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Neuro 321 > Chapter 5 Midterm 2 > Flashcards

Chapter 5 Midterm 2 Flashcards

1
Q

What was a historical controversy in neuroscience?

A

Whether communication in the brain was electrical or chemical

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2
Q

What experiment did Otto Loewi perform?

A

Loewi put a frogs heart in a saline bath, then electrically stimulated the vagus nerve, at the same time he transferred the fluid in this container to another where a heart was immersed but not electrically stimulated. He then recorded both heart rates and found the heart rate of the electrically stimulated heart slowed after stimulation and the heart that wasn’t electrically stimulated also slowed after fluid transfer, proving that neurotransmission was chemical in nature as a chemical (acetylcholine) released from the vagus nerve into the fluid caused the second heart to slow down. Did the reverse experiment to conclude noradrenaline speeds up the heart

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3
Q

What three findings have helped researchers understand parkinsons neural basis?

A
  1. That the substania nigra is a small midbrain nucleus that degenerates and in the brain of a patient who had parkison symptoms on one side of the body, the opposite side had the SN degrading
  2. Chemical examination of the brain of ppl w parkinsons showed that disease symptoms appear when dopamine levels had a 90% loss in the basal ganglia, today is aroudn 80%
  3. we found that injecting a neurotoxin called 6-hydroxydopamine into rats destroyed dopamine containing neurons and produced symptoms of Parkinson’s disease.
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4
Q

When parkinsons is diagnosed what percent of neural damage is done?

A

60-70%

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5
Q

How did joy smell parkinsons?

A

because parkinsons has a chemical signal

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6
Q

When a neuron dies it is not replaced except where?

A

the dentate gyrus of hippocampus and in the striatum next to the ventricle

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7
Q

How was parkinsons tried to be cured?

A

Treat parkinson’s with juvenile cells that were destined to be dopaminergic but the source of cells were aborted fetuses, was abandoned and didn’t work as the disease just kills the neurons

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8
Q

What were the frozen addicts?

A

Addicts that went to sweden for surgery, got fetal tissue and had a benefit. They didn’t have parkisnosn but they took a drug that killed the dopaminergic neurons, got new neruons and it relieved symptoms

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9
Q

what are the parts of a synapse ?

A

There’s a postsynpactic neuron and presynaptic terminal which leads into a cell body. The cell body contains a presynaptic membrane which has protein mlcls that transmit chemical messages. Past the membrane you have a mitochondrion, and then a synaptic vesicle which contains neurotransmitters, these vesicles can be stored in bunches in storage granules. The vesicles release neurotransmitters onto the synaptic cleft where they enter neurotransmitter channels on the postsynaptic receptor where they bind, the postsynaptic membrane contains protein mcls that receive chemical messages.

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10
Q

What is the tripartite synapse?

A

The presynaptic membrane, post synaptic membrane, and glial cell (usually surrounding astrocytes)

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11
Q

What does anterograde mean?

A

That the information flows from presynaptic to postsynaptic

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12
Q

What are the five steps synaptic transmission takes place?

A
  1. Synthesis- have to make neurotranmitter from precursor modules
    2- pack transmitter into vesicle and store it there
    3- then the neurotransmitter is released through exocytosisin response to an action potential
    4- The transmitter crosses the cleft and interacts with the receptor, which effects the post synaptic cell
    5- Inactivation- The transmitter diffuses away, is degraded, taken into the neuron terminal, or taken by an astrocyte
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13
Q

What are receptors?

A

proteins

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14
Q

Why would plants make substances that have drug effects?

A

It’s a form of reproduction for plants seeds to move, we found out how to synthesize and make large quantities of it

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15
Q

Why do drugs work?

A

Because we have receptors for opiates, because you make neurotransmitters called opiodes which the mlcls from these plants can fit into these receptors and work.

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16
Q

What two receptors do we have that allow cannabis to work?

A

CB1 and CB2, which correspond to molecules anandamide and 2 AG

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17
Q

What drug does not work by receptors?

A

alcohol

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18
Q

How are neurotransmitters released?

A

When an action potential reaches the terminal it open calcium channels,
the incoming calcium ions bind to proteins forming a complex, this complex binds to vesicles releasing some from filaments and inducing others to bind to the presynaptic membrane and empty their content by exocytosis onto the postsynaptic receptor sites

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19
Q

What is an omega body?

A

Is when the fusion pore widens, membrane of synaptic vesicle fuses with presynaptic membrane

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20
Q

How is the neurotransmitter released from the presynaptic cell bodyafers its at the presynaptic membrane?

