48 Neurons, Synapses and Signaling Flashcards
1
Q
What cells support the neutrons?
A
Ganglia.
2
Q
What is the nervous system divided into?
A
The central nervous system (CNS) and the peripheral nervous system.
3
Q
What are the basic types of neurons?
A
Sensory neurons, interneurons and motor neurons
4
Q
What are sensory neurons?
A
Neurons that transmit information from SENSORS that detect internal and external stimuli.
(note that the sensory neurone does not actually detect the stimulus, it simply relays it from the sensor)
5
Q
What are some example of external stimuli relayed by sensory neurons?
A
Light, sound, touch, heat, smells taste.
6
Q
What are some example of internal stimuli relayed by sensory neurons?
A
Blood pressure, blood carbon dioxide levels and also muscle tension.
7
Q
What are processing centres in the brain called?
A
Ganglia.
8
Q
What is the basic pattern of flow of information through the various types of neurons?
A
Sensory neurons of the PNS relay the “stimulus” from the sensor to the CNS. When it reaches the CNS is is integrated with other stimuli and processed by interneurons of the brain.
The processed output of the internreurons is relayed through the PNS by “motor neurons’ that trigger a response in an “effector” i.e. muscle.
9
Q
What is the structure of a neuron?
A
Fine projections called ‘dendrites’ receive electrical input and carry them to the “cell body”, which contains a ’nucleus’.
Any outputs are sent through the ‘axon hillock’ (pint between cell body and axon) which initiates the signal that will propagate down the axon.
The axon ends by branching out, leading to many “synaptic terminals”
10
Q
How does the structure of the neuron differ between types of neurons?
A
Interneurons have a vast number of highly branched dendrites and thus can receive input from up to 100,000 other neurons. They also have many axons.
Both sensory neurons and motor neurons have a few axons. Both have relatively few dendrites although motor neutrons tend to have a few more which are also longer.
Sensory neurons are unique in that they have their cell body partly along the axon.
11
Q
Where do the inputs to the dendrite come?
A
Either from the axons of other neurons or from sensory receptors.
12
Q
How does a signal pass between the axon and a dendrite?
A
This connection is called synapse and the gap between the two neutrons is called the “synaptic cleft”
There is a small gap between the “presynaptic neuron” and the “postsynaptic neuron”.
Upon being triggered by an action potential the “presynaptic neuron” releases neurotransmitters that diffuse across the gap (called the “synaptic cleft” ) and trigger the continuation of the signal when they reach the “postsynaptic neuron”
13
Q
What functions doe glia perform?
A
They nourish neurons, insulate the axons and regulate the extracellular fluid that surrounds the neurons.
14
Q
How are signals carried along the axons of neurons?
A
As action potentials.
15
Q
What are action potentials?
A
A wave of depolarisation that travels down the axon due to coordinated diffusion of ions into and out of the neurons.
16
Q
Through what do ions move through during action potentials?
A
“Gated ion channels”
17
Q
What happens to membrane potential as a signal is received at a cell body?
A
If the signal is a EPSP (excitatory post-synaptic potential) the membrane potential will “depolarise” Since the “resting potential” is negative this will increase the voltage.
If the signal is an IPSP (inhibitory post-synaptic potential) it will “hyperpolarise” the membrane and thus bring is farther from the threshold.
18
Q
What conditions lead to the initiation of an action potential?
A
The sum of the depolarisations by EPSPs and of the hyperpolarisations by IPSPs must exceed the voltage “threshold.”
If this threshold is met an action potential is triggered.
19
Q
What does “membrane potential” refer to?
A
The charge difference (voltage) across the membrane due to the difference in ion concentration.
20
Q
What is the baseline “membrane potential” of the neuron called?
A
Its “resting potential”
21
Q
What is the voltage of a typically neuron’s resting potential?
A
-60 to -80 mV
22
Q
What does the negative resting potential indicate?
A
That there is a net negative charge inside the cell.
23
Q
How does the resting potential arise?
A
Sodium-potassium pumps transport Na+ out of the cell and move K+ into the cell. This would lead to a net neutral charge.
The potential is negative because few sodium channels are open and thus very few sodium ions can diffuse back into the cell. Conversely many potassium ions are open at rest and thus allow potassium ions to diffuse out of the cell.
