descent
Patients have a difficult time describing their
symptoms. Symptoms are bizarre and unrelated.
Sometimes they have: Parasthesias (tingling sensation)
of hands that resolvefollowed by in a couple of
months with weakness in leg or visual disturbances
Because they often resolve before the doctor
Eventually, the neurological problems stop resolving
completely, and they occur more frequently. That is
when doctors suspect MS.
Presynaptic vesicles and Mitochondria
Presynaptic vesicles
Emptying of a small number of vesicles into the
synaptic cleft.
voltage gated calcium channels
It causes the neurotransmitter to be released.
It lands on receptor proteins on the post-synaptic cell
called ligand-gated channels (LGC) and opens them
Ions diffuse in or out depending on the type of LGC
Excitatory Postsynaptic Potential (EPSP)
Inhibitory Postsynaptic Potential (IPSP)
Destruction by enzymes or diffusion away, back into
the presynaptic cell to be recycled.
In the synaptic knob of the presynaptic neuron
On the post-synaptic cell membrane
VGC for sodium, allows Na+ to enter the cell
Neurotransmitter Flashcards
75. What types of channels are in the synaptic
knob of the presynaptic neuron, and what ion
crosses that channel?
76. What does calcium do in a neuron?
77. What types of channels are in the dendrite of
the presynaptic neuron?
VGC for calcium, allows Ca++ to enter the cell
78. What does the neurotransmitter do?
It binds to the LGC, which causes nearby VGC’s to
Excitatory and Inhibitory
Depolarization or Hyperpolarization
EPSP: excitatory post-synaptic potential (the dendrite
receiving the signal continues the action potential)
IPSP: inhibitory post-synaptic potential (the dendrite
receiving the signal stops the action potential)
79. What are two categories of VGC’s?
80. The change in voltage causes what?
81. If it causes depolarization, what type of action
potential is it called?
82. If it causes hyperpolarization (going farther
from an action potential, what type of action
potential is it called?
83. By what process are NT’s released, and what
ion triggers it?
84. How does the NT get across the synaptic cleft?
85. What is a graded potential?
86. The effect of a neurotransmitter is dependent
on what 3 factors?
87. What happens to the voltage on the
postsynaptic cell if it experiences an EPSP?
88. What happens to the voltage on the postsynaptic
cell if it experiences an IPSP?
89. Neurotransmitters are released in response to
90. When NTs are released in response to
presynaptic depolarization, what is molecule is
91. In order to allow another cycle of NT release,
binding and signal transmission, what must be
done to the NTs?
92. What do sympathetic neurons do to the heart
rate and blood pressure? What broad group of
responses is this called?
93. What do parasympathetic neurons do to the
heart rate, blood pressure, and food digestion?
What broad group of responses is this called?
94. Is the heart innervated by sympathetic neurons,
parasympathetic neurons, or both?
Causes release of the neurotransmitter
LGC (they bind to neurotransmitters)
Released by exocytosis.
It is triggered by Ca++
the more channels there are, the more the charge
1. The selectivity of the channel (which ions are
allowed to diffuse across membrane; Na+, K+, Cl-)
2. How many ions diffuse across the membrane
3. How long do the ions diffuse across the membrane
The voltage becomes more positive; closer to
The voltage becomes more negative; farther from
PRE-synaptic depolarization
The NTs must be removed by reuptake by presynaptic
nerve or degrading by specific enzymes or a
combination of these.
Increase heart rate
Increase blood pressure
“Fight or Flight” responses
Decrease heart rate
Decrease blood pressure
Increase food digestion
“Rest and Digest” responses
Both. The heart is innervated by both sympathetic and
parasympathetic neurons
Neurotransmitter Flashcards
95. In a dually innervated organ, how will the
organ know if sympathetic or parasympathetic
is barking louder?
96. Why are a lot of organs dually innervated?
97. What neurons can cause excitation in one
organ yet inhibition in another?
98. What happens when the parasympathetic
system is suppressed?
99. If a drug mimics the parasympathetic system,
how will it affect the heart?
100. If a drug mimics the sympathetic system, how
will it affect the heart?
101. What effect does epinephrine have on the heart
102. What effect does atropine have on the heart
103. What two medicines are given when a person’s
heart stops?
104. What complicates the healing for a post-op
heart transplant patient?
105. Why must the post-op heart transplant keep
themselves from becoming overly anxious, angry
or sexually aroused?