A

the vesicle binds to the presynaptic membrane by calcium opening a fusion pore, the fusion pore widens and the membranes of the synaptic vesicles fuses with presynaptic membrane, the proteins on the initial vesicle get removed, and the neurotransmitters get released from the presynapse

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21
Q

What are the four types of inactivating a neurotransmitter?

A

1: Diffusion- neurotransmitter simply diffuses
away from the synaptic cleft and is no longer available to
bind to receptors
2: Degradation: Enzymes in the synaptic cleft break down the neurotransmitter: these pieces are usually recycled/reused
3: Reuptake: the transmitter is brought back into the presynaptic axon terminal is degraded by enzymes, and then used again by being taken into the terminal
4: Astrocyte uptake: nearby astrocytes take up the transmitter, also stores them for re-export to the axon terminal- reason why the tripartite synapse is so important.

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22
Q

What are the 7 variety of synapses?

A

Dendrodendritic, Axodendritic, Axoextracellular, Axosomatic, Axosynaptic, Axoaxonic, axosecretory

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23
Q

What is a Dendrodendritic synapse?

A

Two different dendrites come in close contact and communicate

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24
Q

Whats axoextracellular synapse?

A

The end of an axon doesn’t make a synpatic connection but just releases it’s neurotransmitters and it floats around and interacts with receptors it bumps into.

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25
Q

Whats axosomatic synapse?

A

When axon terminal makes contact on the cell body, usually inhibtory

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26
Q

What’s axosynaptic?

A

The axon terminal makes synaptic contact to another synaptic terminal

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27
Q

What’s axoaxonic?

A

rare, axon terminal ends on another axon

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28
Q

What’s Axosecretory?

A

axon terminal end son tiny blood vessel and secretes transmitter directly into blood

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29
Q

What’s the difference between hormones and neurotransmitters?

A

Just the distance it travels, hormones travel longer distance before it interacts with it’s receptor, hormones have to travel several feet to an internal organ its hormone, if it travels 200 angstroms is a neurotransmitter

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30
Q

What proteins mediate electrical synapses?

A

Gap junctions

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31
Q

What are electrical synapses?

A

Two membranes come so close together that hemichannels go through both membranes and substances cross from one cell to another, fluid can travel between them, allow action potentials to pass from one nueron to the next directly

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32
Q

How do electrical synapses differ from chemical?

A

They’re very fast (flies have them), but less plastic so you can’t learn new info (can’t really teach fly something new)

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33
Q

How do chemicals synapses effect us?

A

Make us plastic, can learn

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34
Q

What are features of inhibitory synapses?

A

Typically located on cell
body- very close to initial segment
– Flat vesicles
– Sparse material on
membranes
– Narrow cleft
– Small active zone

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35
Q

What are features of excitatory synapse?

A

Typically located on
dendrites
– Round vesicles
– Dense material on
membranes
– Wide cleft
– Large active zone

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36
Q

Which synapse is more likely to fail? excitatory or inhibitory?

A

excitatory, as it’s mor eplastic, breaks more important so inhibtory don’t fail

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37
Q

What is the four criteria for a neurotransmitter?

A

1: Transmitter must be synthesized or present in a neuron
2: When released, the transmitter must produce a response in the target cell
3: The same receptor action must happen if you squirt it on the receptor experimentally
4: There must be a mechanism for removal after the transmitters work is done

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38
Q

All motor neurons leaving the spinal cord use what as a neurotransmitter?

A

acetylcholine

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39
Q

What is the renshaw loop?

A

Each motor axon has a main axon projecting to a muscle (leaving spinal cord) and has an axon collateral within the spinal cord that synapses on a nearby CNS (renshaw) interneuron releasing acetylcholine, the interneuron contains the inhibitory transmitter glycine which stops motor neuron excitation as it in turn synapses on the motor neurons cell body creating a loop

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40
Q

When a motor neuron is highly excited how can it’s modulate it’s activity?

A

Through the renshaw loop

41
Q

What can happen if the renshaw loop becomes blocked?

A

motor neurons become overactive, producing convulsions that can choke off respiration and so cause death.

42
Q

What can block the renshaw loop?

A

the toxin strychine

43
Q

What three things can a neurotransmitter also do?

A

1: Carry a message from the presynaptic membrane of one neuron to another by influencing the postsynaptic membrane’s voltage.
2: Change the structure of a synapse.
3: Communicate by sending messages in the opposite direction. These retrograde (reverse-direction) messages influence the release or reuptake of transmitters on the presynaptic side.

