Microstructure & Signaling Flashcards
Cells in the CNS are broken down into two components: ____ cells and ____. The ____ cells are there for support and they are the bulk of the mass of the brain. They are called ____ after glue, they keep everything together. When looking at the brain the majority of what you are looking at is ____ cells.
glia; neurons; glia; glia; glia
Interspersed within the glia cells are the _____ that are responsible for cell signaling.
neurons
The different type of glial cells are ______ cells, ______, and _____ astrocytes ((grey/white) matter).
microglial; oligodendrocytes; fibrous; white
(Astrocytes/Microglial cells) are the MOST common cell type in the CNS.
Astrocytes
(Astrocytes/Microglial cells) supply cells with nutrients from
Blood & CSF.
Astrocytes
(Glucose/Lactate) is not the preferred energy currency of the neurons. The preferred currency is (glucose/lactate). Neurons thrive off of (glucose/lactate). They can deal with (glucose/lactate) but prefer (glucose/lactic acid).
Glucose; lactate; lactate; glucose; lactic acid
One of the key features of astrocytes is to take (glucose/lactic acid), break it down, put it through the Krebs cycle, produce (glucose/lactic acid), and then spoon-feed it to the neurons they are attached to. The neurons are then absorbing the (glucose/lactate) that is being produced from the astrocytes.
glucose; lactic acid; lactate
Astrocytes aid in CNS development by guiding neuroblast migration and provide structural support by grouping neuron clusters and enclosing bundles of (myelinated/unmyelinated) axons.
unmyelinated
Astrocytes create a net around the pial layer so that as the CNS develops through that neuralation process, brain cells stop at the end of that radial process and form a cortex and doesn’t escape out into the periphery. It keeps everything where it is supposed to be so you don’t have ____ mass growing where ____ mass isn’t supposed to be.
brain; brain
(Astrocytes/Oligodendrocytes) secrete growth factors, cytokines, and neurotransmitters.
Astrocytes
(Astrocytes/Microglial cells) play a role in injury response by _____ tissue formation going in and filling in areas where there has been damage.
Astrocytes; scar
(Astrocytes/Microglial cells) play a role in neurotransmission by recycling _______. They also play a role in neurovascular coupling by releasing neurotransmitters to (increase/decrease) blood flow into areas of increased activity.
Astrocytes; neurotransmitters; increase
Astrocytes have _______ feet and these feet but up (line up) against the blood vessels and the feet act as a filtration that is going to be actively creating the blood brain barrier. It is going to be controlling pH and keeping larger molecules from invading into the CNS. So we are trying to keep virus and bacteria out of the CNS by keeping the blood brain barrier. Essentially these feet are making sure that the things that is entering the brain are the things that we want.
perivascular
Microglia are immune effector cells that are derived from (microphages/macrophages). They are also ______ mediators (cytokines and prostaglandins).
macrophages; inflammatory
Oligodendrocytes are responsible for myelination of the (cell body/axons) and along with that process they are going to wrangle everybody ((cell bodies/axons)) together that has similar function so they don’t stray away.
axons; axons
Myelin helps to (increase/decrease) the speed of conduction.
increase
Neurons are considered to be the most important aspect of the (CNS/PNS) because that is where the signal processing and signal transmission occurs.
CNS
The (neurons/dendrites) hang by the cell body. They are like branches of a tree coming off the main stem of the tree. That is responsible for receiving the signal.
dendrites
The (dendrite’s/neuron cell body’s) purpose is to keep the neuron alive through metabolic and repair processes. This is where the golgi bodies are going to be, the mitochondria are going to be.
neuron cell body’s
The (cell body/nucleus) of the cell body is making sure the cell is doing what it needs to do to stay alive.
nucleus
At the end of the cell body is the axon ____ and that is going to be important for generation of the action potential.
hillock
The (axon/dendrite) is where the signal is going to be carried through.
axon
Terminal (arbors/boutons) are where the axon starts to branch off and communicate through neurotransmitters with a neuron downstream of it with the dendrites so it is able to release the neurotransmitters to the cell next to it. That cell potentially goes through action potential depending on how the signaling goes.
arbors
The connection between the terminal arbors and the dendrites are called the ______.
synapse
Where the terminal arbor comes out there is something at the end called the terminal ______. That is where the neurotransmitter are going to be released to go to the receiving dendrite of the cell downstream.
