Hi everyone! Welcome to the next video in Perceptual Motivation and Emotion course. In our first week of class, you've already learned about the main structures of the neuron, and you've also been introduced to the functions of each neuronal structure. Then, last week, you learned about the mechanism that enables the transmission of information within a neuron, namely through a series of events that cause the membrane's resting potential to change into an action potential. If you feel that you have not yet fully understood the concepts taught in previous lectures, I strongly encourage you to revisit chapter 1 in your textbook before you continue watching this presentation of today's topic of discussion.
If last week we covered the topic of the transmission of information within one neuron, then I encourage you to review the following slides. Then today, we'll look at how information is sent from one neuron to the next. In other words, we will be learning about how communication between neurons happens.
But before we look at the processes that underlie communication between neurons, first you need to understand where exactly this exchange of information occurs. Do you still remember the name Santiago Ramon y Cajal that was mentioned in the first week of class? Cajal was a pioneer in the field of neuroscience who managed to use the Golgi staining technique to demonstrate that one neuron is separate from another neuron, with a small gap separating them.
Although Cajal managed to visually demonstrate the existence of these small gaps, Cajal never explained what exactly happens in these gaps that allows for the exchange of information between neurons. Then, in 1906, another scientist by the name of Charles Sherrington began to use the term synapse to refer to the gaps between neurons. Based on his research, Sherrington came up with the conclusion that the physiological processes that underlie information exchange between neurons is unique or different from the transmission of information within one neuron. But before I tell you the gist of Sherrington's research, it is necessary for you to first understand the terms we're going to repeatedly encounter in this topic's discussions. First is the difference between the terms presynaptic and postsynaptic.
In the previous chapter, an explanation of electrical activity in neurons was illustrated using artificial stimulation. The process of depolarization and hyperpolarization can indeed occur when an electrical current is artificially delivered through a microelectrode inserted into the neuron, as we saw last week. However, such an artificial stimulation is typically only found in the strict setting of laboratory experiments. In reality though, our neurons receive information not from microelectrodes inserted into the brain. Instead, our neurons naturally receive information from other neurons found in the nervous system.
That is to say, in real life, there are neurons that function as information senders and there are also neurons that function as information receivers. Since a synapse is defined as a place where two neurons meet, the neuron that sends information must therefore be located before the synapse, and is thus known as a presynaptic neuron. Meanwhile, the neuron that receives information must be located after the synapse, and is therefore known as a postsynaptic neuron.
In addition, You will also come across the term post-synaptic potential, which refers to changes in the electrical potential of a neuron, and which can take the form of either a depolarization or a hyperpolarization in the post-synaptic neuron. Let's return to the Sherrington study mentioned in the previous slide. As already explained, Sherrington's research succeeded in demonstrating the physiological processes that occur at the synapse.
In his study, in which he used a dog as a subject, Sherrington measured the time it took for a dog to respond to a pinch applied to the skin on their leg. Like humans and other vertebrates, when a dog feels a painful sensation or any startling sensation on the skin, the dog will react by bending its leg. You can see an example of this in the animation on the left side of this slide. This reaction, known as the flexion reflex, occurs automatically, or reflexively. Sensory information that triggers reflexive movement is generally transmitted along the reflex arc.
In the picture on the right, it can be seen that in the reflex arc, information about sensation that enters the skin is carried by sensory neurons to interneurons located in the spinal cord, and then the information is sent from the interneurons to motor neurons, which then instruct. the muscles to move. If the incoming sensation is pain, then the muscle movement that occurs automatically causes the leg to bend in an attempt to move away from the source of the pain. Sherrington measured the distance a nerve impulse must travel from the skin to the interneurons and all the way to the muscles, and then he compared this distance to the time it took the dog to bend the leg.
since the pinch was applied to the skin. Through these measurements, Sherrington was able to estimate the speed at which information is transmitted along the reflex arc. Based on his observations of the flexion reflex in the dog's leg, Sherrington drew three conclusions, which suggest that there are unique mechanisms underlying the communication between neurons. First, He found that the rate of transmission of information along the reflex arc is longer than the transmission of information that can be otherwise expected to occur along the length of the axon.
