Neurotransmitter Flashcards

1. Where are dendrites located? • Dendrites are spaced in all directions from neuronal soma. 2. What does this allow them to do? • This allows signal reception from a large spatial area providing the opportunity for summation of signals from many presynaptic neurons

3. When do dendrites transmit signals? • Dendrites transmit signals after the opening of LGC’s

4. When do LGC (Ligand-gated channels) open? • These open when a ligand (neurotransmitter) binds to them. They do not need an action potential to open them. 5. What do LGC’s have receptors for? • Neurotransmitters

6. Where are LGC’s located? • dendrites only 7. Why is it important to understand ion Many human diseases are from dysfunction of ion channels? channels 8. What do positive amino acids repel against? Ions with a positive charge 9. What do negative amino acids repel? Ions with a negative charge 10. What do amino acids on ligand gated channels Ion selectivity (what ions pass) control? 11. What ions have their own ligand gated Sodium, Potassium, and Chloride channel? 12. What would happen to the resting membrane Na+ has a positive charge, so the RMP would become potential (RMP) if the sodium channel opened? less negative and go closer to threshold. 13. What would happen to the resting membrane K+ would leave with its positive charge, so the RMP potential (RMP) if the potassium channel would become more negative and go farther from opened? threshold. 14. What would happen to the resting membrane Cl- has a negative, so the RMP would become more potential (RMP) if the chloride channel negative and go farther from threshold. opened? 15. What is the Excitatory Postsynaptic Potential • The increase in voltage above the normal resting (EPSP) potential (to a less negative value) is called the excitatory postsynaptic potential. 16. What does “postsynaptic” refer to? • Postsynaptic refers to the dendrite of the neuron receiving the signal.

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. 18. What mV is the resting membrane potential? Approximately Minus 70 mV 19. How many mV do we need to reach threshold? We need to get to +30mV to have an action potential 20. What type of action potential opens sodium excitatory postsynaptic potentials (EPSP) channels, EPSP or IPSP? 21. What type of action potential opens K+ and Cl- Inhibitory postsynaptic potentials (IPSP) channels, EPSP or IPSP?

22. When a K+ channel opens, which direction It rushes out of the cell, and the inside of the cell Neurotransmitter Flashcards

does K+ move, and what happens to the inside membrane becomes more negative, farther from of the cell membrane? starting an action potential.

23. When a Cl- channel opens, which direction It rushes into the cell, and the inside of the cell does Cl- move and what happens to the inside membrane becomes more negative, farther from of the cell membrane? starting an action potential. 24. What determines whether a neuron “responds” It depends on temporal (how fast) and spatial (how or not? 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 IPSP’s. 26. If Excitatory and inhibitory postsynaptic potentials are firing at the same time, how do Add up all the charges from the excitatory and you know which one wins? 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 Electrical or mechanical stimulation excitable cell? 30. When a cell membrane is depolarizing, is it Closer to threshold going closer to threshold or farther away? 31. What neurons fire in people with Parkinson’s Both disease: excitatory, inhibitory, or both? 32. What general effect does this cause? Problems with coordinating movement 33. What are the symptoms of people with Parkinson’s disease? They have trouble starting and stopping any motion and shake at rest 34. At threshold, what happens to sodium They open, and sodium rushes into the cell channels? 35. What 2 types of channels allow sodium LGC, when a neurotransmitter binds to it channels to open? VGC, when the cell membrane charges change 36. When do LGC’s open so sodium can enter the When a neurotransmitter (a ligand) binds to them. cell?

37. When do VGC’s open so sodium can enter the When the charge of the inside of the cell membrane cell? goes from negative to positive. Neurotransmitter Flashcards

38. What other ions use VGC’s? Potassium, chloride, and calcium

39. What type of VGC is it when it is selective for It is an inhibitory VGC. If K+ leaves the cell or if Cl- potassium or chloride instead of sodium? enters the cell, the inside becomes more negative, farther from an AP 40. What type of VGC is it when it is selective for It is an excitatory VGC. If Na+ or Ca++ enters the calcium? cell, the inside becomes more positive, making it closer to an AP 41. On what part of a neuron are LGC’s located? Dendrites only 42. On what part of a neuron are VGC’s located? On the axon, from the hillock to synaptic knobs. 43. What happens to Na+ channels during They open. depolarization? 44. Does the amplitude of the action potential No, the amplitude of the action potential does not change? (how strong the AP is) change. 45. Does the frequency of the action potential Yes, the frequency of the action potential does change. change? 46. What is the frequency pattern? The frequency pattern is a code (like Morse Code) that transmits information about the stimulus (light, sound, taste, smell, touch) to the brain. 47. The speed of the Action Potential depends on The size of the neuron fiber (larger is faster) and what two things? whether or not its axon is myelinated (myelinated are faster). 48. How does the action potential event occur? 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 49. Why does the action potential regenerate over There is a refractory period (Na+ channels become and over at each point of diffusion of incoming inactivated). NA+? 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 diet? because a lot of the myelin has not yet been produced.

