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What is a unitary post synaptic potential?

What is a unitary post synaptic potential?


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I am reading the paper Cooperative subnetworks of molecularly similar interneurons in mouse neocortex and have encountered the term: "Unitary (excitatory or inhibitory) post synaptic potential". I know what is an excitatory (or inhibitory) post synaptic potential. But what does the unitary refers to?

Thanks!


What is a unitary post synaptic potential? - Biology

IT is generally believed that synaptic transmission is effected by a quantal release of transmitter substances, such as has been demonstrated for the neuromuscular junction 1 . The quantal nature of synaptic transmission in the central nervous system is more difficult to investigate, one reason being that many presynaptic fibres usually contribute to the EPSP (excitatory postsynaptic potential), whereas at the neuromuscular junction the entire effect is evoked from a single presynaptic fibre. Thus at central synapses the total synaptic action should be described both in terms of the number of unitary EPSPs (the EPSP contributed by a single presynaptic fibre) and the quantal composition of each unitary EPSP. In motoneurones, impulses in Ia afferents (large muscle spindle afferents) usually evoke small unitary EPSPs with a low quantal content 2 , but larger unitary Ia EPSPs with quantal content ``possibly as high as ten or fifteen'' have also been found 3 .


Excitatory synapses

The neurotransmitter at excitatory synapses depolarizes the postsynaptic membrane (of a neuron in this diagram). Example: acetylcholine (ACh)

  • Binding of acetylcholine to its receptors on the postsynaptic cell opens up ligand-gated sodium channels.
  • These allow an influx of Na + ions, reducing the membrane potential.
  • This reduced membrane potential is called an excitatory postsynaptic potential or EPSP.
  • If depolarization of the postsynaptic membrane reaches threshold, an action potential is generated in the postsynaptic cell.

Long-term Depression (LTD)

Long-term depression (LTD) is essentially the reverse of LTP: it is a long-term weakening of a synaptic connection. One mechanism known to cause LTD also involves AMPA receptors. In this situation, calcium that enters through NMDA receptors initiates a different signaling cascade, which results in the removal of AMPA receptors from the postsynaptic membrane, as illustrated in Figure 1. The decrease in AMPA receptors in the membrane makes the postsynaptic neuron less responsive to glutamate released from the presynaptic neuron. While it may seem counterintuitive, LTD may be just as important for learning and memory as LTP. The weakening and pruning of unused synapses allows for unimportant connections to be lost and makes the synapses that have undergone LTP that much stronger by comparison.


Synaptic transmission:

The structure of a cholinergic synapse and neuromuscular junction should be known. The acetylcholine receptor in the first image on the left is more better known as nicotinic cholinergic receptor.

In a cholinergic synapse (this is the only synapse you need to know) an action potential increases permeability of the presynaptic membrane by stimulating the Ca2+ ion gated channels to open. This causes an influx of Ca2+ ions into the presynaptic knob down its concentration gradient by facilitated diffusion. The high concentration of Ca2+ ions causes the vesicles of acetylcholine (neurotransmitters) to fuse with the presynaptic membrane. NB: It is best to say acetylcholine than Ach because it gives you more of an understanding and helps with questions if it says ‘acetylcholine’ instead of Ach. If you are going to use Ach it is important that you know what it is. Acetylcholine leaves the presynaptic knob by exocytosis into the synaptic cleft. Acetylcholine diffuses across the synaptic cleft and binds to the cholinergic receptors causing the Na ligand gated channels to open. This causes an influx of Na+ ions into the postsynaptic neurone making the postsynaptic neurone depolarised and if the threshold is met, an action potential is generated. The acetylcholine is removed from the synaptic cleft by the enzyme acetylcholine esterase into products by complementary shapes to prevent a continuous impulse. NB: Acetylcholine esterase can be abbreviated into Ache however it is best also to refer to this enzyme as acetylcholine esterase as it will help you in questions that have this name. The products are actively transported into the presynaptic knob by the use of Pi from ATP into vesicles to make acetylcholine. The Ca2+ ions are actively transported out of the presynaptic knob by the use of Pi from ATP.

Above is an example of excitatory neurotransmitters. This is where the postsynaptic neurone is depolarised leading to an action potential being fired when the threshold is met. Neurotransmitters can also be inhibitory where they hyperpolarise the postsynaptic neurone by opening the K= ion gated channels open.