106. How can we use the parasympathetic system to
make the heart cells less active?
107. What is the number one way to regulate the
Heart Rate?
108. What are two ways of classifying
109. What are the two types of chemical
classification of NT’s?
110. What is an example of a large molecule NT?
111. What are the 3 small molecule NT categories?
112. What are the two types of functional
classification of NT’s?
113. What are three categories of small molecule
NT’s and examples of each?
The receptors that have the most transmitters bound
will cause the biggest result.
To adjust to their physiology
Sympathetic and Parasympathetic
The sympathetic system will gain more control.
Heart rate will be slower
Heart rate will increase
It increases heart rate by stimulating the sympathetic
nervous system
It increases heart rate by blocking the parasympathetic
nervous system
Epinephrine and atropine
Nerves that innervate the heart are cut and there is no
way to suture them back.
These emotions can release epinephrine because it is a
hormone, not a nerve but the patient no longer has
parasympathetic neurons attached to the heart to
counter the effects of epinephrine.
Use a medicine that opens the potassium channels,
making the inside of the cell more negative
Use a medicine that opens the potassium channels
Chemical classification
Functional classification
Large Molecule
Small Molecule
Amino Acids
1) Cholinergic (Acetylcholine)
2) Catecholamines (epinephrine, norepinephrine,
dopamine, serotonin)
3) Amino Acid NT’s (glutamate, GABA, glycine)
Neurotransmitter Flashcards
114. List 3 large molecule (peptide) NT’s and their
115. What effect does Bradykinin have on blood
122. What effect does Ach, epinephrine,
angiotensin, and ADH have on blood pressure?
116. What is an example of a cholinergic NT?
117. What are the 3 types of catecholamines, and an
example of each?
118. What are the 3 main Amino Acid NT’s?
119. Which ones are excitatory and which are
120. What is an adrenergic neuron?
121. What is a dopaminergic neuron?
122. What is a serotonergic neuron?
123. What are cholinergic neurons?
124. What type of muscle is innervated by
cholinergic neurons?
125. Which NT causes contraction of skeletal
126. Is acetylcholine used by sympathetic neurons,
parasympathetic neurons, or both?
127. How is Acetylcholine removed from the
synaptic cleft?
1) ADH (anti-diuretic hormone, AKA
Vasopressin) increases blood volume, which
increases BP
2) Angiotensin, which causes vasoconstriction,
which also raises BP
3) Bradykinin, which causes vasodilation, which
lowers BP
Lowers it
Raises it
Acetylcholine (Ach)
1) Adrenergic
a) Norepinephrine
b) Epinephrine
2) Dopaminergic
a) Dopamine
3) Serotonergic
a) Serotonin
Glutamate (excitatory)
GABA (inhibitory)
Glycine (inhibitory)
One that makes epinephrine or norepinephrine
One that makes dopamine
One that makes serotonin
Neurons that use the neurotransmitter, Acetylcholine
Skeletal Muscle
Acetylcholine (ACh)
Acetylcholine is removed from the synaptic cleft by
the enzyme, Acetylcholine esterase (AChE)
128. Treatment of Myasthenia gravis is to give a
Acetylcholine (ACh)
medicine that inhibits the enzyme that degrades this
129. What is the very important Amino acid in the
CNS that nearly all excitatory neurons use?
130. What does too little glutamate cause?
Leads to psychosis (delusional, paranoid, lack of
contact with reality.)
131. What does too much glutamate cause?
Excitotoxicity due to unregulated calcium influx.
132. What causes too much glutamate to be
Neuronal death.
133. What common ailment causes neuronal death? Stroke
Neurotransmitter Flashcards
134. What group of medicines are used when a
person has too much glutamate released (such as
after a stroke)?
135. Antagonists to which neurotransmitter helps
stop neuronal death after a stroke?
136. Why are strokes or trauma to the brain so
dangerous in relation to neurotransmitters?
137. What effect does it have when excessive
neurotransmitters are released after a trauma?
138. What causes Parkinson’s and Alzheimer’s
139. What agent is given to those who have stroke?
Glutamate antagonists
When damaged, neurons release a lot of
They cause over-stimulation of nearby neurons, which
then release too much calcium, causing cytotoxicity. It
can kill the cell.
10% of the time it is genetic. 90% of the time it is
caused by calcium dyshomeostasis (The calcium is not
being monitored properly in the body).