44
Q

How can we group neurotransmitters?

A

Group them based on their chemical composition

45
Q

What are the 5 classes/groups of neurotransmitters?

A

small molecule transmitters
peptides
lipids
gases
ion

46
Q

What are the 5 characteristics of the small neurotransmitters?

A

-They are small
- Their main components are derived from the food we eat (diet can influence their activity, important when designing drugs as neuroactive drugs reach bran by digestive tract)
- They are synthesized and packaged at the axon terminal
-Act quickly
-Have relatively short biosynthetic pathways

47
Q

How is the neurotransmitter acetylcholine synthesized and broken down?

A

Inside the cell, the acetyl CoA carries acetate to the synthesis site, and a second enzyme choline acetyltransferase transfers the acetate to choline to make acetylcholine .
After the Ach gets released into the synaptic cleft and reaches receptor sites on postsynaptic membrane, enzyme AchE (acetylcholinesterase) breaks it down by removing acetate from choline and the product are taken back into the cell to be reused.

48
Q

How are amines made?

A

Have tyrosine which turns into L-dopa through enzyme tyrosine hydroxylase, this turns into dopamine, then norepherine, then ephinerpherine through other succesive enzymes

49
Q

How was L-dopa used to help parkinson like symptoms in a patient?

A

L-dopa increased the amount of dopamine neurons in the remaining synapses.

50
Q

Why is the rate at which amines (like dopamine) are produced limited?

A

Because to turn tyorisine into L-dopa, the enzyme tyrosine hydroxylase is limited

51
Q

Why is L-dopa not a cure for parkinsons?

A

because it kills dopamine synapses so more dopamine neurotransmitters in very few synapses stops being effective. Also causes dyskinesias (ballistic movements or choreic movement)

52
Q

What are the six characteristics of the peptide neurotransmitters?

A

1- Are strings of amino acids
2- assembled by ribosomes according to instructions
3- Packaged in a membrane by golgi bodies
-transported to the axon terminal
-not replaced quickly (as they act slowly and are made slowly)
-Do not normally bind to ion channels and have no direct effects on voltage gated channels, activate receptors that indirectly influence cell structure and function

53
Q

What two neurotransmitters are considered the workhorses of the brain?

A

Glutamate and GABA (are peptide neurotransmitters)

54
Q

Is glutamate a transmitter in excitatory or inhibitory synapses?

A

excitatory

55
Q

Is GABA a neurotransmitter in inhibitory or excitatory synapses?

A

Inhibitory

56
Q

Why can neuropeptidetransmitters not be taken as drugs?

A

because digestive processes degrade neuropeptide amino acid chains

57
Q

What are the seven families of peptide transmitters?

A

Opiods (importan tin painregulation), Neurohypophyseals, Secretins (growth hormone relasing factor), Insulins(transports sugars), Gastrins (important in energy balance regulation), Somatostatins, Tachykinis

58
Q

What are some examples of the opiods transmitters?

A

Met-enkephalin, dynorphin, beta-endorphin (responsible for runners high)

59
Q

What are some examples of the neurohypophyseals transmitters?

A

Vasopressin (important in kidney), oxytocin (enables bonding between offspring and mom, and milk)

60
Q

What are some examples of the secretins transmitters?

A

Secretin, motilin, glucagon, growth hormone-releasing factor

61
Q

What are some examples of the insulins transmitters?

A

Insulin, insulin growth factors

62
Q

What are some examples of gastrin neurotransmitters?

A

Gastrin, cholecystokinin

63
Q

What are some examples of the somatostatins neurotransmitters?

A

Somatostatin

64
Q

What are some examples of the tachykinins neurotransmitters?

A

Neurokinin A and B, substance P

65
Q

What does enkephalin mean?

A

in the cephalon

66
Q

What does endorphin mean?

A

endogenous morphine

67
Q

What is the main example of lipid neurotransmitters? Describe them

A

endocannabinoids
(endogenous cannabinoids)
A class of lipid neurotransmitters
synthesized at the postsynaptic
membrane to act on receptors
at the presynaptic membrane
(retrograde)
include anandamide and 2-AG (derived from arachidonic acid, unsat fatty acid)

68
Q

What’s something you have to take with L-Dopa

A

Benzerizide, prevents conversion to L-dopa to dopamine outside of the brain, doesn’t cross blood brain barrier- need it so not everywhere has extra dopamine

69
Q

Can you drive peptide transmitters to exhaustion?

A

yes

70
Q

What is THC?