52. Why is a neuron with myelin more efficient Neurons that have myelin are more efficient because than one without? they use less ATP.

53. What autoimmune disorder destroys the body’s Multiple Sclerosis myelin sheaths?

54. How many people have MS in the United 1 in 1000 States? 55. What is the female to male ratio? 2 to 1 Neurotransmitter Flashcards

56. Who has the highest incidents? Whites of Northern European descent 57. What are the symptoms of MS? 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 58. Why don’t patients report these symptoms to Because they often resolve before the doctor their doctors? appointment 59. How does the diagnostic of MS begin? Eventually, the neurological problems stop resolving completely, and they occur more frequently. That is when doctors suspect MS. 60. What 2 structures are important to the function Presynaptic vesicles and Mitochondria of the synapse? 61. What structure in a neuron contains Presynaptic vesicles neurotransmitter substances to excite or inhibit postsynaptic neurons? 62. What organelle provides most of the energy to Mitochondria synthesize a neurotransmitter? 63. What does membrane depolarization by an Emptying of a small number of vesicles into the action potential cause? synaptic cleft. 64. What structure do presynaptic membranes voltage gated calcium channels contain? 65. Depolarization of the presynaptic membrane Calcium by an action potential opens what channels? 66. When calcium floods into the neuron, what It causes the neurotransmitter to be released. happens? 67. Where does the neurotransmitter go when it is It lands on receptor proteins on the post-synaptic cell released? called ligand-gated channels (LGC) and opens them 68. What happens when the LGC opens? Ions diffuse in or out depending on the type of LGC 69. As the neurotransmitter binds to the receptor Excitatory Postsynaptic Potential (EPSP) (LGC) on the postsynaptic membrane, what 2 Inhibitory Postsynaptic Potential (IPSP) kinds of electrical signals can the neurotransmitter generate? 70. How is the NT removed from the LGC? Destruction by enzymes or diffusion away, back into the presynaptic cell to be recycled. 71. Where are Voltage- gated calcium channels In the synaptic knob of the presynaptic neuron located? 72. Where are receptor proteins for the released On the post-synaptic cell membrane neurotransmitter located? 73. What makes the energy for neurotransmitter Mitochondria synthesis? 74. What types of channels are in the axon of the VGC for sodium, allows Na+ to enter the cell presynaptic neuron, and what ion crosses that channel? 75. What types of channels are in the synaptic VGC for calcium, allows Ca++ to enter the cell knob of the presynaptic neuron, and what ion crosses that channel? 76. What does calcium do in a neuron? Causes release of the neurotransmitter Neurotransmitter Flashcards

77. What types of channels are in the dendrite of LGC (they bind to neurotransmitters) the presynaptic neuron?

78. What does the neurotransmitter do? It binds to the LGC, which causes nearby VGC’s to open. 79. What are two categories of VGC’s? Excitatory and Inhibitory 80. The change in voltage causes what? Depolarization or Hyperpolarization 81. If it causes depolarization, what type of action EPSP: excitatory post-synaptic potential (the dendrite potential is it called? receiving the signal continues the action potential) 82. If it causes hyperpolarization (going farther IPSP: inhibitory post-synaptic potential (the dendrite from an action potential, what type of action receiving the signal stops the action potential) potential is it called? 83. By what process are NT’s released, and what Released by exocytosis. ion triggers it? It is triggered by Ca++ 84. How does the NT get across the synaptic cleft? Diffusion 85. What is a graded potential? the more channels there are, the more the charge changes 86. The effect of a neurotransmitter is dependent 1. The selectivity of the channel (which ions are on what 3 factors? 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 87. What happens to the voltage on the The voltage becomes more positive; closer to postsynaptic cell if it experiences an EPSP? threshold. 88. What happens to the voltage on the postsynaptic The voltage becomes more negative; farther from cell if it experiences an IPSP? threshold. 89. Neurotransmitters are released in response to PRE-synaptic depolarization what? 90. When NTs are released in response to Calcium presynaptic depolarization, what is molecule is needed? 91. In order to allow another cycle of NT release, The NTs must be removed by reuptake by presynaptic binding and signal transmission, what must be nerve or degrading by specific enzymes or a done to the NTs? combination of these. 92. What do sympathetic neurons do to the heart Increase heart rate rate and blood pressure? What broad group of Increase blood pressure responses is this called? “Fight or Flight” responses 93. What do parasympathetic neurons do to the Decrease heart rate heart rate, blood pressure, and food digestion? Decrease blood pressure What broad group of responses is this called? Increase food digestion “Rest and Digest” responses

