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Neuroscience 484 > Synaptic Transmission Basics > Flashcards

Synaptic Transmission Basics Flashcards

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1
Q

Describe gap junctions?

A

Low resistance connections and rapid communication. At gap junctions the two cells are separated by only 3 nm. This narrow gad is spanned by a cluster of 20 different proteins called connexins. 6 connexins combine to form a subunit called a connexons. Two two hemi-channels (connexons) on in each membrane meet to form a gap junction. Energy can flow both ways in gap junctions.

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2
Q

What does it mean that cells at gap junctions are electrically coupled?

A

Current (in the form of ions) pass through gap junctions which are created by two connecting connexons are said to be energetically coupled.

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3
Q

Where are electrical synapses common?

A

Every part of the mammalian CNS

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4
Q

What are postsynaptic potentials (PSP) created?

A

When neurons are energetically couples at the gap junction, a small amount of ionic current flows across the gap junction into the other neuron this causes an electrically mediated post-synaptic potential in the second neuron.

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5
Q

What does is the impact of electrical synapses being bi-directional?

A

When an AP is generated in the second neuron, it will produce a PSP in the first neuron.

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6
Q

How strong is the PSP generated by one neuron?

A

1mV. However, one neuron usually has electrical synapses with many other neurons, so several PSPs occurring simultaneously could be enough to strongly excite a neurons

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7
Q

When are gap junctions most common?

A

Early development

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8
Q

Name a type of response that gap junctions frequently mediate?

A

Escape responses. This is because they are so fast! Passive current flow across the gap junction is virtually instantaneous.

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9
Q

How wide is the synaptic cleft?

A

20-25nm wide. This is 10x the width of the gap junction. The synaptic cleft is filled with fiberous proteins

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10
Q

How do electrical currents flow from one electrical synapse to another?

A

Connexons on the upstream neuron are precisely aligned to connexons of the downstream neuron at the gap junction. Said another way, six presynaptic connexons align with six post-synaptic connexons to form pores that connect the cells.

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11
Q

What is larger, the pore of a connexon or the pore of a voltage-gated ion channel?

A

The pore of a connexon. As a result many substances diffuse between the gap junctions of the pre and post synaptic neurons. In fact in addition to ions, molecules with molecular weights as great at several hundred daltons can diffuse through the gap junction. This mean that ATP and other important intracellular metabolites, as second messenger

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12
Q

What are connexons made of?

A

Connexins. There are several different types of connexins that yield gap junctions with different physiological properties.

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13
Q

How do electrical synapses work?

A

ionic current flows passively from one neuron to another. The source of this current is typically the pre-synaptic action potential.

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14
Q

Are electrical synapses bidirectional?

A

Yes! Although some a uni-directional

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15
Q

What does to mean that electrical transmission is graded?

A

It can occur below action potential threshold and can be hyper-polarizing or depolarizing?

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16
Q

How is it that electrical synapses can he hyper-polarizing or depolarizing?

A

not sure?

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17
Q

Describe the connexin and connexon protein structure?

A

It is a single protein that passes through the membrane four times. So it is called a 4-pass transmembrane protein. It takes six of these proteins to form 1 connexon. Connexons have closed and open configurations regulated, which are regulated by Ca2+, pH and voltage

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18
Q

How is ion movement through connexons facilitated?

A

By polar residues lining the pore.

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19
Q

Why are electrically coupled synapses so fast?

A

Low resistance of the connection

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20
Q

What are the primary factors that determine input resistance Rin?

A

Size and myelination. Larger cells have lower re

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21
Q

Do networks of energetically coupled neurons tend to exhibit higher or lower and what impact doe this have on current required to depolarize them to threshold?

A

Due to increased membrane surface area, networks of coupled neurons tend to have low resistance, which means that a greater current is required for an AP. This reduces the sensitivity of some electrically coupled synapses such that they require synchronous firing form many pre-synaptic neurons in order to generate a threshold depolarization.

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22
Q

Is more or less current required to achieve depolarization in electrically coupled cells as opposed to chemical cells?

A

Using deltaV=delta I * Rin
v=voltage across the membrane
I=current
Rin=in put resistance, which is the inverse of conductance.