Glutamate Antagonist
140. What happens if you don’t have enough
Inhibitory NTs will gain momentum. Too little
glutamate leads to psychosis, perceives reality
differently than normal.
141. What is the major inhibitory neurotransmitter
in CNS?
142. Decreased GABA causes what symptoms?
143. What type of medicines target GABA
receptors to act as GABA agonists?
144. What two substances stimulate GABA
receptors, and so are considered to be GABA
145. When a person is detoxing from alcohol abuse,
what medicine is given, what symptom does it
prevent, and how does the medicine work (what is
its mechanism of action)?
146. What two neurotransmitters are inhibitory?
147. Alcohol stimulates what 2 neurotransmitters?
148. What effect does alcohol have on GABA
149. When GABA receptors are stimulated, what
type of action potential is generated?
150. What effect do IPSP’s have on the reflexes and
151. When alcoholics try to stop drinking all at
once, what type of transmitters gain control?
152. What effect do excitatory NT’s have?
They slow down. Reflexes decrease, speech slurs.
153. Recovering alcoholics need what medicine
while weaning off the alcohol?
Benzodiazepam (valium)
Benzodiazepines (valium) and drinking alcohol
Benzodiazepine (valium) is given to prevent seizures
during detox. Valium binds onto the GABA receptors,
stimulating them. This causes inhibition of the CNS,
preventing seizures.
GABA and Glycine
GABA and Glycine
Alcohol stimulates GABA receptors.
Inhibitory Post Synaptic Potentials (IPSP’s)
Excitatory NTs gain control.
Tremors and visual overstimulation (hallucinations).
Neurotransmitter Flashcards
154. Recovering alcoholics can be given what class
of drugs? What is an example of this medicine?
155. What effects do benzodiazepines (such as
valium) have on GABA receptors?
156. What disorders is valium used for?
157. What organ releases adrenergic
catecholamines, and when are they released?
158. Catecholamines are part of which branch of the
autonomic nervous system?
159. What degrades catecholamines?
160. What effect does an MAO inhibitor have on
the nervous system?
161. What are MAO inhibitors used for?
163. What types of medicines cannot be used on a
patient taking an MAO inhibitor? Why not?
164. What are some examples of Sympathomimetic
165. Where is epinephrine secreted?
166. Is epinephrine excitatory or inhibitory?
167. Where is norepinephrine secreted?
168. What neurotransmitters speed up the heart
rate? To what branch of the ANS does it belong?
169. Where is dopamine secreted?
170. Is dopamine excitatory or inhibitory?
171. What secretes serotonin?
172. Is serotonin excitatory or inhibitory?
173. What causes Parkinson’s disease?
174. What symptoms characterize Parkinson’s?
175. How is Parkinson’s treated?
176. What are the side effects of the treatments?
177. What region of the brain contains the neurons
that move the muscles of the skeleton?
178. What region of the brain regulates body
movements by communicating with the motor
GABA Agonists (drugs that act like GABA), such as
anti- convulsants like Benzodiazepam (valium)
They enhance the effects of GABA, which results in
sedative, hypnotic (sleep-inducing), anxiolytic (antianxiety), anticonvulsant, muscle relaxant, and amnesic
Treating anxiety, insomnia, agitation, seizures, muscle
spasms, alcohol withdrawal and as a premedication for
medical or dental procedures.
Adrenal glands in response to fight or flight emotions
Sympathetic Nervous System (fight or flight)
Mono-amine oxidase (MAO)
Allows catecholamines to excite the nervous system.
Anti-anxiety and anti-depression medications
SYMPATHOMIMETIC (those that imitate
catecholamines). . It doubles the excitatory effect in
the nervous system and can be deadly. The person’s
blood pressure goes up to a crisis level.
Medicines for cardiac arrest, low blood pressure, and
some meds that delay premature labor.
Adrenal gland
Mainly secreted by adrenal gland, and also by some
neurons in the CNS and by the sympathetic postganglionic neurons.
Epinephrine and Norepinephrine; sympathetic
Neurons in the CNS (substantia nigra)
Neurons in the CNS
Mainly excitatory. It can excite one cell but inhibit
It is a loss of dopamine from neurons in substantia
nigra of the midbrain.
Resting tremors, “pill rolling”, Bradykinesia (slow
With L-dopa or MAO inhibitors.
Hallucinations, motor problems.