Neuromuscular junctions work in exactly the same way however:

  • Postsynaptic membrane: The postsynaptic membrane of the muscle is deeply folded to form clefts. This is where acetylcholine esterase is stored. NB: It is important that you say postsynaptic membrane of the muscle and not postsynaptic membrane of a neurone as a postsynaptic neurone is not involved in a neuromuscular junction.
  • Receptors: There are many more receptors on the postsynaptic membrane of the muscle than on the postsynaptic membrane of a neurone.
  • Neurotransmitters: The acetylcholine are excitatory in every neuromuscular junction whereas in the synapse it can be excitatory or inhibitory.

Spatial summation is where many presynaptic neurones connect to one postsynaptic neurone. A small amount of excitatory neurotransmitters can be enough for the threshold to be met in the postsynaptic neurone and causing an action potential to be created. If some neurotransmitters are inhibitory then the overall effect may not be an action potential as it will be difficult to meet the threshold in the postsynaptic neurone. Temporal summation is where there is a quick-fire of two or more action potentials arriving at the same time from one presynaptic neurone. This means more neurotransmitters are released into the cleft making an action potential more likely to occur as the threshold may be met.

Some drugs mimic or inhibit the action of neurotransmitters:

  • If a drug causes an action potential to be triggered, then this is because the drug and the receptor have complementary shapes where it is mimicking the neurotransmitter. These type of drugs are said to be agonists.
  • If a drug does not cause action potential but it is binded to the receptors, then this means that the drug is complementary to the receptor but blocks the receptor so not many receptors are activated. These type of drugs are said to be antagonists.
  • If a drug binds to an acetylcholine esterase, then this means fewer enzyme-substrate complexes will be formed with acetylcholine creating a continuous impulse.
  • If more receptors are stimulated, then this is because the drug releases more neurotransmitters than usual.
  • If less receptors are stimulated, then this is because the drug inhibits the release of neurotransmitters.

NB: Recall of names of drugs and the mechanism of drugs do not need to be recalled in the exam. A piece of information will be given in the exam about a drug and its mechanism and only you have to explain why that has happened which are the bullet points above. These are the only explanations you need to know and are highlighted in green.


What is a unitary post synaptic potential? - Biology

Neurotransmitter receptor sites and their related, voltage-dependent ion channels compose a functional unit in the postsynaptic membrane. These units are called ionotropic receptors. In general, there are four major types of voltage-dependent channels. These control the passage of sodium, potassium, chloride and calcium ions across the membrane. The ion channel affected by a neurotransmitter determines whether or not a generated postsynaptic potential will be excitatory or inhibitory.

There are two different mechanisms, direct and indirect, by which these ion channels may be opened by the binding of a neurotransmitter. The simplest mechanism (ion-channel linked receptors) involves the direct opening of a channel coincident with the binding of a neurotransmitter to the receptor site. This effect is transient (milliseconds in duration). The indirect mechanisms involve a chain of chemical reactions that occur between the binding of a neurotransmitter to a receptor site and the opening of the channel. These are the mechanisms (G-protein linked receptors and chemically-activated ion channels) associated with the metabotropic neurotransmitters described in Tutorial 11 (hyperlink to figure11a, #10), and are sustained in nature (seconds to minutes in duration). The first indirect mechanism entails a metabotropic receptor site that is coupled to a G protein. When the neurotransmitter binds with the receptor site, the G protein nearby is activated. One of three units of the G protein, the alpha-subunit, breaks away and attaches to the ion channel. The binding of the alpha-subunit to the channel triggers its opening. The second type of indirect mechanism discovered involves the same complex (receptor site coupled to G protein) as just described. Except in this case, the activated alpha-subunit of the G protein activates an enzyme in the membrane that produces a second messenger molecule, which initiates a series of chemical events that open the channel.

Figure 12 illustrates the primary ionotropic mechanisms underlying the generation of excitatory and inhibitory postsynaptic potentials.

More recent studies of neurotransmission have yielded a number of additional findings. Most neurotransmitters may combine with a number of different types of receptors. There are dozens of different G proteins in the typical postsynaptic membrane (Eckard & Beck-Sickinger, 2000 Soderling & Beavo, 2000). G proteins were named for guanylate triphosphate, the molecule that activates them each has a specific protein target in the cell. Some of the second messengers created by activated G proteins have widespread effects (such as cyclic AMP). Others may activate certain target molecules (e.g., protein kinase A) that in turn activate other target molecules such as ion channels. In addition, some second messengers (e.g., cyclic AMP) may diffuse into the nucleus of the neuron to change the production of proteins by the genes within. These mechanisms may have long-range effects.