We therefore know, it depends on the size of the post-synaptic neuron. If it is a small post-synaptic neuron resistance will be high (because there are few channels) therefore a low current will be required for depolarization. This is the case for the tail flip of the crayfish. This tail flip is an escape response. Since the post-synaptic neuron is small, only a small current is required for it to depolarize it.

Conversely, the motor neuron that cause the inking response of the Aplasia (sea slug), need the synchronous firing of many presynaptic cell because their large surface area lowers the resistance of the post synaptic neuron meaning that it needs a large depolarization current I, to reach threshold for an AP to fire.

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23
Q

Name two diseases that gap junctions are implicated in?

A

Charcot-Marie-Tooth Disease: Demyelination due to mutations of a Schwann cell connexin (connexin 32). Schwann cell death results in deformation due to imbalance of opposing muscle performance.

A leading cause of hereditary deafness: Caused by mutations leading to loss of connexin 26 in cochlear epithelial cells.

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24
Q

Discuss the role of gap junctions.

A

Found in all cell types and organs and plays a role in development and structural integrity.

At the synapse:
Permits rapid times and is thus key in escape response
Connects groups of cells for synchronicity
Width allows them to transfer metabolites (cAMP, IP3, small peptides, myelination)
Glial cells connect via gap junctions into large network

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25
Describe the importance of the synchronization of neuronal activity that is possible through energetic coupling?
A single electrical pre-synaptic neuron can energetically couple with many post-synaptic neurons thereby creating synchronized activity. For example, brainstem neurons that generate the rhythmic electrical activity that underlies breathing are electrically coupled. I am still not entirely clear on how the allow for synchronization. Something about a large network of simultaneously firing cells.
26
What is the space between chemical synapses called?
The synaptic cleft
27
What happens when calcium enters the pre-synaptic cell?
The transient increase in Ca concentration, allows the NT vesicles to fuse with the pre-synaptic membrane and release their contents into the synaptic cleft.
28
What happens when the NT diffuses across the post-synaptic cleft?
They bind to specific receptors, which causes channels in the post-synaptic membrane to open or sometimes to close. This changes the ability of ions to flow into or out of the post-synaptic cell. This NT induced current flow alters conductance and usually membrane potential of the post-synatpic neuron. This change in membrane potential then changes the likelihood of a neuron firing an AP.
29
How is NT removed from the synaptic cleft?
It is taken up by glial cells or degraded by enzymatic degradation. If this NT remained in the cleft, the action of the AP would continue.
30
How many NT have been identified?
More than 100. They are broadly classified as small molecule neuropeptides and neurotransmitters
31
Do neurons produce more than one type of neuronal transmitters?
Until recently it was believed that neurons produced only one type of neurotransmitter, but there is evidence that some neurons produce two or more neurotransmitters When more than one transmitter is released by a neuron these neurons are called co-transmitters.
32
Where are small molecule NT manufactured?
In the pre-synaptic terminal. The enzymes need to make these NTs are made in the neuronal cell body and then transported to the nerve terminal by slow axonal transport. The precursor materials need to make these NT are pulled into the terminal form the extra cellular space.
33
What are small clear-core vesicles?
Most small-molecule NTs are are packaged into vesicles that are 40-60nm in diameter, the centers of these vesicles appear clear on an electonmicrograph, accordingly these vesicles are referred to as small-clear core vesicles.
34
What defines neuropeptides?
They are synthesized in the cell body of a neuron. As such it is produced a long-way from its secretion site. It is brought to the terminal via fast axonal transport. Because these vesicles are electon dense they are often referred to as large dense-core vesicles.
35
Where is he neuromuscular junction?
The between the spinal motor neurons and the skeletal muscles. Visualize the connection of the spinal chord to the skeletal muscle.
36