Therefore there is a net movement of potassium ions and thus positive charges out of the cell so it becomes more negative.
24
Q
What form of transport are potassium channels and sodium channels?
A
They passively transport the ions through ‘facilitated diffusion’
25
Besides sodium and potassium, what contributes to the membrane potential?
The extracellular fluid has a significantly higher concentration of Chloride ions which actually make the cell less negative.
Conversely the cell is made more negative due to the large anion inside it such as proteins.
26
What does A- (superscript -) refer to?
Large anions i.e. proteins inside the cell.
27
Where are more Cl- ions seen: inside the neuron or in the extracellular fluid? What is the consequence of this?
More are in the extracellular fluid which actually makes the cell less negative.
28
How can the membrane potential be predicted?
Assuming all the ions have a charge of 1+ or 1- Nernst’s equation can be used so that:
Eion = 63 mV (log (ion concentration outside / ion concentration inside) )
Where Eion (E subscript ion) is the ion’s equilibrium potential (in mV) and the ion concentration are measured in moles/millimoles.
29
What does equilibrium potential refer to?
The theoretical membrane potential of the ions when they reach equilibrium i.e. no net flow.
30
How do signals travel down dendrites?
As “graded potentials” i.e. electrotonic potentials.
Unlike action potentials which are ‘all-or-nothing’ these have a variety of strengths and thus can be used to integrate the EPSPs and IPSPs of the various dendrites as they recombine.
31
How are graded potentials formed and what property does this yield?
Graded potentials are formed as ion move into or out of the dendrite. These ions then diffuse through the dendrite, leading to a increase in membrane,
However the further the ions diffuse the more the signal weakness and thus dendrites with synapses closer to cell body initiate stronger IPSPs and EPSPs.
32
How can an action potential portray the strength off a signal?
An action potential, unlike a graded potential, is an all or nothing response and thus the magnitude of the signal can not be encoded in the strength of the action potential.
To encode quantitative information either many separate action potentials must be sent rapidly or many fibres carry the same signal to the same place.
33
What structure leads to the conduction of action potentials?
Voltage-gated ion channels.
34
What conditions trigger an action potential?
The sum of the EPSPs and IPSPs received by the cell body must exceed a ’threshold'
35
What is a typical threshold for an action potential to be triggered?
-55 mV
36
What happens during an action potential?
Resting State: The gates Na+ and K+ channels are closed. The undated channels maintain the resting potential.
Depolarisation: A stimulus opens some Sodium channels at the postsynaptic neuron. The influx of sodium ions depolarises the membrane of the cell body through a graded potential. If the depolarisation reaches the threshold an action potential is generated.
Rising phase: The depolarisation opens the voltage gates sodium channels whereas the potassium gates remain closed. This causes a further influx of sodium ions into the cell and thus the membrane potential increases rapidly.
Falling phase: As the voltage increases the sodium channels become inactivated as the potassium channels open. This causes K+ ions to leave the neuron and thus the membrane depolarises. out of the
Undershoot: The sodium channels close, but some potassium channels are still open causing the membrane potential to drop below resting potential. These potassium channels close and the sodium channels become unblocked (though still closed), the membrane returns to its resting state.
37
What does the period in which the neuron is unable to fire called?
The refractory period.
38
What causes the refractory period of the neuron?
During the falling phase and undershoot of the action potential the sodium channels are not only closed but also blocked by “inactivation loops.” Therefore the sodium channels can’t open until these loops have been removed. Because the sodium ion channels are needed to initiate the action potential the time in which these channels are blocked, called the ‘refractory period’, does not allow any new action potentials to form.
(note that this refractory period is not due to the cell running out of ions etc.)
39
How is volume portrayed through action potentials?
As the sound gets louder the ear sends action potentials at a greater frequency.
40
Where is the action potential initiated?
Generally the axon hillock.
41
Why is the refractory period important to the proper operation of the neuron?
It ensures that the action potential only travels in one direction.
42
Why do action potentials travel in one direction?
An action potential is generated as Na+ flows inward across the membrane at one location.
The depolarization of the action potential spreads to the neighboring region of the membrane, reinitiating the action potential there. Behind this this region, the membrane is repolarizing as K+ flows outward.