A

Is the psychoactive ingredient in cannabis, is similar to anadamide and have same recptors, replacing anamide with THC when you get high

71
Q

Why are lipid neurotransmitters not packed in vesicles?

A

hydrophobic, made rapidly and degraded rapidly

72
Q

Why are lipid neurotransmitters retrograde?

A

They go from post synapytic neuron to presynaptic neuron

73
Q

What receptor is the target of all cannabinoids?

A

CB1

74
Q

What receptor is found at both glutamate and GABA synapses?

A

CB1

75
Q

Do cannabinoids inhibit release of glutamate and GABA?

A

Yes, therefore they dampen both neuronal excitation and inhibition

76
Q

How are you still getting high if cannabinoids dampen both excitatory and inhibitory systems?

A

chnages how frontal cortex interacts with the rest of your brain

77
Q

What are the gaseous neurotransmitters?

A

NO and CO

78
Q

How does viagra work?

A

Changes the enzyme that makes NO and CO

79
Q

How do gaseous neurotransmitters effect heart disease?

A

Effect blood vessels diameter and whether they’re rigid or not

80
Q

How are gaseous neurotransmitters a part of parkinsons?

A

they mediate cell death

81
Q

How do you package CO or NO into a vesicle?

A

You can’t

82
Q

How can nitric oxide remediate cardiac disease?

A

Take a pill of it to relax the heart

83
Q

Is the ion zinc a neurotransmitter? Whats it’s characteristics?

A

Yes, Actively transported, packaged
into vesicles—usually with
another transmitter like
glutamate—and released into
the synaptic cleft

84
Q

How does zinc violate neurotransmitter rules?

A

Not synthesized

85
Q

What makes glutamate excitatory?

A

Nothing, the receptor it interacts with makes it excitatory, always open sodium channels

86
Q

What makes GABA inhibitory?

A

Always ties to a receptor that opens chloride channels

87
Q

What are the two parts of a ionotropic receptor?

A

A binding site for a neurotransmitter and a pore that regulates ion flow, protein decides which ions go through

88
Q

What are metabotropic receptors?

A

The receptor is linked to a G protein, lipid transmitters interact with this class of receptors

89
Q

Describe the two classes of Metabotropic receptors?

A

in the first class, transmitter binds w receptor, receptor releases G proteins, the alpha subunit of the g PROTEIN binds to the ion channel and lets the ions flow
2nd class- the alpha subunit binds to an enzyme, activates DNA, and makes new channels or fewer channels

90
Q

Why can’t you say a neurotransmitter is either or inhibitory and excitatory?

A

Because sometimes it’s both, can be ionotropic in one location and metabotropic in one location.

91
Q

How does the fast pathway work?

A

the hypothalmus sends a message down the spinal cord, the adrenal gland makes epinephrine which is released into the circulatory system, activates bodies cells, endocribe glands, and the brain

92
Q

How does the slow pathway work?

A

Hypothamus releases slow CRH into pitituary gland, this releases ACTH, this causes adrenal cortex to relase cortisol which activate the bodys cells, endocrine glands, and brain

93
Q

What autonomic control?

A

Ach excites autonomic ganglion in sympathetic releases NE neurons (fight or flight system)
Ach excites autonomic ganglion in parasympathetic which releases ACh neurons

94
Q

NE receptors on the heart are what? Ne receptors on the gut are what?

A

excitatory, inhibitory

95
Q

Basal forebrain in rat does what?

A

makes acetylcholine and pumps it out

96
Q

What are five systems that don’t release neurotransmitters to postsynaptic neuron right there in the brain?

A

Cholinergic- maintains attention and EEG, role in memory, death of cholinergic neurons related to alzheimers
Dopaminergic- has serveral independent systems, one in parkinsons is called nigrostriatal pathway, is the do it again pathway
Noradrenergic system- involved in maintaining emotional tone and depression
Serotonergic system- involved in maintaining waking EEG pattern, related to OCD, tics, and schizophrenia, and depression

97
Q

What happened to the frozen addicts?

A

took MPTP which converted to MPP+ which killed dopamine cells in the nigrosriatum, took L dopa to initiate movement, and got fetus tissue to get dopamine cells

98
Q

What is the one way a synapse doesn’t change to code for learning?

A

the number of neurotransmitter particles in a vesicle stays constant

99
Q

In which ways does the neuron change to code for learning?

A

Increased axonal support, number of vesicles, size of cleft, spine size/area, density of contact zones, terminal size, protein transport for spine construction and change in dendrite stem length and width.

Neuro 321 (11 decks)

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