Two distinct systems of metabotropic receptors have been described, the cyclic nucleotide and the phosphoinositide systems. In the primary type of cyclic nucleotide system, the activating enzyme is coupled to the receptor via a G protein. The G protein can either stimulate or inhibit the adenylate cyclase via its influence on the receptor. When the G protein activates this enzyme, cyclic AMP is produced (adenosine monophosphate). A series of reactions involving protein phosphorylations and dephosphorylations follow, resulting in the opening of specific ion channels a synaptic potential is generated. A less common cyclic nucleotide system using the enzyme, guanylate cyclase, occurs predominantly in the cerebellum (Morris & Scarlata, 1997 Sharma & Duda, 1997 Sharma, Duda, Goraczniak & Sitaramayya, 1997).

The phosphoinositide system is considerably more complex (Catt, Hunyady & Balla, 1991 Conti & Jin, 1999 Pacheco & Jope, 1996). In one example of this type of system, the enzyme (phosphoinositidase C) is fixed deep within the lipid membrane layer adjacent to the neuroreceptors. Like the adenylate cyclase system, a G protein coupled to a neuroreceptor activates the enzyme. Triphosphoinositide is hydrolysed and the molecule, inositol triphosphate (IP3) is created. IP3 triggers the release of calcium ions from storage sites within the cell. The calcium, acting as a third messenger, initiates a series of protein phosphorylation reactions, which in turn open ion channels (e.g., potassium channels). The ionic flow generates the postsynaptic potential signaling an action potential. As mentioned before, the metabotropic response to neurotransmitter binding is much slower (10-30 X) than the more direct ionotropic response.

Catt, K.J., Hunyady, L. & Balla, T. (1991). Second messengers derived from inositol lipids. Journal of Bioenergy and Biomembranes, 23(1), 7-27.

Conti, M., & Jin, S.L. (1999). The molecular biology of cyclic nucleotide phosphodiesterases. Progress in Nucleic Acid Research and Molebular Biology, 63, 1-38.

Eckard, C.P. & Beck-Sickinger, A.G. (2000). Characterisation of G-Protein-coupled Receptors by Antibodies. Current Medical Chemistry, 7(9), 897-910.

Morris, A.J. & Scarlata, S. (1997). Regulation of effectors by G-protein alpha- and beta gamma-subunits. Recent insights from studies of the phospholipase c-beta isoenzymes. Biochemical Pharmacology, 54(4), 429-435.

Pacheco, M.A. & Jope, R.S. (1996). Phosphoinositide signaling in human brain. Progress in Neurobiology, 50(2-3), 255-273.

Sharma, R.K. & Duda, T. (1997). Plasma membrane guanylate cyclase. A multimodule transduction system. Advanced Experimental Medical Biology, 407, 271-279.

Sharma, R.K., Duda. T., Goraczniak, R. & Sitaramayya, A. (1997). Membrane guanylate cyclase signal transduction system. Indian Journal of Biochemistry and Biophysics, 34(1-2), 40-49.

Soderling, S.H. & Beavo, J.A. (2000). Regulation of cAMP and cGMP signaling: new phosphodiesterases and new functions. Current Opinions in Cell Biology, 12(2), 174-179.

Suggestions for further study

SUGGESTED READINGS:

Alkon, D.L. (1989, July). Memory storage and neural systems. Scientific American, 261(1), 42-50.

Beardsley, T.M. (1990, October). Cannabis comprehended. The "assassin of youth" points to a new pharmacology. Scientfic American, 263(4), 38.

Changeux, J.P. (1993, November). Chemical signaling in the brain. Scientific American, 269(5), 58-62.

Dunant, Y & Israel, M. (1985, April). The release of acetylcholine. Scientific American, 252(4), 58-66.

Erickson, D. (1991, May). Open channels. Hormone derivatives may combat PMS and epilepsy. Scientific American, 264(5), 124.

Holloway, M. (1991, August). Profile: Solomon H. Snyder. The reward of ideas that are wrong. Scientfic American, 265(2), 29-30.