As the region behind the front of the action potential is depolarising it is in its refractory period. Therefore it can not carry an action potential.
Therefore because the region behind the action potential is in its ‘refractory period’ the action potential can not travel backwards and depolarise the cell body.
43
What are the major factors in deterring the rate of an action potential down an axon?
The diameter of the axon (thicker=faster) and whether or not the axon is ‘myelinated’ (surrounded by a myelin sheath.)
44
How are myelin sheaths produced?
By glial cells. In the CNS specialise glia called Oligodendrocytes produce the myelin sheaths. In the PNS they are produced by Schwann cells (also a form of glial cell)
45
In what animals are myelinated axons seen?
Vertebrates only
46
What are the myelin sheaths made of and why is the important?
They are mostly lipids. This is important as they are poor conductors of electricity.
47
How do myelin sheaths increase the rate of action potential conduction?
In a non-myelinated axon the membrane is not insulated so the membrane potentials dissipate over short distances. Therefore the volatge-gated sodium channels must be close for the influx of ions at one to trigger the next. However because their is a latency each time one channel is opened the more channels the signal has to pass through, the slower the signal will propagate.
In myelinated axons the membrane is insulated and thus the membrane potentials dissipate less rapidly. Therefore the voltage-gated ion channels can be farther apart.
Such voltage gated ion-channels are found exclusively at the “nodes of ranvier” between myelin sheaths. As the signal passes between the nodes of ranvier to insulation allows it to travel purely through electrical conduction. Since this is much faster than moving through various voltage-gated channels the signal jumps between nodes of ranvier.
This jumping is called ’saltatory conduction'
48
What disease is caused by malfunctioning myelin sheaths and what happens specifically?
In “multiple sclerosis” the myelin sheaths harder (skleros=hard) and deteriorate. This impairs saltatory conduction leading to a degradation of nervous function.
49
How do signals travel across the synapse?
When an action potential arrives at the Axon terminal it depolarises the membrane. This triggers voltage-gated Ca2+ channels to open.
The elevated concentration of Ca2+ causes synaptic vesicles in the axon terminal to fuse with the presynaptic membrane. This releases neurotransmitters into the synaptic cleft.
These neurotransmitters diffuse across the synaptic cleft and binds to ligand-gated ion channels in the postsynaptic membrane. This triggers opens ion channels that Na+ and K+ to diffuse through i.e K+ out and Na+ ion.
This depolarises the membrane and thus triggers a graded potential. (since it depolarises the membrane this is an EPSP)
50
How do a synapse trigger an IPSP or an EPSP?
Based on the neurotransmitter released and the ligand-gated channels it can bind to determine if an IPSP or an EPSP is generated.
An EPSP is triggered when the neurotransmitter activates a ligand-gate ion channel that is permeable to both K+ and Na+. As Na+ moves into the cell and K+ leave the net movement of charge is into the membrane so it becomes more positive.
In an IPSP the neurotransmitter activates a ligand-gated ion channel that is permeable only to K+ or Cl-. The diffusion of Cl- into the neuron or K+ out lowers the membrane potential farther form the threshold and thus is an IPSP.
51
In a neuron, what are the concentration gradients of Sodium and of Potassium?
There is a greater concentration of Sodium ions out side the cell so it will tend to diffuse in and polarise the neuron.
There is a greater concentration of K+ ions inside the cells so they tend to diffuse out and hyperpolarise the neuron.
52
What are the vesicle that release the neurotransmitters during an action potential called?
Synaptic vesicles.
53
In what class of synapses is the signal propagated using neurotransmitters?
“Chemical synapses” (the vast majority.)
54
What are the ligand-gated ion channels also known as?
Ionotrophic receptors.
55
If a single EPSP is not sufficient, how can the threshold be reached?
Through the summation of multiple EPSPs (and IPSPs)
56
In what ways can summation of EPSPs occur?
Spacial summation and temporal summation.
57
What is spacial summation?
Two different dendrites are activated simultaneously. Their individually small EPSPs are thus combined, along with any IPSPs
58
How does the sodium-potassium ion pump work?
For each stroke i.e. ATP use it moves 3 sodium ions outside the neurone and moves three in.
59
What is temporal summation?