Second, Sherrington noticed that although a single sensory stimulus may be too weak to produce a response, as for example if a given pinch doesn't trigger a dog's flexion reflex, several weak stimuli if given successively at the same location, can produce a response. The same is true for several weak stimuli that are applied at the same time in several different locations. Third, Sherrington also observed that one group of muscles is excited or stimulated, another muscle group undergoes relaxation.
Let's look at the implications of each. of Sherrington's discoveries. Previously, I've described how Sherrington found that the speed of information transmission along the reflex arc is slower than the speed of information transmission that usually occurs down the length of an axon. To be more precise, although the axon should be able to transmit information at a speed of about 40 meters per second, it turned out that information transmission along the reflex arc only has a speed of approximately 15 meters per second. Based on these findings, Sherrington then suggested that there must be some unique process that slows down the transmission of information along the reflex arc, and that this process must occur in the gaps that separate these neurons.
Or in other words, the slowing down is due to some process that occurs at synapses. This conclusion is then considered as evidence of the existence of synapses. It's also assumed that the physiological processes underlying communication between neurons are different from the physiological processes that underlie information transmission within a neuron. Even so, at that time, no one knew exactly what processes were taking place at the synapse that distinguished it from the processes occurring at the axon.
Moreover, Sherrington also saw that even though one brief stimulus applied to a dog's leg might be too weak to trigger a motor reflex, when multiple brief stimuli are applied consecutively to the same location within a brief period of time, The resulting cumulative effect may be strong enough to produce a response. In other words, although a single brief weak stimulation or a sub-threshold stimulation may quickly decay and cannot trigger an action potential, its effect can be combined with the effects of other brief stimulations that quickly follow it, and the resulting cumulative effect is strong enough to trigger an action potential. This cumulative effect is is known as temporal summation. In addition, neurons can also respond to several weak stimuli or sub-threshold stimuli, which come at the same time but at different locations. This combined effect of multiple synaptic inputs originating from different locations is known as spatial summation.
To make it easier for you to distinguish between them, remember that the word Temporal relates to tempo or time, thus referring to the cumulative effect related to the time the input is received, while the word spatial is closely related to space, so that it refers to the cumulative effect related to the location of the input. If you have trouble imagining the concepts of temporal and spatial summation, Perhaps imagining the following scenario will help. Imagine a friend pokes you on your arm, but you can't feel it because the touch is too weak.
Even though one weak touch doesn't have any effect, if your friend then repeatedly pokes you at the same place on your arm, then the effects of these several consecutive pokes would combine into a bigger effect. So eventually you'll be able to feel it too. This is an analogy of temporal summation.
Then imagine another scenario in which your friend pokes you in the arm, again, with a poke that's too weak for you to feel. Although one single weak poke can't be felt, but if your friend gives a weak poke at several different but adjacent places on your arm, then the effects of these multiple pokes can be combined into a more intense cumulative effect. Eventually, you'll be able to feel the incoming sensation too. This kind of effect occurs in spatial summation.
At the top of this image, you can see an illustration of temporal summation. Here, several inputs enter successively at the same location, and the combined effect of these inputs. is large enough to generate an action potential in the postsynaptic neuron.
Meanwhile, in the bottom image, you can see how spatial summation occurs. Recall that in spatial summation, inputs that enter at different locations are combined to produce a larger effect, thus triggering an action potential along the axon of the postsynaptic neuron. Here is a graph that represents the change in membrane potential of a neuron.
In section 1, you can see a depiction of a sub-threshold depolarization, meaning that the depolarization is not large enough to reach the excitation threshold. In this instance, an action potential does not occur. In the next section, in section 2, The incoming stimulus also causes a subthreshold depolarization, but this time you can see that before the depolarizing effect of the first stimulus completely wears off, there is a second stimulus that comes shortly after the first stimulus.
