- Anatomy of a neuron
- Overview of neuron structure and function
- The membrane potential
- Electrotonic and action potentials
- Saltatory conduction in neurons
- Neuronal synapses (chemical)
- The synapse
- Neurotransmitters and receptors
- Q & A: Neuron depolarization, hyperpolarization, and action potentials
- Overview of the functions of the cerebral cortex
How neurons communicate with each other at synapses. Chemical vs. electrical synapses.
- Neurons communicate with one another at junctions called synapses. At a synapse, one neuron sends a message to a target neuron—another cell.
- Most synapses are chemical; these synapses communicate using chemical messengers. Other synapses are electrical; in these synapses, ions flow directly between cells.
- At a chemical synapse, an action potential triggers the presynaptic neuron to release neurotransmitters. These molecules bind to receptors on the postsynaptic cell and make it more or less likely to fire an action potential.
A neuron’s signaling, however, is much more exciting—no pun intended!—when we consider its interactions with other neurons. Individual neurons make connections to target neurons and stimulate or inhibit their activity, forming circuits that can process incoming information and carry out a response.
How do neurons "talk" to one another? The action happens at the synapse, the point of communication between two neurons or between a neuron and a target cell, like a muscle or a gland. At the synapse, the firing of an action potential in one neuron—the presynaptic, or sending, neuron—causes the transmission of a signal to another neuron—the postsynaptic, or receiving, neuron—making the postsynaptic neuron either more or less likely to fire its own action potential.
Electrical or chemical transmission?
At the end of the 19th and beginning of the 20th century, there was a lot of controversy about whether synaptic transmission was electrical or chemical.
- Some people thought that signaling across a synapse involved the flow of ions directly from one neuron into another—electrical transmission.
- Other people thought it depended on the release of a chemical from one neuron, causing a response in the receiving neuron—chemical transmission.
We now know that synaptic transmission can be either electrical or chemical—in some cases, both at the same synapse!
Chemical transmission is more common, and more complicated, than electrical transmission. So, let's take a look at chemical transmission first.
Overview of transmission at chemical synapses
Chemical transmission involves release of chemical messengers known as neurotransmitters. Neurotransmitters carry information from the pre-synaptic—sending—neuron to the post-synaptic—receiving—cell.
As you may remember from the article on neuron structure and function, synapses are usually formed between nerve terminals—axon terminals—on the sending neuron and the cell body or dendrites of the receiving neuron.
A single axon can have multiple branches, allowing it to make synapses on various postsynaptic cells. Similarly, a single neuron can receive thousands of synaptic inputs from many different presynaptic—sending—neurons.
Inside the axon terminal of a sending cell are many synaptic vesicles. These are membrane-bound spheres filled with neurotransmitter molecules. There is a small gap between the axon terminal of the presynaptic neuron and the membrane of the postsynaptic cell, and this gap is called the synaptic cleft.
When an action potential, or nerve impulse, arrives at the axon terminal, it activates voltage-gated calcium channels in the cell membrane.
, which is present at a much higher concentration outside the neuron than inside, rushes into the cell. The allows synaptic vesicles to fuse with the axon terminal membrane, releasing neurotransmitter into the synaptic cleft.
The molecules of neurotransmitter diffuse across the synaptic cleft and bind to receptor proteins on the postsynaptic cell. Activation of postsynaptic receptors leads to the opening or closing of ion channels in the cell membrane. This may be depolarizing—make the inside of the cell more positive—or hyperpolarizing—make the inside of the cell more negative—depending on the ions involved.
In some cases, these effects on channel behavior are direct: the receptor is a ligand-gated ion channel, as in the diagram above. In other cases, the receptor is not an ion channel itself but activates ion channels through a signaling pathway. See the article on neurotransmitters and receptors for more info.
Excitatory and inhibitory postsynaptic potentials
When a neurotransmitter binds to its receptor on a receiving cell, it causes ion channels to open or close. This can produce a localized change in the membrane potential—voltage across the membrane—of the receiving cell.
- In some cases, the change makes the target cell more likely to fire its own action potential. In this case, the shift in membrane potential is called an excitatory postsynaptic potential, or EPSP.
- In other cases, the change makes the target cell less likely to fire an action potential and is called an inhibitory post-synaptic potential, or IPSP.
An EPSP is depolarizing: it makes the inside of the cell more positive, bringing the membrane potential closer to its threshold for firing an action potential. Sometimes, a single EPSP isn't large enough bring the neuron to threshold, but it can sum together with other EPSPs to trigger an action potential.
IPSPs have the opposite effect. That is, they tend to keep the membrane potential of the postsynaptic neuron below threshold for firing an action potential. IPSPs are important because they can counteract, or cancel out, the excitatory effect of EPSPs.
Spatial and temporal summation
How do EPSPs and IPSPs interact? Basically, a postsynaptic neuron adds together, or integrates, all of the excitatory and inhibitory inputs it receives and “decides” whether to fire an action potential.