When a dendrite is activated the membrane gradually depolarises. If a second action potential is received before the membrane fully depolarises these EPSPs (or IPSPs) are combined to yield a stronger depolarising effect.
60
Why is temporal/spatial summation important?
It allow the neuron to integrate multiple inputs and allows IPSPs to regulate EPSPs i.e. two simultaneous IPSPs could nullify a single EPSP.
61
What factors determine the strength of the postsynaptic potential?
Many, including how many ligand-gated ion channels are present and the amount of neurotransmitter released by the synaptic vesicles.
62
Besides a ligand-gated ion channel, what can a neurotransmitter bind to?
In some synapses it binds to a “metaboropic receptor"
63
What happens when a metabotropic receptor binds to a neurotransmitter?
It activates a signal transaction pathway in the postsynaptic cell by releasing a second messenger.
This allows them to modulate the responsiveness of postsynaptic neurons such as by controlling the number of open potassium channels to modulate the resting potential and thus make it easier or harder for an EPSP to reach the threshold.
64
How do metabotrophic receptors differ in purpose from ligand-gated ion channels?
Ligand-gated ion channels lead to a temporary increase or decrease in membrane potential and thus trigger or suppress action potentials.
Metabotropic receptors modulate the postsynaptic neuron and thus ‘fine tune’ the neuron to be more or less sensitive etc.
65
How do ligand-gate ion channels and metabotropic receptors differ in chronology?
Ligand-gated ion channels have a rapid response that last for a brief time.
The responses initiated by metabotropic are longer lasting (minutes or even hours) but take longer to begin.
66
What is an example of a specific metabotropic receptor and its signal pathway?
When the neurotransmitter norepinephrine binds to its metabotropic receptor, the neurotransmitter-receptor complex activates a G protein, which in turn activates adenylyl cyclase (ATP to cAMP) cAMP activates protein kinase A, which phosphorylates specific ion channel proteins in the postsynaptic membrane, causing them to open or close.
Because of the amplifying effect of the signal transduction pathway, the binding of a single neurotransmitter molecule to a metabotropic receptor can open or close many channels.
67
What are neurotransmitters divided into?
5 groups: Acetylcholine, Amino Acids, Biogenic Amines, Neuropeptides and Gases
68
What neurotransmitters are in the group Acetylcholine?
Just Acetylcholine - its in a class of its own
69
What neurotransmitters are in the group Amino Acids?
GABA, Glutamate and Glycine
70
What neurotransmitters are in the group Biogenic Amines?
Norepinephrine, Dopamine and Serotonin
71
What neurotransmitters are in the group Neuropeptides?
Many, including ’Substance P’ and Met-enkephalin
72
What neurotransmitters are in the group Gases?
Nitric Oxide (NO) and Carbon monoxide (CO)
73
What is ‘Met-enkephalin’ a type of?
Endorphin
74
What is an example of an endorphin?
Met-enkephalin
75
What does “GABA” stand for?
Gamma-aminobutyric acid
76
In what organism is acetylcholine found?
Vertebrates and invertebrates.
77
What is the function of acetylcholine?
It acts in two places: at neuromuscular junctions and in the heart.
78
What is a neuromuscular junction?
A place where the axons synapse with the skeletal muscle cells.
79
How does acetylcholine act as neuromuscular junctions?
It acts as a ligand that opens the ligand-gated ion gates and thus leads to an EPSP.
This excitatory activity is soon terminated by acetylcholinesterase, an enzyme in the synaptic cleft that hydrolyzes the neurotransmitter.
80
What is special about the acetylcholine receptors?
The ones found at the neuromuscular junctions are actually found throughout the PNS and CNS.
These receptors bind not only to acetylcholine but also to Nicotine, expelling the physiological and psychological effects of this stimulant.
81
How does acetylcholine act in the heart?
It binds to metabotropic receptors that are found in the heart (and throughout the CNS).
In heart muscle, acetylcholine released by neurons activates a signal transduction pathway. The G proteins in the pathway inhibit adenylyl cyclase and open potassium channels in the muscle cell membrane. Both effects reduce the rate at which the heart pumps. Thus, the effect of acetylcholine in heart muscle is inhibitory rather than excitatory.