What are end plates?
The synapse that the neuromuscular junction.
37
What is end plate potential (EPP)
It is the change membrane potential across the end plate at the neuromuscular junction. Said another way EPP is the depolarization of a muscle neuron that occurs when the pre-synaptic motor neuron fires an AP. Moreover, EPPs are evoked by the stimulation of the pre-synaptic motor neuron. This usually causes a sufficient depolarization in the post-synaptic muscle cell to produce an action potential.
38
What is an MEPP?
A miniature EPP. They are spontaneous and occur in the absence of pre-synaptic stimulation. MEPPs are 1mV and EPPs tend to be over 50 mV.
39
What happens if the neuromuscular junction is bathed in a solution that has a low concentration of Ca?
The post-synaptic muscle cell produces sub-threshold EPPs that are to sufficient to depolarize the cell and cause a contraction. In fact, they are about the same size as MEPPs. This tells us that no matter how little Ca there is in the extra cellular fluid interfering with the fusion and release of pre-synaptic vesicles, at least enough NT released to cause an MEPP change in potential. Moreover, it is not possible to release an amount of NT less than what is required to cause a random MEPP.
40
What is the quantal nature of NT release?
The NTs are released from the pre-synaptic neuron tend to occur multiples of a specific amount. Moreover, it is quantal. One of the ways that we know this is that EPP amplitude tends to occur as integer multiples of the mean MEPP amplitude. Moreover, a repsonse to a neurotransmitter either happens in a certain amount or a multiple of that amount or it does't happen at all.
41
What is the significance of the quantal natures of NTs?
Realizing this led to the understand of vesicular transport of NT. These vesicles are what create this quantal nature.
42
How many molecules of Ach are present in a single vesicle?
10,000. Interestingly this number corresponds very well to the amount of Ach required for an MEPP. This, of course, supports the idea that these quanta arise of the discharge of the contents of a single vesicle of Ach
43
What toxin do puffer fish produce and what does it do?
They produce TTX and it blocks all sodium channels
44
What is the drug 4-amino pyridine or 4-AP?
Increases the number of quanta released by a single action potential. It works by blocking K+ channels to prevent the repolarization of the cell. Varying the amount of 4-AP applied to the presynaptic cells
45
How was it proven that each vesicle that fused whit he presynaptic membrane was responsible for a single quata?
John Heuser among others correlated vesicle fusion with the number of quanta (MEPPs) in post-synaptic cell. They treated the presynaptic cell with 4-AP in order to increase the release of quanta. They then used the electron microscopy to count the vesicle fusion. They were abel to draw an entirely linear correlation between the number of quanta released and the number of vesicles fussing.
46
What is a quanta?
The amplitude in mV created by one MEPP. Now we know that a quanta is the amount of EPP created by the release of one NT vesicle, at the time that was not understood and each unit of potential neurotransmitter. IN a sense they were equivalent to MEPPs.
47
How is the fusion of NT vesicles with the presynaptic membrane visualized?
With an electron microscopical technique called freeze-fracture microscopy.
48
What is endocytosis?
The process by which fused vesicles are taken back into the cytoplasm of the nerve terminal.
49
What happened to capacitance when synaptic vesicles fuse the pre-synaptic terminal during NT release?
The membrane capacitance (Cm) increases because capacitance is proportional to surface area
50
What happens to the length of the AP when TTX or TEA is applied? How did this shed light on the role of Ca as the agent that triggered NT release.
A clamped cell with TTX can still produce and AP because the depolarization caused by the clamp is enough to open Ca channel even through the Na channnels are closed. This provided evince that that Ca mediated release, not Na because NT only need Ca to be released. Further when TEA did not NT release in a clamped cell what was in a calcium rich solution. The only thing that blocked NT release in cells sufficiently depolarized to open the Ca channels was the addition of Cadmium (Ca channel blocker).
51
What type of current makes the membrane potential becomes more negative?
An outward current is when positive ions leave the cell and the membrane potential becomes more negative or hyperpolarizes the cell
52
What is an outward current?