- The integration of postsynaptic potentials that occur in different locations—but at about the same time—is known as spatial summation.
- The integration of postsynaptic potentials that occur in the same place—but at slightly different times—is called temporal summation.
For instance, let’s suppose that excitatory synapses are made on two different dendrites of the same postsynaptic neuron, as shown below. Neither synapse can produce an EPSP quite large enough to bring the membrane potential to threshold at the axon hillock—the place where the action potential is triggered, boxed below. If both subthreshold EPSPs occurred at the same time, however, they could sum, or add up, to bring the membrane potential to threshold.
On the other hand, if an IPSP occurred together with the two EPSPs, it might prevent the membrane potential from reaching threshold and keep the neuron from firing an action potential. These are examples of spatial summation.
What about temporal summation? A key point is that postsynaptic potentials aren’t instantaneous: instead, they last for a little while before they dissipate. If a presynaptic neuron fires quickly twice in row, causing two EPSPs, the second EPSP may arrive before the first one has dissipated, bumping the membrane potential above threshold. This is an example of temporal summation.
A synapse can only function effectively if there is some way to "turn off" the signal once it's been sent. Termination of the signal lets the postsynaptic cell return to its normal resting potential, ready for new signals to arrive.
For the signal to end, the synaptic cleft must be cleared of neurotransmitter. There are a few different ways to get this done. The neurotransmitter may be broken down by an enzyme, it may be sucked back up into the presynaptic neuron, or it may simply diffuse away. In some cases, neurotransmitter can also be "mopped up" by nearby glial cells—not shown in the diagram below.
Anything that interferes with the processes that terminate the synaptic signal can have significant physiological effects. For instance, some insecticides kill insects by inhibiting an enzyme that breaks down the neurotransmitter acetylcholine. On a more positive note, drugs that interfere with reuptake of the neurotransmitter serotonin in the human brain are used as antidepressants, for example, Prozac.
Chemical synapses are flexible
If you've learned about action potentials, you may remember that the action potential is an all-or-none response. That is, it either happens at its full strength, or it doesn't happen at all.
Synaptic signaling, on the other hand, is much more flexible. For instance, a sending neuron can "dial up" or "dial down" the amount of neurotransmitter it releases in response to the arrival of an action potential. Similarly, a receiving cell can alter the number of receptors it puts on its membrane and how readily it responds to activation of those receptors. These changes can strengthen or weaken communication at a particular synapse.
Presynaptic and postsynaptic cells can dynamically change their signaling behavior based on their internal state or the cues they receive from other cells. This type of plasticity, or capacity for change, makes the synapse a key site for altering neural circuit strength and plays a role in learning and memory. Synaptic plasticity is also involved in addiction.
In addition, different presynaptic and postsynaptic cells produce different neurotransmitters and neurotransmitter receptors, with different interactions and different effects on the postsynaptic cell. For more information, take a look at the article on neurotransmitters and receptors.
At electrical synapses, unlike chemical synapses, there is a direct physical connection between the presynaptic neuron and the postsynaptic neuron. This connection takes the form of a channel called a gap junction, which allows current—ions—to flow directly from one cell into another.
Electrical synapses transmit signals more rapidly than chemical synapses do. Some synapses are both electrical and chemical. At these synapses, the electrical response occurs earlier than the chemical response.
What are the benefits of electrical synapses? For one thing, they're fast—which could be important, say, in a circuit that helps an organism escape from a predator. Also, electrical synapses allow for the synchronized activity of groups of cells. In many cases, they can carry current in both directions so that depolarization of a postsynaptic neuron will lead to depolarization of a presynaptic neuron. This kind of bends the definitions of presynaptic and postsynaptic!
What are the downsides of electrical synapses? Unlike chemical synapses, electrical synapses cannot turn an excitatory signal in one neuron into an inhibitory signal in another. More broadly, they lack the versatility, flexibility, and capacity for signal modulation that we see in chemical synapses.
Want to join the conversation?
- is there any thing between the synaps any fluid or anyting else?(17 votes)
- I know this article talked about the flexibility of synapses, but I still don't understand how different kinds of signals can be transmitted. Does a certain neuron only send one kind of signal only (different signals would be sent by different neurons) or does a certain neuron send multiple kinds of signals by sending different kinds of neurotransmitters? If the former, how are specific cells targeted? If the latter, how are specific neurotransmitters released?(13 votes)
- Each neuron may be connected to up to 10,000 other neurons, passing signals to each other via as many as 1,000 trillion synaptic connections.
Meaning that a certain neuron sends multiple kinds of signals by sending different kinds of neurotransmitters.
Functionally related neurons connect to form neural networks (also known as neural nets or assemblies). The connections between neurons are not static, though, they change over time. The more signals sent between two neurons, the stronger the connection grows.
When stimulated by an electrical pulse, neurotransmitters of various types are released, and they cross the cell membrane into the synaptic gap between neurons. These chemicals then bind to chemical receptors in the dendrites of the receiving (post-synaptic) neuron. In the process, they cause changes in the permeability of the cell membrane to specific ions, opening up special gates or channels which let in a flood of charged particles (ions of calcium, sodium, potassium, and chloride).