bouton
The cell membrane is a very specific structure with respect to function of the neurons. It is a phospholipid bilayer, so you have two layers of (fat/water) cells. You have the outer lipid bilayer, on the inside you have a (fat/fluid) matrix and then another layer of cell sitting right underneath it.
fat; fluid
In neurons the function of the cellular membrane is very important because we have channels embedded into the cellular membrane and that cellular membrane and the channels that are embedded in it are critical for the function of the neurons ability to receive and send ______.
action potentials
The way that the neurons function the way that they do is through a combination of electrical and chemical signaling. (Chemical/Electrical) signaling within the cell functions to be able to carry the message down to the terminal bouton. (Chemical/Electrical) signaling functions down at the business end of the terminal bouton.
Electrical; Chemical
In order to create that electrical potential we have these open channels and there is inflow and outflow of different ions to be able to keep that electrical ionic flow to be able to provide the ______
action potential
The cell internally has a negative charge with respects to the extracellular space. With respects to the outside world the neuron itself is negatively charged at _ mV.
-70
The neuron membrane maintains a very specific resting potential through osmotic radiance. The body is trying to maintain homeostasis at a certain level and things are going to move from areas of (low/high) concentration to areas of (low/high) concentration.
low; high
When the cell is at rest we have (gated/ leakage/non-gated) channels. There is no cover over that gate to restrict what flows in and what flows out.
leakage/non-gated
When the neuron is at rest and it doesn’t need to generate an action potential you have this (active/passive) diffusion of ions in and out of the cell based on diffusion gradients. That maintains that resting potential of that _mV.
passive; -70
When we start to get to the business end of what the neuron does which is generate an action potential, this is where (non-gated/gated) channels come into play.
gated
(Ligand/Mechanical) gated channels are the channels that we are most familiar with. A neurotransmitter of a certain type binds on to a _____, kind of like a key-home mechanism. The right key fits, you open up the gate, there is an influx and out flux of certain ions, and you have generation of an ______. These gated channels also respond to (chemical/mechanical) stimulus and are involved in synapses.
Ligand; receptor; action potential; chemical
(Ligand/Mechanical) gated channels don’t respond to neurotransmitters using a key home mechanism. They respond to (chemical/mechanical) stimulus. You get the appropriate (chemical/mechanical) stimulus, the gate opens up, and you have an influx and outflux of different ions that changes the resting potential to generate an action potential. So where we are going to see these types of channels are where we have to produce (chemical/mechanical) stimuli: muscle spindles, joint receptors, and golgi tendon organs.
Mechanical; mechanical; mechanical; mechanical
(Mechanical/Voltage) gated channels are typically lining the axon of the neuron and they open and close depending on voltage changes. So if it is at -70mV, it stays (closed/open), if it changes to -50mV those channels (close/open) up. These channels respond to a change in resting membrane potential, these are going to be important for continuing the action potential down the length of the axon.
Voltage; closed; open
When we have the resting membrane potential, we have a good amount of open diffusion graded channels. You are going to have subtle changes within that electrical voltage and when that happens we depend on these things called ____ pumps to actively pump certain ions, either negatively or positively charged out of that intracellular space into the extracellular space just to be able to maintain -70mV. You don’t want voltage changes happening when you don’t want it to. In order to prevent that erroneous firing we have ion pumps monitoring everything. They actively pump (Ca+/Na+) out of the cell, even if [Na] is higher in extracellular.
ion; Na+
When something comes and attaches to the dendrite from the neuron above it that is signaling through, most likely a _______ , that is what is going to kick off the electrical response that generates the action potential .
neurotransmitter
The cell is at rest and then something happens. We either have a ligand neurotransmitter that is binding to a ligand gated channel or we have a mechanical stimulus of some sort that results in a stimulus. When that stimulus occurs it opens the channel that is going to cause an influx of an ion and we are going to get to what we call a (synapse/threshold). So the neurotransmitter that binds doesn’t have to get the whole cell to action potential. All it has to do is change it enough to get to that (synapse/threshold). In this particular scenario, the (synapse/threshold) is -55 mV. And once it gets the cell to -55mV the rest of the gates are going to start coming into the picture, opening up and resulting in an all or none response where the action potential is going to form and at the end of that we have neurotransmitter release at the terminal (arbor/bouton).