When the cell becomes hyperpolarized (more negative), either by negative current flowing in or positive current flowing out
53
What is in an inward current?
When a cell is depolarized (more positive). This occurs through either positive current flowing in or negative current flowing out.
54
What causes clear-core verses dense core vesicles to be released?
Low-frenwucny stimulation raises the Ca concentration close to the membrane favoring the release of small clear core NTs docked that the presynaptic specialization. High frequency stim causes increase of Ca concentration inside and outside the membrane. This global increase in Ca causes large dense-core vesicles containing peptides to be released in addition to the small molecule clear core vesicles. Moreover, high frequency stim is required to attain a significant enough Ca for large vesicle release
55
What is synapsin's role in NT release?
It reversibly binds to synaptic vesicles. It also keeps the vesicles bound to the reserve pool by crosslinking with each other an actin. When it is phosphorylated by CamKII, the vesicle dissociate from the reserve pool and make their way to the plasma membrane
56
How are reserve pool vesicle mobilized?
By the phosphorylation of synapsin by protein kinases, most notably Ca calmodulin-dependent protein kinase (CaMKII), which allows synapsin to dissociate from vesicles so they they can make their way to the plasm membrane and attach
57
What is ATPase?
An enzyme that turns ATP into ADP and a free phosphate ion.
58
What does priming of vesicles do in exocytosis?
It makes them fusion comportment
59
Name several proteins the regulate the assembly of SNARE proteins?
NSF, SNAP
60
What does SNARE mean?
SNAP receptors
61
Name several proteins involved in vesicle priming?
munc-13, nSec-1, complesin, snapin, syntaphilin and tomosyn
62
What is the purpose od priming vesicles?
To organize the SNARE proteins into the correct conformation for membrane fusion
63
What is the name of two prominent membrane vesicle proteins? One of them is a snare protein and one is not.
synaptobrevin is a SNARE protein synaptotagmin, not a SNARE protein. Binds Ca and then binds to SNARE proteins and the plasma membrane
64
What are the names of two prominent SNARE proteins found primarily in the plasma membrane?
syntaxin and SNAP-25
65
Where does Ca bind once it enters the neuron?
Ca binds to synaptotgmin, which was on the vesicle membrane. Then Ca bound synaptotagmin bind to SNAREs (Syaptobrevin, syntax and SNAP-25), which have already come together. After that, the whole thing is bound to the plasma membrane
66
Name the primary SNARE proteins and their roles?
Synaptobrevin is the in the vesicle membrane, it brings the vesicle to the contact with the SNARE proteins of the membrane. The SNARE proteins of the plasma membrane are called syntaxin and SNAP-25. These three proteins come together to form a helical complex that brings the vesicle in the correct position for release
67
What is synaptotagmin?
It is a Ca sensor protein in the membrane of vesicle. It catalyzes membrane vesicle fusion with the plasma membrane by fusing with the SNARE complex.
68
What happens if one of the 19 gene necessary for synaptotagmin is deleted in mice?
those mice die soon after birth
69
What happens when synapsin is phsophoylated by CaMKII?
The vesicle that has been phosphorylated leaves the reserve pool and migrates to the plasma membrane were it can then form the SNARE complex between synaptobrevin on the vesicle and syntax and SNAP-25 in the plasma membrane.
70
What is the vesicular monoamine transporter?
Uses a protein gradient with a low pH to drive moneamines into vesicles. Vesicles with low NT amounts will have smaller quanta. Transporters exchange protons fromt eh vesicles for neurotransmitter. The proton rich acidic interior is created by proton pump in the vesicle membrane. This protein pump brings acidity on the vesicle down to 5.5pH
71
Describe the impact of clostridium bacteria?
It causes botulism when ingested or tetanus when it contaminates puncture wounds. Botulism can cause paralysis due to impaired NT release Tatanus blocks the release of inhibitory transmitters from interneurons in the spinal cord producing hyper excitation of skeletal muscles. Both disorders have the same cause. Both toxins cleave snare proteins involved and are thus inhibitory. Botulinum toxins are taken up by motor neurons. Tetanus toxins are taken up by interneurons. Their different points of uptake are responsible for their different effect. Inhibiting motor neurons as it does in botulinum causes paralysis. Inhibiting interneurons prevents inhibitory NTs from firing thus causing excruciating pain.