Meaning that upon stimulation, many neurotransmitters are being released into the synaptic cleft.
But there a thing called membrane capacitance. Another direct measure of exocytosis is the increase in membrane area due to the incorporation of the secretory granule or vesicle membrane into the plasma membrane. This can be measured by increases in membrane capacitance (Cm).
The specific capacitance is mainly determined by the thickness and dielectric constant of the phospholipid bilayer membrane and is similar for intracellular organelles and the plasma membrane.
There are only differences between fast secreting neurotransmitters (Acth, dopamine) and slow releasing neuropeptides from neuroendocrine cells.(12 votes)
- The 'Synaptic Cleft' has an approximately 20 nm separation, How do the axion/dendrite pre/post synaptic terminals maintain their correct separation, that is, how do they stop themselves from touching or stop themselves from separating too far?
And if there is indeed- Failures in this gap separation, then what would be the diseases associated with both the touching condition and the over separation condition of the terminals?(9 votes)
- In the Synaptic Cleft, there are neurotransmitters that are diffusing from one neuron to the next neuron, and then undergoing receptor-mediated endocytosis with the receptors in the "receiving" neuron (which should require space for receiving them). These neurotransmitters would diffuse away from the synaptic cleft or an enzyme would help clear the rest of the neurotransmitters. I believe that for these enzymes to be able to "sweep away" those neurotransmitters, some space is needed. Furthermore, as only milliseconds pass between some action potentials, the synaptic cleft maintains its distance.(2 votes)
- in "Overview of transmission at chemical synapses," it was stated that a depolarization of the membrane causes an influx of Ca2+ ions into the cell. However, doesn't this influx on positive charge cause depolarization of the cell?
I don't understand why depolarizing the membrane would stimulate further depolarization. Wouldn't hyper-polarization of the membrane cause this?(6 votes)
- You got confused because both carry a positive charge. I will tell you that speaking of the number of ions, this is almost minor.
Yes, we say an influx of Ca+ ions, but there are not many Ca+ ions. Sometimes, only one is enough to bind to SNARE complex of one vesicle to release neurotransmitters-(6 votes)
- what makes an EPSP or IPSP, how are they determined to be excitatory or inhibitory?(5 votes)
- EPSPs are graded potentials that can initiate an AP in the axon, whereas IPSPs produce a graded potential that lessens the chance of an AP in an axon.
I found one paper where it was investigated, but again - Cell-autonomous molecular mechanisms that control the balance of excitatory and inhibitory synapse function remain poorly understood; no proteins that regulate excitatory and inhibitory synapse strength in a coordinated reciprocal manner have been identified.
The knockdown of cadherin-10 reduces excitatory but increases inhibitory synapse size and strength.
- Where is the ACTH broken down into ethanoic acid and choline by the acetylcholinesterase, in the cleft, or postsynaptic neuron? It is definitely broken down after it enters the postsynaptic neuron, right? Why ACTH can not go back to the presynaptic neuron directly, but has to be broken down and brought back?(4 votes)
- Acetylcholine interacts with postsynaptic receptors a few milliseconds before it is being degraded down by acetylcholinesterase. Then both taken up by presynaptic nerve terminal and recycled.
Meaning that degradation happens in the synaptic cleft, actually on the postsynaptic neurons, but right after it already finished its role.
- How did cell membrane evolve in synaptic clefts?(3 votes)
- A primordial neurosecretory apparatus in choanoflagellates was identified and it was found that the mechanism, by which presynaptic proteins required for secretion of neurotransmitters interact, is conserved in choanoflagellates and metazoans. Moreover, studies on the postsynaptic protein homolog Homer revealed unexpected localization patterns in choanoflagellates and new binding partners, both of which are conserved in metazoans.
I think this paper will satisfy you, everyzhing int he one place:
- Why are the neurotransmitter molecules cleaved so fast in the synaptic cleft ( 50molecules/ms)?(3 votes)
- Because it could cause potential disadvantages:
1. further delaying of response
2. overcrowding of neurotransmitters and too enhanced answer
3. what if new stimulation happens in a short time and neurotransmitters are not recycled? Who would respond to it then?(2 votes)
- how do synapses affect your reaction time?(3 votes)
- They little delay the reaction.
The overall synaptic delay and estimated number of synapses (ENOS) of simple tactile reaction neuronal circuits of normal subjects did not significantly vary with site of tactile stimulation or effector organ.
The overall synaptic delay in the tactile reaction neuronal circuits between SOS and the left and right big toes were significantly lower in sniffers than in control subjects. This may be due to a decrease in either the average synaptic delay, the number of synapses, or both in the tactile reaction neuronal circuits between sites of stimulation and big toes (but not index fingers) in sniffers.
- Can we see electrical synapses in FMRI just like its name electrical? Do the both look like the same in FMRI?(3 votes)