Horgan, J. (1992, April). D2 or not D2. A barroom brawl over an "alcoholism gene". Scientific American, 266(4), 29, 32.

Kalil, R.E. (1989, December). Synapse formation in the developing brain. Scientific American, 261(6), 76-79, 82-85.

Keynes, R.D. (1979, March). Ion channels in the nerve-cell membrane. Scientific American, 240(3), 126-132, 134-135.

Lester, H.A. (1977, February). The response to acetylcholine. Scientific American, 236(2), 106-116, 118.

Linder, M.E. & Gilman, A.G. (1992, July). G proteins. Scientific American, 267(1), 56-61, 64-65.

Llinas, R.R. (1982, October). Calcium in synaptic transmission. Scientific American, 247(4), 56-65.

McEwen, B.S. (1976, July). Interactions between hormones and nerve tissue. Scientific American, 235(1), 48-58.

Myers, C.W. & Daly, J.W. (1983). Dart-poison frogs. Scientific American, 248(2), 120-133.

Nathanson, J.A. & Greengard, P. (1977, August). "Second messengers" in the brain. Scientific American, 237(2), 109-119.

Neher, E. & Sakmann, B. (1992, March). The patch clamp technique. Scientific American, 266(3), 28-35.

Rennie, J. (1990, January). Nervous excitement. Scientific American, 262(1), 21.

Satir, B. (1975, October). The final steps in secretion. Scientific American, 233(4), 29-37.

Simons, K. & Ikonen, E. (1997). Functional rafts in cell membranes. Nature, 387, 569-572.

Snyder, S.H. (1977, March). Opiate receptors and internal opiates. Scientific American, 236(3), 44-56.

Snyder, S.H. (1985, October). The molecular basis of communication between cells. Scientific American, 253(4), 132-141.

Stryer, L. (1987, July). The molecules of visual excitation. Scientific American, 257(1), 42-50.

Winson, J. (1990, November). The meaning of dreams, Scientific American, 263(5), 86-88, 90-92, 94-96.


What is EPSP

An Excitatory Postsynaptic Potential (ESPS) refers to an electric charge in the postsynaptic membrane, which makes the postsynaptic membrane to generate an action potential. The EPSP is caused by the binding of the excitatory neurotransmitters, which are released from the presynaptic membrane. The excitatory neurotransmitters are released from the vesicles of the presynaptic nerve. Several EPSPs generating an action potential is shown in figure 1.

Figure 1: EPSPs Generating an Action Potential

The main excitatory neurotransmitter is glutamate. The acetylcholine serves as the excitatory neurotransmitter at the neuromuscular junction. These excitatory neurotransmitters bind to the receptors and open the ligand-gated channels. This causes the flow of the positively-charged sodium ions into the postsynaptic cell. The depolarization of the postsynaptic membrane generates an action potential on the postsynaptic nerve.


What is a unitary post synaptic potential? - Biology

C2006/F2402 '11 -- Key to Recitation Problems # 12

1. Hint: Will one EPP cause the muscle to contract?

Answer:
A. Muscle will contract briefly and then relax. (This is called a twitch). One EPP (end plate potential) is enough to stimulate muscle contraction, but multiple stimuli are needed to sustain a contraction. (One EPSP is not enough to fire an action potential in the post-synaptic neuron, but one EPP is enough to cause a contraction in the post-synaptic skeletal muscle cell.)

B. Neither. It was a motor neuron of the somatic nervous system.

2. This table contains most of the important features. Students should know all of the skeletal vs smooth columns, except the parts which are starred. (These, and the cardiac column, are included for reference.) There may be other aspects of 'compare and contrast' which are not explicitly mentioned.

Note table above does not include bridge cycle. All three use ATP during bridge cycle see handout for details in skeletal muscle.

3. The idea here is to compare and contrast the IPSP, EPSP, EPP, receptor potential, AP in skeletal muscle membrane, & AP in cardiac muscle membrane. It can't hurt to make a table as above. Here are some of the important differences:

Types of potentials: The first 4 are graded local potentials AP's are self regenerating, long distance, all or nothing. The first 4 represent input into a cell an AP indicates output. The first 3 are found at a synapse (on post synaptic side) an AP occurs in the membrane of an axon (of a neuron) or the part of the muscle membrane outside the synapse/endplate. Receptor potentials are found in the specialized sensory/receptor cells where the receptor proteins are located.