72
Name another protein machinery that has a prodound impact on the function of the vesicle release machinery?
Munc-18. Dysfunctional Munc-18 protein have defective NT release.
73
What is the structure of clathrin?
Triskelion (there legged appearance) proteins that assemble around vesicles that are endocytosing. Once the vesicle is assembled they take off.
74
What s myasthenia syndrome? Why does it matter?
Disorders caused abnormal transmission at the neuromuscular synapse leads to weakness and fragility of skeletal muscles. Seems to result from insuffient NT in the synaptic cleft, which can occur for many reasons. A well-known type is Lamber-eatton myasthenia syndrome or LEMS. The number of quanta contained in EPPS is greatly reduced, although the amplitude of a spontaneous MEPP is unchanged showing the vesicles are full. Evidence shows that changes are due to the loss of voltage gated Ca channels. This is due to LEMS patients have many antibodies in their blood that bind to Ca channels
75
What protein causes the pinching off of the membrane
dynamin
76
What removes the calthrin coat?
An ATPase called Hsc70 and auxilin recruits Hsc70 to the coated vesicle.
77
What does Actin do in endocytosis?
It moves the clathrin coated vesicles right before auxilin recruits Hsc to remove the coats.
78
What are omega structures?
fusing vesicles
79
Name the types of endocytosis?
``` Clathrin mediated (slow) Ultrafast Bulk endocytosis (very high-stim) ```
80
What regulates the pore opening at gap junctions?
Most commonly voltage, but Ca and pH can too.
81
Are gap junctions always excitatory?
Yes
82
How are neurotransmitters defined?
1. ) Substance must be present int a presynaptic neuron 2. ) Substance must be released in response to a depolarization and the release must be Ca dependent 3. ) Specific receptors for a substance must be present on the post synaptic cell
83
What is the difference between an agonist and an antagonist?
an agonist perfectly mimics a ligand. An antagonist prevents the ligand mediated response.
84
Where are peptides made?
In the rough ER
85
Describe the synthesis of classical neurotransmitters?
Enzymes required for NT synthesis are produced in the RER and packaged into vesicles in the golgi. They then travel along microtubules via slow axonal transport. Precursors are taken into the axon terminal assembled with the appropriate enzyme loaded into vesicles and secreted. They are then broken down in the extra cellular space or taken back in to the pre-synaptic membrane.
86
What is EPC?
End plate current. Current resulting from the summed opening of many ion channels.
87
What is it called when the EPC reverses?
The reversal potential
88
What is the equation for the EPC?
EPC=g (Vm-Erev)
89
ACh receptors are permeable to what ions?
Equally permeable to N and K. We know this because when the extracellular concentration of either ion is changed, the Erev changed. Low
90
What generates the EPC,?
Influx of Na
91
How many times can neuropeptides be used?
Once.
92
What has a reversal potential more positive than the AP threshold?
An EPSP
93
What has a reversal potential more negative than the AP threshold?
An IPSP
94
Do IPSP's depolarize or hyperpolarize cells?
Counter-intuitively they can do either. As long as the reversal potential is below the threshold potential both circumstances will be inhibitory
95
Do EPSPs hyperpolarize for depolarize cells?
Depolarize
96
Name the biogenic amines?
dopamine, norepinephrine, epinephrine, serotonin and histamine
97
What are the precursors of Ach?
acetyl coenzyme A--synthesized from pyvurvate made from glucose and choline, which is found in the plasma. ACh is made in the nerve terminal in a reaction catalyzed by choline acetyltransferase (CAT).
98
How does choline enter the neuron?
It is taken into the axon terminal by a high-affinity Na-dependent choline co-transporter (ChT). The transporter sends out one Na+ molecule for each Choline molecule it takes in.
99
How is Ach loaded into vesicles?
Ach transporter (VAChT) loads about 10,000 molecules into each vesicle. The acidic pH inside the vesicle provide the energy necessary to pack it. The VAChT replaced ACh for H+
100
How does the action of AcH end?
Not by reuptake, but by enzymatic breakdown. The enzyme that breaks ACh down is called acetylcholinesterase (AChE). It leaves acetate and choline in the synaptic cleft. The choline can be transported again into the neuron and synthesized again into ACh. ACh is removed from the cleft in 1ms. There is also a bit of diffusion
101
How does sarin work?