82
What can cause unusual levels of acetycholine?
The nerve gas ’sarin’ inhibits acetylcholinesterase causing a buildup of acetylcholine and thus paralysis and death.
Certain bacteria release a toxin that inhibits the release of acetylcholine. This lead to “botulism” which inhibits acetylcholine’s effects at triggering muscles and thus is used in ‘Botox.'
83
What is ‘glutamate’?
An amino acid neurotransmitter that is the most common neurotransmitter in the CNS and binds to several types of ligand-gated ion channels to cause an EPSP in the postsynaptic cell.
84
What is ‘GABA’?
An amino acid neurotransmitter that is the neurotransmitter at most of the inhibitory synapses of the brain. Binding of GABA to receptors in postsynaptic cells increases membrane permeability to Cl-, resulting in an IPSP.
85
What is ‘glycine’?
An amino acid neurotransmitter that acts at inhibitory synapses outside of the CNS.
86
How can glycine functionality be affected?
It binds to ionotropic receptors that are inhibited by strychnine, a chemical often used in rat poison.
Thus when the poison is present the activity of glycine is indirectly impaired.
87
How can the functionality of GABA be affected?
The widely prescribed drug diazepam (Valium) reduces anxiety through binding to a site on a GABA receptor.
88
How can anxiety be treated medically?
With diazepam (Valium) which reduces anxiety by binding to a site on a GABA receptor
89
What are biogenic amines chemically?
Neurotransmitters that are synthesised from amino acids.
90
What is ’norepinephrine’ as a neurotransmitter?
A biogenic amine neurotransmitter that acts as an excitatory neurotransmitter in the autonomic nervous system (part of the PNS)
Out side of the nervous system it is a hormone.
91
How is dopamine synthesised?
From tyrosine.
92
How is serotonin synthesised?
From tryptophan
93
What is ‘dopamine’ and ’serotonin’?
Biogenic amines that are released by the brain to mediate sleep, mood, attention and learning.
94
How can ‘dopamine’ and ’serotonin’ be affected?
Some psychoactive drugs like LSD and mescaline yield their hallucinatory effects by binding to the receptors in the brain that are typically bound by dopamine and serotonin.
95
What neurotransmitter is involved in Parkinson’s?
Dopamine (caused by degradation of substantia nigra)
96
What disease is related to serotonin?
Severe depression which can be treated by drugs that increase the concentration of biogenic amines.
Prozac, for example, enhances the effect of serotonin by inhibiting its reuptake after release.
97
How are neuropeptides formed?
Typically by the cleavage of larger proteins.
98
What is ’substance P’?
A neuropeptide that is a key excitatory neurotransmitter that mediates our perception of pain through metabotropic receptors.
99
On what do neuropeptides act?
On metabotropic receptors and thus all have modulatory effects.
100
What are endorphins?
Neuropeptides that are secreted by the body to act as analgesics i.e. suppress pain.
101
How do many pain killers work?
Many, like morphine and heroin (opiates), bind to the receptors that typically bind to endorphins.
102
When specifically are endorphins released?
During periods of intense physical or emotional stress i.e. childbirth.
103
What effects do endorphins have?
Besides suppressing pain they decrease urine output, depress respiration, and produce euphoria, as well as other emotional effects.
104
How does nitric oxide differ from other neurotransmitters?
It is not released from synaptic vesicles and is instead produced on demand as it breaks down quickly.
It does not trigger a postsynaptic potential but instead diffuses through the tissue to act as a ‘local regulator’ i.e. to tell the smooth muscle of the surrounding blood vessels to dilate.
105
How does Viagra work?
By suppressing an enzyme that otherwise terminates the action of NO.
106
How does Carbon monoxide act as a neurotransmitter?
Carbon monoxide is generated by the enzyme 'heme oxygenase', one form of which is found in some groups of neurons in the brain and PNS.
In the brain, CO regulates the release of hypothalamic hormones.
In the PNS, it acts as an inhibitory neurotransmitter that hyperpolarizes the plasma membrane of intestinal smooth muscle cells.
107
What is the movement of signals between node of randier called.
Saltatory conduction
108
What does 'saltatory conduction' refer to?
The "jumping" of signal between nodes of ranvier due to the insulating properties of the myelin sheath