The motor cortex
The basal nuclei
Neurotransmitter Flashcards
179. What region of the brain inhibits some motor
neurons so that unwanted body movements do not
180. What region of the brain regulates stopping,
starting, and coordination of movements?
181. What region of the brain is like a strict parent
that ties their kids up to keep them from doing wild
182. What region of the brain secretes dopamine?
183. What effect does dopamine have on the basal
184. What region of the brain, and which NT are
like bosses who tie up the basal nuclei? How does
this effect movement?
185. What are the 2 reasons basal nuclei do not
work correctly?
186. What are the 2 most common disorders of the
basal nuclei?
187. Parkinson’s disease is a problem in what
region of the brain?
188. What NT is secreted by that region of the
189. People with Parkinson’s disease lack which
190. What happens when there is not enough
191. What are the four cardinal symptoms of
Parkinson’s disease?
192. What disease has symptoms that are the
opposite of Parkinson’s disease?
193. What types of movements are seen in
Huntington’s disease?
194. What area of the brain is damaged in
Huntington’s disease?
195. What is the function of the basal nuclei in the
brain (between the corpus callosum and thalamus)?
196. Most regions in the brain use what NT?
197. The basal nuclei in the brain use what NT?
198. What happens if the basal nuclei are damaged?
The basal nuclei
The basal nuclei
The basal nuclei
The substantia nigra
It inhibits the basal nuclei (inhibits the inhibitor). That
allows the excitatory neurons to allow the body to
The substantia nigra and dopamine are like bosses that
tie up the basal nuclei (the parent). With the inhibitor
(parent) tied up, the kids (muscles) are no longer tied
up, so they throw a party (body movements occur)
Either the basal nuclei themselves are dysfunctional or
the dopamine levels are not correct
Parkinson’s Disease (dopamine problem) and
Huntington’s Disease ( basal nuclei problem)
Substantia nigra of the midbrain.
The brain cannot initiate body movements.
1) Tremor (pill-rolling tremor at rest)
2) Bradykinesia (slowness of movement) They
have trouble initiating movements (taking the
first step, getting up from a seated position,
begin to reach out for something)
3) Rigidity (neck and shoulders first)
4) Postural instability (frequent falls)
Huntington’s disease
Sudden, jerky movements. Their body writhes around
like they are dancing (chorea).
The basal nuclei.
It inhibits some motor neurons so that unwanted body
movements do not occur
Excitatory neurotransmitters
GABA (inhibitory)
Excitatory neurons are no longer inhibited, so they
make the body move when movement is not intended.
Neurotransmitter Flashcards
199. Describe the malfunction in the brain of
someone with Huntington’s disease.
200. What are other symptoms in a person with
Huntington’s disease?
201. How does one get Huntington’s disease, and at
what age does it manifest?
202. What is the effect of taking too much of the
street drug, “Meth”?
203. If you lose excitatory neurons, what neurons
gain an advantage?
204. What do Parkinson’s patients have problems
205. What is the treatment for Parkinson’s disease?
206. What stem cell research is being tried for
Parkinson’s disease?
207. Serotonin is synthesized from what amino
208. What medicines are serotonin reuptake
209. What neurotransmitter is released by the street
drug, ecstasy?
210. What NT is called the mood elevator, feel
good transmitter?
211. What is the effect of taking an SSR inhibitor?
212. When is this medicine prescribed?
213. What is phenylalanine (an amino acid)
converted into?
214. What is tyrosine converted into?
215. What is L-Dopa converted into?
216. What is dopamine converted into?
217. What is norepinephrine converted into?
218. Write the pathway of phenylalanine 
219. Catecholamines (such as epinephrine) are
made from which amino acid?
Since the basal nuclei are damaged, the inhibition of
the motor cortex is removed, so excitatory neurons go
unchecked, and the person has sudden jerky
Cognitive decline and psychiatric problems
It is genetic and hereditary (50% chance of each child
getting it if one parent has it).
Age of onset is usually 35-45 years of age.
It kills dopaminergic neurons, causing Parkinson’s
Inhibitory neurons
Starting movements, and coordinating the
excitatory/inhibitory stimulus to muscles while
walking. Stopping motions is also hard. They need a
trained dog to pull them up from a seated position and
help them to take the first step, and to stop them when
they want to stop.
An MAO inhibitor or L-dopa, which can cross BBB,
unlike dopamine.