Size/Effects: An EPSP is not enough to generate an AP in the membrane of the post synaptic neuron. An EPP is large enough to generate an AP in the muscle membrane and subsequently a twitch in the muscle.

Ion flow/potential changes: EPPs and EPSPs are excitatory (depolarizing) IPSPs are inhibiting (hyperpolarizing). A net flow of positive ions going into the cell causes EPPs and EPSPs positive ions going out, or negative ions going in, cause IPSPs.

Channels: The first 3 result from ligand gated channels an AP from voltage gated channels. (Receptor potentials result from ligand, photon, or mechanically gated channels.)

Summation: EPSPs and IPSPs are algebraically summed. If the total is enough to reach threshold, the neuron fires an AP. If the total stimulation to neuron or muscle is enough, there will be multiple APs, but all of the same size. Summation leads to more frequent APs, but no change in shape of AP. If enough EPPs generate multiple APs in the muscle membrane, the subsequent twitches will add up, leading to larger contractions. The contraction will be proportional to the amount of stimulation up to a point -- once the muscle is maximally contracted it will remain so (tetanus) until stimulation stops.
Receptor potentials are also summed stimulation leads to a proportional increase in the number of APs or a proportional release of transmitter (generating APs in the next cell), depending on the set up.

Two types of AP: AP in skeletal muscle (& nerve) is relatively short. AP in cardiac muscle is prolonged (by opening Ca ++ channels and delayed opening of K + channels**). The result is a long refractory period in cardiac muscle, relative to the length of the contraction (twitch). Therefore multiple APs can generate multiple twitches which can be summed in skeletal muscle, but not cardiac. Other factors being equal, the size of the skeletal muscle contraction is proportional to the stimulation the size of the cardiac contraction is not.

4. How to compare and contrast the RMP vs pacemaker potential?

The RMP (resting membrane potential) is stable -- it remains at a constant (negative) value in non-pacemaker cells (until the cell is stimulated). The RMP is caused primarily by K + leaving the cell through leak channels. The Na + /K + pump establishes a high [K + ] inside the cell, and some K + leaks out. The RMP reaches a steady state when the chemical gradient -- pushing K + out -- is balanced by the potential difference across the membrane -- pulling K + in.

In pacemaker (autorhythmic) cells, there is no stable RMP. After a spike (AP) the membrane potential repolarizes, and reaches a negative value. Then it gradually depolarizes without any input from nerves or ligands, because of the spontaneous opening/closing of the appropriate channels. (Either less K + moves out than usual, and/or more Na + and Ca ++ move in.**) The gradual change in in polarization = pacemaker potential the membrane eventually depolarizes to threshold and an AP is fired. Therefore the cell fires APs spontaneously without any input.

The slope of the pacemaker potential determines the frequency of reaching threshold, and the intervals between APs. The slope can be altered by ligands that affect channel states these ligands alter ion flow, change the slope of the pacemaker potential, and alter the frequency of APs.

**Reminder: You do not need to memorize what channels are responsible for the pacemaker potential and the AP in the pacemaker cell (or prolonged AP in the cardiac muscle cell). This year the handout does not have the channels for the pacemaker cells. However, it does show the channels for cardiac contractile cells, and you should be able to explain how the changes in channels and permeabilities shown on handout 21-C produce the changes in the shape of the AP.

5. A. DTX probably blocks (repolarization).

B. DTX should affect (amount of AcCh released per AP).

C. DTX probably (increases AP width)

D. DTX causes (increased opening of Ca ++ channels).

How more Ca ++ is released: DTX will not change the RMP it will change the amount of time it takes to return to the RMP. Therefore it will increase the AP width, which will in turn increases the amount of opening of voltage gated Ca ++ channels. Since the voltage remains high for a longer time, the Ca ++ channels will remain open longer, and more Ca ++ will come in to the cell.
If cell remains longer at higher voltage, it may be easier to trigger an AP, and APs may be more frequent. It was okay if you said this in addition to the correct answer it wasn't given credit as an answer by itself. For the explanation, it was okay to explain either why there might be more APs or longer (wider) APs.
Why more AcCh released? Ca ++ causes exocytosis and release of neurotransmitter. If more Ca ++ channels are opened, or opened longer, more AcCh will be released per AP.

Note that the 'extra' Ca ++ is in the presynaptic cell, not in the post synaptic muscle. It is the 'extra' AcCh that causes overexcitability of the muscle.