threshold; threshold; threshold; bouton
For the most part it is going to be ______ channels that open up. ______ is a positive ion so they are going to open up because you add a ligand or a mechanical stimulus to that channel. ______ ions are going to come rushing into the cell and because of that we are going to get that bump up from -70mV to -55mV. Once we get to that -55mV we have (mechanical/voltage) gated channels are going to open up and bring us the rest of the way.
sodium; Sodium; Sodium; voltage
Once we get the rest of the way down from the voltage gated channels, it is like a dominoe effect and it just travels all the way down through to the axon ____ where that signal is going to continue on down to the _____ itself. That is where conduction of the signal occurs.
hillock; axon
The way that the signal is propagated is that the cell got to threshold (-55mV). That triggers (mechanical/voltage) gated ions to open up. Within this particular region (red circle) there is an influx of sodium that is coming in and that sodium is going to diffuse out to the rest of that axonal space through intracellular fluid. As the sodium starts to diffuse out, the surrounding area starts to (increase/decrease) in voltage. More voltage gated channels open up and that area becomes more (positive/negative). So you get a consistent downstream of diffusion of sodium that is happening down the length of the axon until that potential change reaches the terminal (arbor/bouton) and you have an action potential that is generated.
voltage; increase; positive; bouton
Myelination occurs and in this space (the whole length of the axon) you don’t have any leakage of ions that you don’t want into the system. So as sodium comes in, it is going to be more highly concentrated. And because it is highly concentrated, that diffusion is going to travel down further and it is going to open up the sodium channels resulting in that downward gradient. The reason saltatory conduction is (slower/faster) is because the channels only have to open up where the gaps in the ____ are because you don’t have the leakage of ions in and out. You have a stronger solution getting down, it is traveling further, and it is just a more efficient process because the condition is right for a faster transmission of the signal.
faster; myelin
So what we essentially have is a (lower/higher) concentration of sodium sitting on the extra cellular milieu, and more potassium and (more/less) sodium sitting in the internal cell. So keep in mind, that’s going to be an important thing to keep in mind. There’s more sodium (inside/outside) than (inside/outside). And the inside is overall (negative/positive).
higher; less; outside; inside; negative
We have the axon hillock trigger zone going to threshold (negative 55, negative 50 millivolts). That starts to get these voltage channels warmed up and starting to open and (increase/decrease) sodium within that local zone right there. So much sodium is going to flood in at that area, is going to go to positive 20 or whatever that action potential number is for that particular nerve. Why is that necessary? The reason it’s necessary is because this whole thing is driven by diffusion. If we don’t get enough sodium coming into that area to drive that local concentration of sodium to positive 20, positive 30, you’re not going to have enough ions to diffuse down the rest of the way. We call that continuous propagation. And that’s what happens in (myelinated/unmyelinated) axons.
increase; unmyelinated
So here we have diffusion that’s happening going left and to the right. But the area that just went to positive, a positive 30, and went through its action potential and was involved in opening up the sodium channels for its neighbors. Down stream is starting to clean house with the sodium and potassium. They starting to kick in. And it’s dumping three (potassium/sodium) out for two (potassium/sodium) that are coming in. And upstream of where the action potential just happened, that part of the axon is starting to get (positive/negative) again. So the issue is you’re going to have some, some sodium that’s traveling to the right, some traveling to the left. If it’s traveling to the left, that’s getting kicked out. So you have this potential for a loss of sodium through the length of the axon. So there’s a chance one, it’s going to be very slow because it depends on that long diffusion gradient to be able to make it down the hallway of the axon down to the terminal button. There’s also a chance that the action potential might not occur because you’ve lost a good bunch of sodium and there was not enough sodium to reach threshold for the neighbors downstream. That’s where the benefit of myelination and saltatory conduction comes into play.
sodium; potassium; negative;
The nodes of ____ are the openings along the axon where myelination (is/ is not) occurring.
ranvier; is not
We call this green area here the leading edge of the action potential because that’s where the (lowest/highest) concentration of sodium is to drive further osmosis and diffusion of sodium downstream.
highest
That section of the axon behind the leading edge is going to be (positive/negative). It’s going to go through repolarization. Repolarization occurs due to the closing of the (Na+/K+) gates and opening of the (Na+/K+) gates.