94. Is the heart innervated by sympathetic neurons, Both. The heart is innervated by both sympathetic and parasympathetic neurons, or both? parasympathetic neurons 95. In a dually innervated organ, how will the The receptors that have the most transmitters bound organ know if sympathetic or parasympathetic will cause the biggest result. is barking louder? 96. Why are a lot of organs dually innervated? To adjust to their physiology 97. What neurons can cause excitation in one Sympathetic and Parasympathetic Neurotransmitter Flashcards

organ yet inhibition in another? 98. What happens when the parasympathetic The sympathetic system will gain more control. system is suppressed? 99. If a drug mimics the parasympathetic system, Heart rate will be slower how will it affect the heart? 100. If a drug mimics the sympathetic system, how Heart rate will increase will it affect the heart? 101. What effect does epinephrine have on the heart It increases heart rate by stimulating the sympathetic rate? nervous system 102. What effect does atropine have on the heart It increases heart rate by blocking the parasympathetic rate? nervous system 103. What two medicines are given when a person’s Epinephrine and atropine heart stops? 104. What complicates the healing for a post-op Nerves that innervate the heart are cut and there is no heart transplant patient? way to suture them back. 105. Why must the post-op heart transplant keep These emotions can release epinephrine because it is a themselves from becoming overly anxious, angry hormone, not a nerve but the patient no longer has or sexually aroused? parasympathetic neurons attached to the heart to counter the effects of epinephrine. 106. How can we use the parasympathetic system to Use a medicine that opens the potassium channels, make the heart cells less active? making the inside of the cell more negative (hyperpolarized). 107. What is the number one way to regulate the Use a medicine that opens the potassium channels Heart Rate? 108. What are two ways of classifying Chemical classification neurotransmitters? Functional classification

109. What are the two types of chemical Large Molecule classification of NT’s? Small Molecule 110. What is an example of a large molecule NT? Peptides 111. What are the 3 small molecule NT categories? Cholinergic Catecholamines Amino Acids 112. What are the two types of functional Metabotropic classification of NT’s? Ionotropic 113. What are three categories of small molecule 1) Cholinergic (Acetylcholine) NT’s and examples of each? 2) Catecholamines (epinephrine, norepinephrine, dopamine, serotonin) 3) Amino Acid NT’s (glutamate, GABA, glycine)

114.List 3 large molecule (peptide) NT’s and their 1) ADH (anti-diuretic hormone, AKA effect Vasopressin) increases blood volume, which increases BP 2) Angiotensin, which causes vasoconstriction, which also raises BP 3) Bradykinin, which causes vasodilation, which Neurotransmitter Flashcards

lowers BP 115.What effect does Bradykinin have on blood Lowers it pressure? 122. What effect does Ach, epinephrine, Raises it angiotensin, and ADH have on blood pressure? 116.What is an example of a cholinergic NT? Acetylcholine (Ach) 117.What are the 3 types of catecholamines, and an 1) Adrenergic example of each? a) Norepinephrine b) Epinephrine 2) Dopaminergic a) Dopamine 3) Serotonergic a) Serotonin 118.What are the 3 main Amino Acid NT’s? Glutamate (excitatory) 119.Which ones are excitatory and which are GABA (inhibitory) inhibitory? Glycine (inhibitory) 120.What is an adrenergic neuron? One that makes epinephrine or norepinephrine 121.What is a dopaminergic neuron? One that makes dopamine 122.What is a serotonergic neuron? One that makes serotonin 123.What are cholinergic neurons? Neurons that use the neurotransmitter, Acetylcholine 124.What type of muscle is innervated by Skeletal Muscle cholinergic neurons? 125.Which NT causes contraction of skeletal Acetylcholine (ACh) muscle? 126.Is acetylcholine used by sympathetic neurons, Both parasympathetic neurons, or both? 127.How is Acetylcholine removed from the Acetylcholine is removed from the synaptic cleft by synaptic cleft? the enzyme, Acetylcholine esterase (AChE)