What is the difference between mEPSCs and sEPSCs?

Answer: In electrophysiology, mini excitatory postsynaptic currents are recorded in bath applied tetrodotoxin, while spontaneous excitatory post synaptic currents are done in bath applied GABAA inhibitor.

Taken from https://www.researchgate.net/publication/7099009_Enhanced_group_II_mGluR-mediated_inhibition_of_pain-related_synaptic_plasticity_in_the_amygdala/figures?lo=1&utm_source=bing&utm_medium=organic

MEPSCs and sEPSCs are both measures that examine the influence of excitatory neurotransmitters on a neuron. Both mEPSCs and sEPSCs are measured in a whole cell recording configuration. Because current is being recorded here, the experimenter must be in voltage clamp. The major difference is that in recording mEPSCs, the spontaneous activity of the network is eliminated due to the voltage-gated sodium channel inhibitor tetrodotoxin (TTX).

Inhibitory events can also be measured in this same way. The release of GABA is called an IPSC, or an inhibitory postsynaptic current. To measure sIPSCs, pharmacological inhibition of excitatory neurotransmitters must be performed, possible with DNQX or CNQX for blockade of AMPA type receptors, and APV for blockade of NMDA type receptors. Usually to measure inhibitory events, the cell must be clamped at a positive potential, or an internal solution containing a modified concentration of chloride must be used.

Deviations in membrane potential can also be measured in this way. The recording must be performed in a current clamp configuration for membrane potential to be measured. In this case, the events are called EPSPs, or excitatory postsynaptic potentials.

Spontaneous or miniature excitatory events are usually analyzed with software such as MiniAnalysis by Synaptosoft. They are generally difficult to identify since there may be multiple events at once. They generally have a much more rapid rise time with a slower time course of decay. Both frequency of events and amplitude of events are relevant physiologically. A change in presynaptic release mechanisms is often manifested as an increase in mEPSC frequency. A change in postsynaptic receptor expression or function is manifested as an increase in mEPSC amplitude.


Crash Course Nervous System 2: How Action Potentials Work

Post 2 in the Crash Course series on how the nervous system works: Action Potential!

Neurons are extraordinary cells. Beyond being intricately branched and gigantic relative to most cells, every second hundreds of billions of electrical impulses called action potentials are transmitted in your body. Before we check out how that works, it’s useful to refresh a few electricity terms.

Voltage is a difference in electrical charge. In neurons, voltage is measured in milivolts (1/1000th of a volt) and is called membrane potential. The greater the charge difference, the greater the membrane potential. Current is the flow of electricity. In neurons, currents refer to the flow of positive or negative ions across cell membranes. But before we get to the flow of current, let’s understand the default or “resting state” of a neuron:

Neuron Resting Potential via Crash Course

Your body is separated from the outside world by skin. This allows the internal state of your body to have different conditions than the outside world. Neurons have their own “skin” in the form of a cell membrane. It has ion gates – macromolecules made of many proteins – that change shape when specific molecules are present, allowing other specific ions (charged particles) to pass through the cell membrane. The movement of these ions changes the charge of the cell, causing a cascade of activity.

When neurons are at rest and not receiving electrical signal. their internal charge is negative thanks to the activity of a remarkable macromolecular machine: the sodium-potassium pump. This trans-membrane protein actively pumps sodium ions across their concentration gradient to the outside of the cell.

Sodium potassium pump maintains an electrochemical gradient inside neurons (shown in teal). The purple molecule at bottom right is ATP, providing energy to activate the pump. For every two positively charged potassium ions (blue) it pumps in, it pumps out three positively charged potassium ions (red), making it more positively charged outside the neuron. Via Crash Course

In addition to sodium potassium pumps, neurons have many types of ion channels.

Ion channels allow many charged ions to pass across a cell membrane. As charged particles rapidly diffuse across the membrane, they depolarize it, thus changing its charge.

Here are a few different types of ion gates:

The most common ion channels are voltage gated. They open at certain membrane potential thresholds. Via crash course

Other ion channels include Ligand gates (red), activated by neurotransmitters such as acetylcholine, and Mechanical gates (yellow), activated by physical stretching. via Crash Course

How an Action Potential Works

When all these gates are closed, a neuron is at rest. It’s polarized with a static membrane potential voltage of -70 mV .