Stem cells research involves injecting stem cells to
cause the remaining neurons to replicate and help them
get more control.
anti-depressant drugs
- It helps serotonin stay in the cleft longer, causing the
person to feel better, having an elevated mood. It is
prescribed for depression.
tyrosine (another amino acid)
Phenylalanine  TYROSINE  L-DOPA 
dopamine  norepinephrine  epinephrine
Tyrosine, which is made from phenylalanine
Lack of the enzyme to convert phenylalanine to
Neurotransmitter Flashcards
221. If you lack that enzyme, what happens?
Waste products (ketones) build up in the blood, and
are toxic to neurons.
222. What are the symptoms of PKU?
Seizures, poor motor development, mental retardation
223. How do you get PKU?
It is genetic. When you marry your sibling or first
cousin, you are more likely to have a child with PKU
224. How is PKU screened for?
It is part of what is tested for in routine heel stick
blood sample in newborns
225. When a person is diagnosed with PKU, how do Prevented by dietary restriction of phenylalanine.
you prevent the symptoms?
They cannot have whole protein during childhood,
when the nervous system is developing (until age 20).
After that, they can go off the diet, but ketones will
begin to accumulate.
226. How will a person feel if there are too many
They start to feel sluggish, and can’t finish a task on
ketones in the body?
time. They need to go back on the diet for a while.
227. What happens to a female and her fetus if there A woman must stay on the diet during pregnancy or
is too many Ketones during pregnancy?
the ketones will cross the placental and kill the neurons
of her baby.
228. What types of foods should be avoided for a
person with phenylketonuria?
Artificial sweeteners such as Sweet N Low and diet
sodas are high in phenylalanine, and must be avoided
in PKU patients.
229. What are the two types of ACh receptors?
• Muscarinic ACh receptors
• Nicotinic ACh receptors
230. What are muscarinic Ach receptors (mAChR)?
They are Ach receptors that area more sensitive to
muscarine than to nicotine
231. What effect do muscarinic substances have?
Activate the parasympathetic nervous system (rest and
digest). Increased saliva, tears, and diarrhea.
Muscarinic ACh receptors
232. When this receptor is stimulated, there is
increased saliva, tears, and diarrhea
233. What is the antidote for overdose of
muscarinic substances?
234. Do muscarinic substances use G-proteins to
activate a nearby ion channel?
235. What are nicotinic Ach receptors (nAChR)?
236. What effect do nicotinic substances have?
237. Do nicotinic substances use G-proteins to
activate a nearby ion channel?
They are Ach receptors that area more sensitive to
nicotine than to muscarine
Acts as a stimulant: increases dopamine (in the reward
center of the brain), which causes euphoria and
relaxation, and it is addictive.
Nicotine has a higher affinity for acetylcholine
receptors in the brain than those in skeletal muscle
No; they open ion channels directly.
Neurotransmitter Flashcards
238. What body part contains both muscarinic and
nicotinic receptors?
239. What are the two types of adrenergic
240. What are the 2 types of adrenergic receptors?
241. What are the 2 types of alpha receptors?
242. What effect do the alpha 1 receptors have on
blood vessels and GI motility?
243. What effect do the alpha 2 receptors have on
blood vessels and GI motility?
244. What 2 receptors, when stimulated, causes
vasodilation, which decreases blood pressure?
245. Do Alpha 2 and Beta 2 receptors slow the
heart rate?
246. Are Alpha 2 and Beta 2 receptors used by the
parasympathetic neurons?
247. What are the 2 types of beta receptors?
248. What effect do the beta 1 receptors have on
heart rate and cardiac output?
249. What effect do the beta 2 receptors have on
blood vessels, GI motility, and bronchioles?
250. What protein is used by adrenergic receptors?
251. What are ionotropic receptors?
252. What are Metabotropic receptors?
253. What are 5 examples of ionotropic receptors?
254. What are 3 types of metabotropic receptors?
Skeletal muscle, which contracts when Ach binds
Alpha adrenergic receptors
Alpha 1 receptors
Alpha 2 receptors
Beta adrenergic receptors
Beta 1 receptors
Beta 2 receptors
Alpha and Beta adrenergic receptors
Alpha 1 and Alpha 2
Vasoconstriction (increases BP)
Decreases GI motility
Vasodilation (decreases BP)
Decreases GI motility
Alpha 2 receptors
Beta 2 receptors
No, only Beta 1 has an effect on the heart rate, and it
increases it.