128.Treatment of Myasthenia gravis is to give a Acetylcholine (ACh) medicine that inhibits the enzyme that degrades this neurotransmitter. 129.What is the very important Amino acid in the Glutamate. 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. released? 133.What common ailment causes neuronal death? Stroke

134.What group of medicines are used when a Glutamate antagonists person has too much glutamate released (such as after a stroke)? 135.Antagonists to which neurotransmitter helps Glutamate stop neuronal death after a stroke? 136.Why are strokes or trauma to the brain so When damaged, neurons release a lot of dangerous in relation to neurotransmitters? neurotransmitters Neurotransmitter Flashcards

137.What effect does it have when excessive They cause over-stimulation of nearby neurons, which neurotransmitters are released after a trauma? then release too much calcium, causing cytotoxicity. It can kill the cell. 138.What causes Parkinson’s and Alzheimer’s 10% of the time it is genetic. 90% of the time it is disease? caused by calcium dyshomeostasis (The calcium is not being monitored properly in the body). 139.What agent is given to those who have stroke? Glutamate Antagonist

140.What happens if you don’t have enough Inhibitory NTs will gain momentum. Too little glutamate? glutamate leads to psychosis, perceives reality differently than normal.

141.What is the major inhibitory neurotransmitter GABA in CNS? 142.Decreased GABA causes what symptoms? Seizures

143.What type of medicines target GABA Anticonvulsants receptors to act as GABA agonists? 144.What two substances stimulate GABA Benzodiazepines (valium) and drinking alcohol receptors, and so are considered to be GABA agonists? 145.When a person is detoxing from alcohol abuse, Benzodiazepine (valium) is given to prevent seizures what medicine is given, what symptom does it during detox. Valium binds onto the GABA receptors, prevent, and how does the medicine work (what is stimulating them. This causes inhibition of the CNS, its mechanism of action)? preventing seizures. 146.What two neurotransmitters are inhibitory? GABA and Glycine 147.Alcohol stimulates what 2 neurotransmitters? GABA and Glycine 148.What effect does alcohol have on GABA Alcohol stimulates GABA receptors. receptors? 149.When GABA receptors are stimulated, what Inhibitory Post Synaptic Potentials (IPSP’s) type of action potential is generated?

150.What effect do IPSP’s have on the reflexes and They slow down. Reflexes decrease, speech slurs. muscles? 151.When alcoholics try to stop drinking all at Excitatory NTs gain control. once, what type of transmitters gain control? 152.What effect do excitatory NT’s have? Tremors and visual overstimulation (hallucinations).

153.Recovering alcoholics need what medicine Benzodiazepam (valium) while weaning off the alcohol? 154.Recovering alcoholics can be given what class GABA Agonists (drugs that act like GABA), such as of drugs? What is an example of this medicine? anti- convulsants like Benzodiazepam (valium) 155.What effects do benzodiazepines (such as They enhance the effects of GABA, which results in valium) have on GABA receptors? sedative, hypnotic (sleep-inducing), anxiolytic (anti- anxiety), anticonvulsant, muscle relaxant, and amnesic action 156.What disorders is valium used for? Treating anxiety, insomnia, agitation, seizures, muscle spasms, alcohol withdrawal and as a premedication for Neurotransmitter Flashcards