Resting state membrane potential via Crash Course

But say a stimuli hits a neuron, triggering an ion channel to open. As ions pass into the cell (much faster than shown below), they alter the membrane’s charge. Watch the white line to the right. It rises as voltage approaches a very important threshold: -55 mV.

It’s all about getting to -55 mV. Sodium ions (red) enter neuron. Via Crash Course

Why -55 mV? At this threshold, thousands of voltage gated sodium channels open. A flood of positively charged sodium ions enter the cell and it becomes rapidly positively charged or depolarized. But this change in charge won’t last long.

Sodium gates (purple) let forth a flood of positive sodium ions (red) into the neuron, resulting in depolarization. Via Crash Course

As a neuron reaches an internal charge of around +30 mV, a conformational shape change happens in the sodium channels. They close and voltage gated potassium channels open, allowing positively charged potassium ions to leave the cell.

Membrane repolarization. Sodium channels (light purple) close. Potassium channels (dark purple) open and diffuse positively charged ions out of the cell. via Crash Course

This drops the internal charge of the neuron briefly below its resting state of -70 mV, activating the sodium potassium pumps to finish the job and bring the neuron to a maintained homeostasis. The entire process lasts 1-2 ms (1/1000th of a second).

Action potential moves through a neuron branch. Via Crash Course

In this manner, action potentials propagate down neuron branches as chain reactions, causing a wave of depolarizations and repolarizations. Action potentials only travel in one direction.

So an action potential is moving along a branch when suddenly it reaches the end, the point of no return: a synapse.

A number of things can happen when an action potential reaches a synapse. To keep it simple, let’s consider the case of a chemical synapse, the type of junction that uses neurotransmitters.

Action potentials here activate local voltage gated calcium channels, releasing a flow of positive ions into the cell. The calcium causes sack like structures full of neurotransmitters called vesicles to release their contents into the synaptic cleft, the area between two neurons.

An action potential reaches the end of the line: a chemical synapse. Via Crash Course

Neurotransmitters are released from vesicles into the synaptic cleft, a region less than five millionths of a centimeter wide. They bind to receptor sites on the postsynaptic cell, triggering either excitation or inhibition. Via Crash Course

There are many types of neurotransmitters. Some are excitatory others are inhibitory.

Here’s how excitatory and inhibitory neurotransmitters differ when it comes to the electrodynamics of neurons (see post 1 for a refresher on membrane potential). All images by Crash Course:

Inhibitory neurotransmitters push neurons farther away from their threshold for having an action potential (hyperpolarization), making it harder for them to fire. Via Crash Course Excitatory neurotransmitters bring neurons closer to their threshold for having an action potential (depolarizing them), making it easier for them to fire. Via Crash Course

It’s neither a single synapse nor a single neurotransmitter that matters. There are over one hundred different types of neurotransmitters and over 100 trillion synapses in your brain. A single neuron can have thousands or even tens of thousands of synapses. As Hank Green points out in this video, “the likelihood of a postsynaptic neuron developing an action potential depends on the sum of the excitation and inhibition in an area.” This is commonly called constructive signal summation and is illustrated by EyeWire’s first scientific discovery (Nature 2014).

A few more Action Potential Factoids

Immediately following an action potential, neurons have a refractory period, a brief bit of time where they are not responsive to further stimuli. If another stimuli reaches a neuron during this period, it will not cause an action potential, no matter how strong the incoming signal is. This results in action potentials only propagating in one direction.

Neurons have consistent voltage thresholds: -55 mV activation,

+30 mV repolarization. They vary their signals then not by Voltage (amplitude) but by frequency and speed (conduction velocity).

Weaker stimuli tend to produce slower, lower frequency signals while stronger or more intense stimuli tend to produce more rapid, higher frequency signals.

Myelinated (insulated) neurons, such as are found in white matter and the peripheral nervous system, send the fastest signals.

Myelinated action potential travels oh so fast because it effectively “leaps” from one myelin gap (nodes of ranvier) to the next. Via Crash Course

In the central nervous system, Myelin is produced by cells called Oligodendrocytes, which wrap around axons.

Oligodendrocyte merrily making myelin sheaths. Via Crash Course

Thanks for reading. Be sure to subscribe to Crash Course on YouTube and let us know what you think about this post in EyeWire chat. For science!


Watch the video: Temporal vs. Spatial Summation (January 2023).