Like many insecticides, it works by inhibiting the action of AChE (acetylacholineesteorase). When AChE is not broken down in the cleft, the build-up o ACh depolarized the post-synaptic cell and renders it indifferent to further ACh release, which causes paralysis.
102
What is nAChR?
It is the nicotinic ACh receptor, it named this because nicotine binds here. The channel is a not-selective cation channel
103
Describe the structure of the nicotinic receptor?
Five subunits. There are homomertic and heteromeric, depending on if the subunits are the same or different.. IN either structure they will require 2 alpha subunit where the ACh binds. Each of the five subunits is made of four domains 2 molecules of ACh must bind to open the channel. Each subunit of the ACh receptor has four domains
104
How is an AP prevented, so the only EPPs can be studied?
Curare, a nitotinic receptor antagonist. At low dosed it will block some, but not all of the nAChR. Enough to prevent an AP. As long as threshold isn't reached EPP only can be studied.
105
What is the graphic relationship between EPP and EPC?
Opposite. An inward (downward sloping) current makes the membrane potential more positive (upward sloping).
106
What is the graphic relationship between EPP and EPC?
Opposite. An inward (downward sloping) current makes the membrane potential more positive (upward sloping).
107
How current flows through an average ACh receptor?
2.7pa. At an average endplate there might be 200,000 ACh receptors
108
What domain lines the channel pore of the nACh receptor?
M2. Thus the M2 domain is very important because of the role that it plays in ion selectivity. The M2 domain is lined with negatively charged amino acids, which attract the positive cations.
109
How is the nACh pore closed?
Hydrophobic leucine ring pores come together to block anything from flowing through the channel. When open an threeonine ring aids in passages through the pore of cations.
110
How to animal toxins that work on ACh receptors work?
The toxins bind to ACh receptors an prevent musclues from responding to the ACh. Thus they cannot contract.. Interestingly cobras have evolved an extra sugar on their ACh receptor so that their own toxins cannot bind.
111
What is myasthenia Gravis and what role does ACh play in it?
Causes muscle and impaired facial movements. Patients produce anti bodies that attach nicotine receptors leading to a loss of post-synaptic response. In MG the first AP might look normal, but over time, responses dwindle. Blocking acetylcholinesterase is one of the most effective ways to treat the disease.
112
Describe the structure of the muscarinic receptor?
The receptor is a single molecule with 7 transmembrane domains. Basically, the receptor is one subunit. The receptor connects to the G-protein, which connects to the channel.
113
What are metabotropic ACh receptors called?
muscarinic receptors. So named because muscarin is an agonist for the receptor.
114
Where in the brain are muscarinic receptors highly expressed?
In the straitum and the forebrain where they can inhibit dopamine release. They also regulate the heart, smooth muscle and glands
115
How does the muscarinic receptor cause the heart to slow down?
Muscarinic receptor activation open K channels, which causes K to flow out of the neuron. The flow of K out of the neuron hyper polarizes the cell, which is inhibitory. Also, preventing the low-threhold t-type calcium channel from opening is also inhibitory. This is why stimulating the vagus nerve slows down the heart
116
How is channel permeability established?
The resides determine what can flow through.
117
What are the different types of mucscarinic domains?
There are five types and each are coupled to different G-protiens, they cause a variety of slow slow post-synaptic responses.
118
What is the rate limiting step in ACh synthesis?
the availability of choline and acetyl-CoA
119
What is choline?
It is a macronutrient. Not synthesized
120
What receptor mediated the effects of ACh in the brain?
muscarinic ACh
121
What causes Myasthenia gravis?
EPPs and MEPPs are much smaller than usual. The synaptic cleft widens and the number of ACh receptors declines dramatically. This is due to antibodies attacking ACh receptors. One way to treat it is by administering acetylcholinesterase inhibitors, which prevent the acetylcholinesterase enzyme from breaking down ACh in the synaptic cleft.
122
What type of ACh receptors are in the heart?
Muscarinic
123
How do muscarinic ACh receptors change ionic flow?
They inhibit Ca current and enhance K current

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