No, they are adrenergic receptors, so they are used by
the sympathetic neurons, although their effect helps
the parasympathetic system by turning down the
sympathetic effects (making the water hotter by
turning down the cold water)
Beta 1 and Beta 2
Increases HR
Increases CO
Vasodilation (decreases BP)
Decreases GI motility
Opens bronchioles
Those that bind to a NT and have a channel that
extends into cell. They are the receptor and the
They need a series of enzymatic actions to change a
gated channel somewhere else. The binding of the NT
outside of the cell activates a G-protein on the inside
of the cell which breaks apart into two pieces. One of
those pieces goes somewhere else in the membrane to
open up another channel.
Nicotinic AChR
Serotonin receptors
Glutamate receptors
GABA receptors
Glycine receptors
Muscarinic AChR
Alpha and Beta Adrenergic receptors
Dopaminergic receptors
Neurotransmitter Flashcards
255. What 2 things happen when the G-protein is
256. What is one change that can occur during Gprotein activation?
257. What are the three sequences of events in a
metabotropic receptor?
258. What 2 types of receptors does Ach bind to?
259. What type of receptor does Norepi and epi
bind to?
260. What receptors use G-proteins?
261. Where are G-proteins found?
262. What are the 2 types of G-proteins?
263. Which type of G-protein will lead to events
that increase the activity of a cell?
264. When the G-proteins breaks into two pieces,
one of them acts as a second messenger. What does
this second messenger do?
265. What do G-Proteins of sympathetic s neurons
266. What do G-Proteins of parasympathetic s
neurons activate?
267. Why is kinase activity important?
268. What are the 3 categories of small molecule
269. Name the 5 neurotransmitters that use
ionotropic receptors. Which are inhibitory?
270. Name the 4 neurotransmitters that use
metabotropic receptors.
271. What are acetylcholine receptors called?
272. What are the two types of Ach receptors?
273. What are the three categories of
It breaks into two pieces. One of the pieces is called
the second messenger, which is the part that opens the
nearby ion channel. It also activates other enzymes
inside the cell, which may cause various changes.
• These changes include activation of gene
transcription (to form new proteins, changing
the metabolism; used especially in making new
Step 1: NT binds to receptor
Step 2: The G proteins activate
Step 3: Second messenger activates another protein
called the late effector protein
Muscarinic and nicotinic receptors
adrenergic receptors
Muscarinic Ach, adrenergic and dopaminergic
Every cell in the body
GS (stimulating G protein)
GI (inhibiting G protein)
GS (stimulating G protein)
activates another protein called the late effector protein
protein kinase A
protein kinase B
Phosphorylates (puts a phosphate molecule on) other
proteins in a cell. This changes the activity level of the
Acetylcholine (Ach), Catecholamines, and Amino
Acid NT’s
Nicotinic Ach
GABA (inhibitory)
Glycine (inhibitory)
Muscarinic Ach
Muscarinic and Nicotinic
Neurotransmitter Flashcards
274. What are the 2 NT’s which are adrenergic?
275. What is the NT that is dopaminergic?
276. What is the NT that is serotonergic?
277. What are the 3 Amino Acid NTs? Which are
278. What are the three types of Catecholamines?
GABA (inhibitory)
Glycine (inhibitory)
1. Adrenergic catecholamines:
• Norepinephrine
• Epinephrine
2. Dopaminergic catecholamine:
• Dopamine
3. Serotonergic catecholamine:
• Serotonin
Summary Slide
279. What are the three types of metabotropic
receptors, and which branch of the ANS uses each?
muscarinic acetylcholine (mostly used by postganglionic parasympathetic neurons)
Alpha and Beta adrenergic receptors (mostly
used by post-ganglionic sympathetic neurons)
Dopaminergic (mostly sympathetic)
Neurotransmitter Flashcards
280. Sympathetic neurons that secrete ACh use
• Muscarinic and nicotinic
what receptors?
281. Sympathetic neurons that secrete epinephrine
• adrenergic receptors (metabotropic)
primarily use what receptors?
282. Parasympathetic neurons that secrete
• Parasympathetic neurons do not secrete
epinephrine use what receptors?
283. Are metabotropic receptors used by
• Both
sympathetic, parasympathetic, or both?