negative; Na+; K+
There’s a section of repolarization that occurs called overshoot or hyperpolarization. And that happens because again, it’s not a precise process during the process of kicking out the sodium and bringing in as much potassium as the channels can bring in. There is an undershoot and it goes (above/below) negative 70 until things come to homeostasis again to negative 70 millivolts. So essentially, the K+ gates remaining (open/closed) results in hyperpolarization/undershoot.
below; open
In an absolute refractory period there’s no other action potential that can be generated on top of that action potential already occurring. Every sodium channel is (closed/open) right now to try to bring in as much sodium as it can to that leading edge to allow for diffusion of that sodium down that axonal gradient. There’s no more sodium that can be open. No stimulus can generate another action potential.
open
In the relative refractory period the Na+ channels are (closed/opened) and the suprathreshold stimuli can generate an action potential. So if you have a stimulus that is called supra threshold, you have a stimulus that comes in, that’s negative 30, negative 20, something that’s above negative 55. It might be able to generate another action potential to go further downstream, resulting in a (lesser/greater) release of neurotransmitters because you’ve had two action potentials following.
closed; greater
The area that sits (behind/ in front of) the peak of the action potential can still go through another action potential if there is a supra-threshold stimulus.
behind
At the area of the chemical synapse, which is the meeting of the terminal bouton and its homologue on the dendrites of the nerve below, we have what’s called a ______.
synapse
The presynaptic membrane belongs to the terminal (arbor/bouton) of the transmitting nerve.
bouton
The postsynaptic membrane sits on the (terminal bouton/dendrite) of the receiving nerve.
dendrite
Neurotransmitters are hacked in synaptic (clefts/vesicles). As the action potential gets down to that terminal bouton, these synaptic vesicles make contact with that (pre/post) synaptic membrane. And it’s going to release neurotransmitters into an area called the synaptic (clefts/vesicles), where it’s going to bind with the neurotransmitter receptor.
vesicles; pre; cleft
Neurotransmitter removal is typically an enzymatic degradation. So ______, one of the most common neurotransmitters that we have in the central and peripheral nervous system is responsible for the resulting contraction of a skeletal muscle at the neuromuscular junction. So what we have is acetylcholine esterase, which is the enzyme. It’s going to break apart the ligand receptors relationships. It’s going to pull the acetylcholine off of that ligand and the neurotransmitter will flow back into the synaptic (vesicle/cleft). Then it’s going to be diffused out of this cleft area and (astrocytes/microglial cells) are going to absorb the acetylcholine that has been broken up by the acetylcholine esterase. And then endopinocytosis (the purple structure) is going to be absorbed back into the (pre/post) synaptic membrane.
acetylcholine; cleft; astrocytes; pre
If the neurotransmitters are not broken down you will stay in a (relaxed/contracted) position.
contracted
Type (A/B) fibers are heavily myelinated and are responsible for heat, cold, touch, pressure, muscle, joint receptors, and “fast” pain
A
Type (B/C) fibers are myelinated but they’re not as heavily myelinated as type A fibers and we see these type of fibers in autonomic nervous system sensory response. They tell us what’s going on for visceral regulation, as well as motor nerves that are coming out of the spinal cord.
B
Type (B/C) fibers are unmyelinated and are responsible for slow visceral pain.
C
Myelination has an impact on conduction speed, but temperature also has an effect on conduction speed. Cold results in (slower/faster) conduction. Warm results in (slower/faster) conduction. The faster conduction you have, the more likelihood that you have the signal being conducted from the axon hillock all the way down to the terminal bouton. The colder it is, the less chance you have of that action potential reaching the terminal bouton, resulting in a neurotransmitter release.
slower; faster
Post Synaptic Potentials (PSPs) are driven by the type of neurotransmitters that are being released at the presynaptic membrane where there is the sending neuron to the receiving neuron. So we have an excitatory postsynaptic potential (EPSP). These are excitatory presynaptic neurons that are releasing neurotransmitters that result in (depolarization/repolarization) (+ ions pulled in to neuron).