medical or dental procedures. 157.What organ releases adrenergic Adrenal glands in response to fight or flight emotions catecholamines, and when are they released? 158.Catecholamines are part of which branch of the Sympathetic Nervous System (fight or flight) autonomic nervous system? 159.What degrades catecholamines? Mono-amine oxidase (MAO) 160.What effect does an MAO inhibitor have on Allows catecholamines to excite the nervous system. the nervous system? 161.What are MAO inhibitors used for? Anti-anxiety and anti-depression medications 162. 163.What types of medicines cannot be used on a SYMPATHOMIMETIC (those that imitate patient taking an MAO inhibitor? Why not? 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. 164.What are some examples of Sympathomimetic Medicines for cardiac arrest, low blood pressure, and medicines? some meds that delay premature labor. 165.Where is epinephrine secreted? Adrenal gland 166.Is epinephrine excitatory or inhibitory? Excitatory 167.Where is norepinephrine secreted? Mainly secreted by adrenal gland, and also by some neurons in the CNS and by the sympathetic post- ganglionic neurons. 168.What neurotransmitters speed up the heart Epinephrine and Norepinephrine; sympathetic rate? To what branch of the ANS does it belong? 169.Where is dopamine secreted? Neurons in the CNS (substantia nigra) 170.Is dopamine excitatory or inhibitory? Inhibitory 171.What secretes serotonin? Neurons in the CNS 172.Is serotonin excitatory or inhibitory? Mainly excitatory. It can excite one cell but inhibit another. 173.What causes Parkinson’s disease? It is a loss of dopamine from neurons in substantia nigra of the midbrain. 174.What symptoms characterize Parkinson’s? Resting tremors, “pill rolling”, Bradykinesia (slow movement) 175.How is Parkinson’s treated? With L-dopa or MAO inhibitors. 176.What are the side effects of the treatments? Hallucinations, motor problems. 177.What region of the brain contains the neurons The motor cortex that move the muscles of the skeleton? 178.What region of the brain regulates body The basal nuclei movements by communicating with the motor cortex? 179.What region of the brain inhibits some motor The basal nuclei neurons so that unwanted body movements do not occur? 180.What region of the brain regulates stopping, The basal nuclei starting, and coordination of movements? 181.What region of the brain is like a strict parent The basal nuclei that ties their kids up to keep them from doing wild things? 182.What region of the brain secretes dopamine? The substantia nigra Neurotransmitter Flashcards

183.What effect does dopamine have on the basal It inhibits the basal nuclei (inhibits the inhibitor). That nuclei? allows the excitatory neurons to allow the body to move. 184.What region of the brain, and which NT are The substantia nigra and dopamine are like bosses that like bosses who tie up the basal nuclei? How does tie up the basal nuclei (the parent). With the inhibitor this effect movement? (parent) tied up, the kids (muscles) are no longer tied up, so they throw a party (body movements occur) 185.What are the 2 reasons basal nuclei do not Either the basal nuclei themselves are dysfunctional or work correctly? the dopamine levels are not correct 186.What are the 2 most common disorders of the Parkinson’s Disease (dopamine problem) and basal nuclei? Huntington’s Disease ( basal nuclei problem) 187.Parkinson’s disease is a problem in what Substantia nigra of the midbrain. region of the brain? 188.What NT is secreted by that region of the Dopamine brain? 189.People with Parkinson’s disease lack which Dopamine NT? 190.What happens when there is not enough The brain cannot initiate body movements. dopamine? 191.What are the four cardinal symptoms of 1) Tremor (pill-rolling tremor at rest) Parkinson’s disease? 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) 192.What disease has symptoms that are the Huntington’s disease opposite of Parkinson’s disease? 193.What types of movements are seen in Sudden, jerky movements. Their body writhes around Huntington’s disease? like they are dancing (chorea). 194.What area of the brain is damaged in The basal nuclei. Huntington’s disease? 195.What is the function of the basal nuclei in the It inhibits some motor neurons so that unwanted body brain (between the corpus callosum and thalamus)? movements do not occur 196.Most regions in the brain use what NT? Excitatory neurotransmitters 197.The basal nuclei in the brain use what NT? GABA (inhibitory) 198.What happens if the basal nuclei are damaged? Excitatory neurons are no longer inhibited, so they make the body move when movement is not intended. 199.Describe the malfunction in the brain of Since the basal nuclei are damaged, the inhibition of someone with Huntington’s disease. the motor cortex is removed, so excitatory neurons go unchecked, and the person has sudden jerky movements. 200.What are other symptoms in a person with Cognitive decline and psychiatric problems Huntington’s disease? 201.How does one get Huntington’s disease, and at It is genetic and hereditary (50% chance of each child what age does it manifest? getting it if one parent has it). Age of onset is usually 35-45 years of age. 202.What is the effect of taking too much of the It kills dopaminergic neurons, causing Parkinson’s Neurotransmitter Flashcards street drug, “Meth”? symptoms. 203.If you lose excitatory neurons, what neurons Inhibitory neurons gain an advantage? 204.What do Parkinson’s patients have problems Starting movements, and coordinating the doing? 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. 205.What is the treatment for Parkinson’s disease? An MAO inhibitor or L-dopa, which can cross BBB, unlike dopamine. 206.What stem cell research is being tried for Stem cells research involves injecting stem cells to Parkinson’s disease? cause the remaining neurons to replicate and help them get more control. 207.Serotonin is synthesized from what amino tryptophan acid? 208.What medicines are serotonin reuptake anti-depressant drugs inhibitors? 209.What neurotransmitter is released by the street Serotonin drug, ecstasy? 210.What NT is called the mood elevator, feel Serotonin good transmitter? 211.What is the effect of taking an SSR inhibitor? - It helps serotonin stay in the cleft longer, causing the 212.When is this medicine prescribed? person to feel better, having an elevated mood. It is prescribed for depression. 213.What is phenylalanine (an amino acid) tyrosine (another amino acid) converted into? 214.What is tyrosine converted into? L-Dopa 215.What is L-Dopa converted into? Dopamine 216.What is dopamine converted into? Norepinephrine 217.What is norepinephrine converted into? Epinephrine 218.Write the pathway of phenylalanine  Phenylalanine  TYROSINE  L-DOPA  epinephrine dopamine  norepinephrine  epinephrine 219.Catecholamines (such as epinephrine) are Tyrosine, which is made from phenylalanine made from which amino acid? 220.What is PHENYLKETONURIA (PKU)? Lack of the enzyme to convert phenylalanine to tyrosine 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 Neurotransmitter Flashcards