284. When Sympathetic neurons try to speed up the
• adrenergic (alpha and beta); use norepinephrine
heart rate, they will stimulate which receptors? What
as the NT
NT do they use?
285. When they do this, are they using an ionotropic
• Metabotropic because they bind G-protein.
or metabotropic receptor? Why?
286. When Parasympathetic neurons try to slow the
• muscarinic receptors use ACh as the NT
heart rate, they will stimulate which receptors? What
NT do they use?
287. When they do this, are they using ionotropic or
• Metabotropic because they bind G-protein.
metabotropic receptors? Why?
Note for clarification:
All sympathetic and parasympathetic preganglionic neurons secrete ACh.
All postganglionic parasympathetic neurons also secrete ACh.
Postganglionic parasympathetic neurons use muscarinic receptors.
About 98% of postganglionic sympathetic neurons secrete epi or norepi, but 2% of postganglionic sympathetic
secrete Ach, so those are the ones that would use muscarinic receptors as well.
286) What is flaccid paralysis?
When the muscle cannot contract at all. The muscle
stays weak and floppy.
287) What is spastic paralysis?
288) Name four sodium VGC blockers. Do they
cause flaccid or spastic paralysis?
When the muscle stays in contraction. You still cannot
move the muscle properly, but in this case, the muscle
is too rigid.
They all cause flaccid paralysis
289) Which of the above four sodium VGC blockers Lidocaine
will DIRECTLY block the sodium channel?
290) Which one is from shellfish toxins?
291) Which one is from a puffer fish?
292) Which one is a local anesthetic?
293) How does lidocaine cause flaccid paralysis?
It inhibits action potentials by blocking sodium VGC
so you can’t have an action potential.
294) Can you get an action potential if a sodium
VGC blocker is present?
Neurotransmitter Flashcards
295) What type of paralysis is caused by a sodium
VGC blocker?
296) How are botulism toxin and curare similar?
297) How are botulism toxin and curare different?
298) Name one vesicle blocker
299) What is botulism, and where does it come
300) Where might botulism be found in your house?
301) What symptom does botulism cause, and what
is the cause of death?
302) What are two medicinal uses for botulism
303) Name 2 muscarinic Ach blocker/competitors
304) Is atropine considered a sodium VGC blocker?
They both cause flaccid paralysis because muscles
cannot contract.
Botulism causes flaccid paralysis by inhibiting ACh
RELEASE, while curare blocks ACh RECEPTORS.
It is a protease (an enzyme that breaks down proteins).
It is from a bacterium
Undercooked turkey and dented cans of food.
Inhibits ACh neurotransmitter release; muscles can’t
contract; flaccid paralysis. Cause of death is from
suffocation because the diaphragm is paralyzed.
Botox injections and migraines.
Atropine and opium derivatives
No, it is a mACH blocker. It still causes flaccid
paralysis, but not by directly blocking the sodium
VGC. Instead, mACH receptors are metabotropic (use
the G protein), so atropine blocks the Na+ VGC
305) What kind of paralysis do ACh blockers cause? Flaccid paralysis
306) What types of muscles can atropine effect?
Heart, smooth muscle (such as intestines), and glands.
307) Do muscarinic Ach blockers affect the
They block the parasympathetic nervous system so the
sympathetic system, parasympathetic system or
sympathetic gets more control.
both? Do they activate that system or block it?
308) What effect on the intestines will a muscarinic Flaccid paralysis of the intestines
Ach blocker have?
309) What is a medicinal use for atropine?
If the heart has slowed down too much or stopped,
inject atropine to block the mACh receptors in the
heart, and heart rate increases.
310) What type of muscle is the iris made of?
311) If you block Ach, what happens to the pupil?
The iris relaxes, opening the pupil, so it is dilated.
312) What group of illegal drugs stimulates
Chemical warfare drugs (other than sarin gas).
muscarinic Ach receptors? What effect does it
Causes parasympathetic system to increase activity.
Person has gut motility, diarrhea, sweat, salivation.
313) How does sarin gas differ from other chemical Sarin gas inhibits ACh-ase
warfare drugs?
The other chemical warfare drugs imitate ACh by
irreversibly landing on the muscarinic ACh receptors.
314) How is sarin gas the same as other chemical
Their effects are the same: spastic paralysis and death
warfare drugs?
by suffocation. They both also stimulate the
parasympathetic nervous system, so the victim has
increased gut motility, diarrhea, sweat, salivation
while they are suffocating to death.