depolarization
An inhibitory post synaptic potential is referred to as an IPSP. A nerve that’s responsible for an IPSP are referred to as inhibitory presynaptic neurons. And the neurotransmitters that that particular neuron releases actually makes the nerve more (positive/negative). So it resulted in a hyperpolarization at the post-synaptic membrane or to the receiving neuron. So what’s happening there is the nerve starts to shut down more and more and more. It results in more (positive/negative) ions being pulled into the postsynaptic membrane. Now It’s going from negative 70 to negative 90, negative 100. That nerve is going to be much harder to pull into action potential and result in a downstream neurotransmitter release.
negative; negative
Glutamate, Acetylcholine, Norepinephrine, and Dopamine are the most common types of (excitatory/inhibitory) neurotransmitters. All of these will result in (repolarization/depolarization) of the downstream nerve and eventually going through the action potential process.
excitatory; depolarization
GABA (Gama aminobutyric acid - Hyperpolarize postsynaptic membrane via influx of chloride), serotonin, and dopamine are examples of (excitatory/inhibitory) neurotransmitters.
inhibitory
(Agonists/Antagonists) are typically exogenous compounds. They bind to the neurotransmitter sites and mimic the activity of the neurotransmitter equating to a similar response of the downstream nerve. Some examples are poppy and tobacco.
Agonists
(Agonists/Antagonists) are typically exogenous compounds. They bind to the neurotransmitter sites but have no effect on the neuron. They just take up space and the intended NT cannot bind to it. An example is coffee.
Antagonists
As an (agonist/antagonist), we see acetylcholine in the neuromuscular junction and it enhances the response of dopamine (the reward center). Examples of (agonists/antagonists) include nicotine in tobacco and muscarine in mushrooms. Nicotinic receptors are found in the NM junction, PNS, and SNS.
agonist; agonists
Examples of (agonists/antagonists) are adenosine which is a neurotransmitter and plays a role in drowsiness and relxation, caffeine which is a competing antagonist, naloxone/naltraxone which are opiate antagonists competing antagonists. In these (agonists/antagonists) there is a CNS response to increased adenosine receptors which leads to central sensitization. Caffeine is a competing antagonist because it is going to bind to those adenosine receptors and you stay alert as a result of that competing antagonist. These types of competing antagonists result in something called central sensitization which is an important concept to us because it has been implicated in chronic pain.
antagonists; antagonists
So here what we see is an example of a more typical presynaptic and postsynaptic membrane setup where you have 4, 5, 6 presynaptic neurons connecting to a postsynaptic neuron. In this picture here, we have three neurons that are responsible for releasing EPSPs, and two neurons that are responsible for IPSPs. So in this particular scenario, depending on what the central nervous system is trying to signal, if none of these EPSP neurons are brought into the picture and just the IPSP transmitting neurons are brought to action potential, what we are going to have is we’re going to have (depolarization/inhibition) of this postsynaptic neuron. Vice versa. If the IPSPs are not stimulated and just the EPSP, presynaptic neurons are stimulated, the nerve (is going/is not going) to go to potential. If all five of these go off, then we have three EPSP generating neurons and two IPSP generating neurons. So the net effect that we’re going to have is an overall (EPSP/IPSP) response at this postsynaptic neuron.
inhibition; is going to; EPSP
So we mentioned temperature slowing down or speeding up conduction. The reason for that is diffusion. Remember the whole process is predicated upon sodium diffusing further down. Colder temperature equates to (less/more) diffusion and warmer temperature equates to (less/more) diffusion.
less; more
So this is just another example of temporal summation. If we have a four hertz stimulus, which we’ll just call it a very low stimulus. If we have a little bump in the threshold, then it starts to go back into depolarization before the next one comes. The next one comes, it gets higher, it gets polarized a little bit, it gets a little positive. But it starts to back off because the rate of stimulus just is not great enough. If we take a look at this picture here, we have an eight hertz potential. Here. The first stimulus comes and it starts to get depolarized. And then as it starts to depolarize again before it gets all the way down to the basement and its resting potential. Another one quickly comes and brings it up a little bit higher, starts to go down, but it doesn’t go down all the way. Another one comes, another one comes, each one building on top of each other until you get to a threshold type of the stimulus. And that’s something that we will see in temporal summation. So low-frequency at the four hertz, the action potential might not even get to threshold versus eight hertz because you have so many, you have so many frequencies, you have so many stimulations happening within a certain time span. You have a summative effect resulting in (smaller/larger) magnitude depolarization.
larger