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 Artificial sweeteners such as Sweet N Low and diet person with phenylketonuria? sodas are high in phenylalanine, and must be avoided in PKU patients. END OF SECTION ONE (THE QUIZ #8 MATERIAL IS CRANIAL NERVES FLASHCARDS, SPINAL CORD FLASHCARDS, AND SECTION ONE OF THESE FLASHCARDS) 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. 232.When this receptor is stimulated, there is Muscarinic ACh receptors increased saliva, tears, and diarrhea 233.What is the antidote for overdose of atropine muscarinic substances? 234.Do muscarinic substances use G-proteins to Yes activate a nearby ion channel? 235.What are nicotinic Ach receptors (nAChR)? They are Ach receptors that area more sensitive to nicotine than to muscarine 236.What effect do nicotinic substances have? 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 237.Do nicotinic substances use G-proteins to No; they open ion channels directly. activate a nearby ion channel? 238.What body part contains both muscarinic and Skeletal muscle, which contracts when Ach binds nicotinic receptors? there. 239.What are the two types of adrenergic Alpha adrenergic receptors receptors? Alpha 1 receptors Alpha 2 receptors Beta adrenergic receptors Beta 1 receptors Beta 2 receptors 240.What are the 2 types of adrenergic receptors? Alpha and Beta adrenergic receptors 241.What are the 2 types of alpha receptors? Alpha 1 and Alpha 2 242.What effect do the alpha 1 receptors have on Vasoconstriction (increases BP) blood vessels and GI motility? Decreases GI motility Neurotransmitter Flashcards

243.What effect do the alpha 2 receptors have on Vasodilation (decreases BP) blood vessels and GI motility? Decreases GI motility 244.What 2 receptors, when stimulated, causes Alpha 2 receptors vasodilation, which decreases blood pressure? Beta 2 receptors 245. Do Alpha 2 and Beta 2 receptors slow the No, only Beta 1 has an effect on the heart rate, and it heart rate? increases it. 246. Are Alpha 2 and Beta 2 receptors used by the No, they are adrenergic receptors, so they are used by parasympathetic neurons? 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) 247.What are the 2 types of beta receptors? Beta 1 and Beta 2 248.What effect do the beta 1 receptors have on Increases HR heart rate and cardiac output? Increases CO 249.What effect do the beta 2 receptors have on Vasodilation (decreases BP) blood vessels, GI motility, and bronchioles? Decreases GI motility Opens bronchioles 250.What protein is used by adrenergic receptors? G-Protein 251.What are ionotropic receptors? Those that bind to a NT and have a channel that extends into cell. They are the receptor and the transporter 252.What are Metabotropic receptors? 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. 253.What are 5 examples of ionotropic receptors? Nicotinic AChR Serotonin receptors Glutamate receptors GABA receptors Glycine receptors 254.What are 3 types of metabotropic receptors? Muscarinic AChR Alpha and Beta Adrenergic receptors Dopaminergic receptors 255.What 2 things happen when the G-protein is It breaks into two pieces. One of the pieces is called activated? 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. 256.What is one change that can occur during G- • These changes include activation of gene protein activation? transcription (to form new proteins, changing the metabolism; used especially in making new memories). 257.What are the three sequences of events in a Step 1: NT binds to receptor metabotropic receptor? Step 2: The G proteins activate Step 3: Second messenger activates another protein called the late effector protein 258.What 2 types of receptors does Ach bind to? Muscarinic and nicotinic receptors Neurotransmitter Flashcards