Neurotransmitter Flashcards
315) How are sarin gas and insecticides the same?
How are they different?
316) What drug can be administered to a victim of a
Sarin gas or other chemical warfare attack?
317) What edible substance stimulates muscarinic
Ach receptors? What effect does it have?
318) Name a nicotinic Ach blocker/competitor.
319) Where does it come from?
320) What type of paralysis does it cause?
321) How does it cause death?
322) Why can a person eat the meat of an animal
that was killed by curare?
323) Where are nicotinic Ach receptors found in the
324) What effect does curare have on action
325) Name 2 reversible acetylcholine esterase
326) What type of paralysis do they cause?
327) What are the medicinal uses for these drugs?
328) What is myasthenia gravis?
329) What is ptosis?
330) What receptors are attacked and destroyed by
the immune system of a person with myasthenia
331) What is the treatment for myasthenia gravis?
332) How does neostigmine work?
333) Is physostigmine used to treat myasthenia
gravis? Explain.
334) What is the effect of a medicine that inhibits
acetylcholine esterase (Ach-ase)?
335) Too much of an Ach-ase inhibitor will cause
what type of paralysis?
336) Is Neostigmine reversible? What is the
consequence of that?
337) Name 2 irreversible Ach-ase inhibitors
338) What happens to an insect when an insecticide
is used?
They are both irreversible ACh-ase inhibitors.
Treatment for both includes atropine, but treatment for
sarin gas also requires artificial ventilator and pressure
Atropine, if you can administer it immediately.
Some poisonous mushrooms. It can kill you.
Curare; comes from tree sap
Paralyzes diaphragm
The enzymes in the GI system deactivate it.
Skeletal muscle
It is a sodium VGC blocker, which blocks the sodium
channel so you can’t have an action potential (like
lidocaine). It causes flaccid paralysis since muscles
cannot contract.
Neostigmine and Physostigmine
Spastic paralysis
They are used to treat myasthenia gravis.
An autoimmune disease that causes ptosis.
droopy eyelids
Nicotinic Ach receptors are destroyed. It usually just
affects some of the receptors, beginning in the eyelid
muscles, then progressing down the face.
It inhibits acetylcholine esterase (Ach-ase)
No. It works in the same way as neostigmine (they are
both reversible ACh-ase inhibitors), but physostigmine
is not medically useful for myasthenia gravis because
its effect on skeletal muscle is too weak.
The acetylcholine will be released but not all of it will
be degraded so the muscles can keep contracting for
Yes, so you need to keep taking it daily. That is what
makes it useful as a medicine.
Insecticides and sarin gas
Ach accumulates and acts as a constant stimulus. The
muscles go into spastic paralysis and the insect
Neurotransmitter Flashcards
339) How does curare differ from insecticides?
340) What is the main difference between
insecticides/sarin gas and
341) What is the treatment for a person exposed to
sarin gas?
342) Name one inhibitory neuron blocker
343) What does it do?
344) What type of paralysis does tetanus toxin
345) What is the treatment for tetanus toxin?
346) What effect does Black Widow spider venom
347) How are insecticides similar to Black Widow
spider venom?
348) How are insecticides different than Black
Widow spider venom?
349) What effect does Brazilian Wandering Spider
(banana spider) spider venom have?
Insecticides allow excess Ach to accumulate and cause
spastic paralysis. Curare blocks the Ach receptors,
causing flaccid paralysis.
Insecticides/sarin gas are irreversible Ach-ase
inhibitors. Neostigmine/physostigmine are reversible
Ach-as inhibitors.
They need to be on a ventilator and pressure chambers
for a few weeks.
Tetanus toxin
Blocks release of inhibitory neurotransmitters (GABA
and glycine)
An Ach blocker like atropine or a sodium VGC
blocker like curare.
Causes Ach release; spastic paralysis
Causes spastic paralysis
Insecticides are irreversible Ach esterase inhibitors.
Black Widow spider venom directly causes excessive
ACh release
It has a lot of nitrous oxide and it blocks the
degradation of nitrous oxide. It acts like tetanus toxin,
causing spastic paralysis.
350) What is the most venomous of all spiders,
causing the most human deaths?
Brazilian Wandering Spider (banana spider)
351) What is a medicinal use for the venom of the
Brazilian Wandering Spider (banana spider)?
It causes penile erection, so is used in Viagra.