259.What type of receptor does Norepi and epi adrenergic receptors bind to? 260.What receptors use G-proteins? Muscarinic Ach, adrenergic and dopaminergic 261.Where are G-proteins found? Every cell in the body 262.What are the 2 types of G-proteins? GS (stimulating G protein) GI (inhibiting G protein) 263.Which type of G-protein will lead to events GS (stimulating G protein) that increase the activity of a cell? 264.When the G-proteins breaks into two pieces, activates another protein called the late effector protein one of them acts as a second messenger. What does this second messenger do? 265.What do G-Proteins of sympathetic s neurons protein kinase A activate? 266.What do G-Proteins of parasympathetic s protein kinase B neurons activate? 267.Why is kinase activity important? Phosphorylates (puts a phosphate molecule on) other proteins in a cell. This changes the activity level of the cell. 268.What are the 3 categories of small molecule Acetylcholine (Ach), Catecholamines, and Amino neurotransmitters? Acid NT’s 269.Name the 5 neurotransmitters that use Nicotinic Ach ionotropic receptors. Which are inhibitory? Glutamate GABA (inhibitory) Glycine (inhibitory) Serotonin 270.Name the 4 neurotransmitters that use Muscarinic Ach metabotropic receptors. Norepinephrine Epinephrine Dopamine 271.What are acetylcholine receptors called? Cholinergic 272.What are the two types of Ach receptors? Muscarinic and Nicotinic 273.What are the three categories of Adrenergic catecholamines? Dopaminergic Serotonergic 274.What are the 2 NT’s which are adrenergic? Norepinephrine Epinephrine 275.What is the NT that is dopaminergic? Dopamine 276.What is the NT that is serotonergic? Serotonin 277.What are the 3 Amino Acid NTs? Which are Glutamate inhibitory? GABA (inhibitory) Glycine (inhibitory) 278.What are the three types of Catecholamines? Catecholamines 1. Adrenergic catecholamines: • Norepinephrine • Epinephrine 2. Dopaminergic catecholamine: • Dopamine 3. Serotonergic catecholamine: Neurotransmitter Flashcards

• Serotonin

Summary Slide

279. What are the three types of metabotropic • muscarinic acetylcholine (mostly used by post- receptors, and which branch of the ANS uses each? ganglionic parasympathetic neurons) • Alpha and Beta adrenergic receptors (mostly used by post-ganglionic sympathetic neurons) • Dopaminergic (mostly sympathetic)

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? epinephrine 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 Neurotransmitter Flashcards

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? When the muscle stays in contraction. You still cannot move the muscle properly, but in this case, the muscle is too rigid.

288) Name four sodium VGC blockers. Do they Lidocaine cause flaccid or spastic paralysis? Tetrodotoxin Saxitoxin Curare They all cause flaccid paralysis 289) Which of the above four sodium VGC blockers Lidocaine will DIRECTLY block the sodium channel? Curare 290) Which one is from shellfish toxins? Saxitoxin 291) Which one is from a puffer fish? Tetrodotoxin 292) Which one is a local anesthetic? Lidocaine 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 No VGC blocker is present?

295) What type of paralysis is caused by a sodium Flaccid VGC blocker? 296) How are botulism toxin and curare similar? They both cause flaccid paralysis because muscles cannot contract. 297) How are botulism toxin and curare different? Botulism causes flaccid paralysis by inhibiting ACh RELEASE, while curare blocks ACh RECEPTORS. 298) Name one vesicle blocker Botulism 299) What is botulism, and where does it come It is a protease (an enzyme that breaks down proteins). from? It is from a bacterium 300) Where might botulism be found in your house? Undercooked turkey and dented cans of food.

301) What symptom does botulism cause, and what Inhibits ACh neurotransmitter release; muscles can’t is the cause of death? contract; flaccid paralysis. Cause of death is from suffocation because the diaphragm is paralyzed. 302) What are two medicinal uses for botulism Botox injections and migraines. Neurotransmitter Flashcards

toxin? 303) Name 2 muscarinic Ach blocker/competitors Atropine and opium derivatives 304) Is atropine considered a sodium VGC blocker? 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 indirectly. 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? smooth 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. have? 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.

315) How are sarin gas and insecticides the same? They are both irreversible ACh-ase inhibitors. How are they different? Treatment for both includes atropine, but treatment for sarin gas also requires artificial ventilator and pressure chamber. 316) What drug can be administered to a victim of a Atropine, if you can administer it immediately. Sarin gas or other chemical warfare attack? 317) What edible substance stimulates muscarinic Some poisonous mushrooms. It can kill you. Ach receptors? What effect does it have? 318) Name a nicotinic Ach blocker/competitor. Curare; comes from tree sap 319) Where does it come from? 320) What type of paralysis does it cause? Flaccid 321) How does it cause death? Paralyzes diaphragm 322) Why can a person eat the meat of an animal The enzymes in the GI system deactivate it. that was killed by curare? 323) Where are nicotinic Ach receptors found in the Skeletal muscle body? Neurotransmitter Flashcards

324) What effect does curare have on action It is a sodium VGC blocker, which blocks the sodium potentials? channel so you can’t have an action potential (like lidocaine). It causes flaccid paralysis since muscles cannot contract. 325) Name 2 reversible acetylcholine esterase Neostigmine and Physostigmine blockers 326) What type of paralysis do they cause? Spastic paralysis 327) What are the medicinal uses for these drugs? They are used to treat myasthenia gravis. 328) What is myasthenia gravis? An autoimmune disease that causes ptosis. 329) What is ptosis? droopy eyelids 330) What receptors are attacked and destroyed by Nicotinic Ach receptors are destroyed. It usually just the immune system of a person with myasthenia affects some of the receptors, beginning in the eyelid gravis? muscles, then progressing down the face. 331) What is the treatment for myasthenia gravis? Neostigmine 332) How does neostigmine work? It inhibits acetylcholine esterase (Ach-ase) 333) Is physostigmine used to treat myasthenia No. It works in the same way as neostigmine (they are gravis? Explain. both reversible ACh-ase inhibitors), but physostigmine is not medically useful for myasthenia gravis because its effect on skeletal muscle is too weak. 334) What is the effect of a medicine that inhibits The acetylcholine will be released but not all of it will acetylcholine esterase (Ach-ase)? be degraded so the muscles can keep contracting for longer. 335) Too much of an Ach-ase inhibitor will cause Spastic what type of paralysis? 336) Is Neostigmine reversible? What is the Yes, so you need to keep taking it daily. That is what consequence of that? makes it useful as a medicine. 337) Name 2 irreversible Ach-ase inhibitors Insecticides and sarin gas 338) What happens to an insect when an insecticide Ach accumulates and acts as a constant stimulus. The is used? muscles go into spastic paralysis and the insect suffocates.

339) How does curare differ from insecticides? Insecticides allow excess Ach to accumulate and cause spastic paralysis. Curare blocks the Ach receptors, causing flaccid paralysis. 340) What is the main difference between Insecticides/sarin gas are irreversible Ach-ase insecticides/sarin gas and inhibitors. Neostigmine/physostigmine are reversible neostigmine/physostigmine? Ach-as inhibitors. 341) What is the treatment for a person exposed to They need to be on a ventilator and pressure chambers sarin gas? for a few weeks. 342) Name one inhibitory neuron blocker Tetanus toxin 343) What does it do? Blocks release of inhibitory neurotransmitters (GABA and glycine) 344) What type of paralysis does tetanus toxin Spastic cause? 345) What is the treatment for tetanus toxin? An Ach blocker like atropine or a sodium VGC blocker like curare. 346) What effect does Black Widow spider venom Causes Ach release; spastic paralysis have? Neurotransmitter Flashcards

347) How are insecticides similar to Black Widow Causes spastic paralysis spider venom? 348) How are insecticides different than Black Insecticides are irreversible Ach esterase inhibitors. Widow spider venom? Black Widow spider venom directly causes excessive ACh release 349) What effect does Brazilian Wandering Spider It has a lot of nitrous oxide and it blocks the (banana spider) spider venom have? degradation of nitrous oxide. It acts like tetanus toxin, causing spastic paralysis.

350) What is the most venomous of all spiders, Brazilian Wandering Spider (banana spider) causing the most human deaths?

351) What is a medicinal use for the venom of the It causes penile erection, so is used in Viagra. Brazilian Wandering Spider (banana spider)?

END OF SECTION TWO EVERYTHING ON THIS DOCUMENT WILL BE ON THE LECTURE UNIT 4 EXAM