The depolarizing effect of the second stimulus is then combined with the depolarizing effect of the first stimulus. Even so, you can see that this combined effect is still not sufficient to reach the excitation threshold. Then, in section 3, there is a combination of three depolarizing stimuli, and the combination of all three is large enough to reach the excitation threshold, and an action potential is therefore triggered. As previously explained, this combined effect can appear temporarily, which is depicted in section 3, as well as spatially, as seen in the fourth section.
Also note that in this graph, a depolarization is denoted as an EPSP. which stands for excitatory postsynaptic potential, and which refers to the graded depolarization of the postsynaptic neuron. Meanwhile, on the right side, you can see that a graded hyperpolarization is denoted by the notation IPSP, which is short for inhibitory postsynaptic potential.
If you recall the explanation in the previous chapter regarding graded potentials, then you should already know that graded depolarizations and hyperpolarizations occur briefly and do not occur in an all-or-none nature like action potentials do. A graded potential also doesn't last very long, as it decays or loses its effect over distance and time. Sherrington's Third Discovery relates to this concept of graded potential. You probably know that in order to bend and straighten your legs, you need a pair of antagonistic muscles, or muscles that work in an opposing manner.
To bend your legs, you contract your flexor muscles. But as your flexor muscles contract, the extensor muscles of the same leg must relax. You can demonstrate this yourself by trying to bend one of your limbs, let's say your arm.
When you bend your arm, the bicep muscles, which act as flexors, contract, while at the same time, the tricep muscles, which act as extensors, relax. The same principle applies to the muscles on a dog's leg. Dogs bend their legs by contracting their flexor muscles. while simultaneously relaxing their extensor muscles.
According to Sherrington, when a group of neurons is stimulated, there will inevitably be another group of neurons that are inhibited or blocked. When bending the leg, for example, there are motor neurons that excite the flexor muscles, but at the same time, there are also motor neurons that send messages to inhibit the extensor muscles from being stimulated. If the flexor muscle stimulation is triggered by depolarization, then to inhibit the extensor muscle, the message sent must be in the form of hyperpolarization, because hyperpolarizations make it difficult for muscles or for neurons to trigger an action potential.
And it's the interneurons in the spinal cord that are responsible for sending these excitatory and inhibitory messages simultaneously. Because graded depolarization increases the likelihood of an action potential occurring, graded depolarization in postsynaptic neurons is also known as EPSP because of its excitatory nature, meaning that it increases the chances of an action potential occurring. Whereas a graded hyperpolarization in postsynaptic neurons is also known as IPSP, because of its inhibitory nature, in that it inhibits or decreases the possibility of an action potential occurring in the postsynaptic neuron.
At this point, you are encouraged to pause your video to carefully examine the image on your screen to better understand the concepts of excitatory and inhibitory effects described in the previous slide. The same picture can also be found on page 46 in your Kalat textbook. Do you remember that our brain consists of about 86 billion neurons?
With so many neurons at our disposal, you should be able to imagine that each presynaptic neuron must be in charge of sending information to many postsynaptic neurons. And conversely, one postsynaptic neuron must have the ability to receive information from many other presynaptic neurons. This means that each neuron must integrate a lot of incoming information before it is able to pass on the information to the next set of neurons. Since the received message can be in the form of either an EPSP or an IPSP, and the information can be combined both temporally and spatially.
This implies that in each neuron, the probability of triggering an action potential will depend on the ratio of all EPSPs and all IPSPs that occur at several locations over a certain period of time. Only when the combined total of all EPSPs and IPSPs received by a neuron depolarizes the membrane to the excitation threshold, would an action potential be initiated. The postsynaptic potentials that are caused by neurotransmitter chemicals can be either depolarizing, often but not always resulting in an excitatory postsynaptic potential, or EPSP, or hyperpolarizing, resulting in an inhibitory postsynaptic potential, or IPSP.
Post-synaptic potentials generally move passively along the dendritic membrane, gradually becoming smaller as they spread. Therefore, the post-synaptic potentials from more distant synapses will decay more than PSPs from synapses closer to the integration zone at the axon hillock. The post-synaptic potentials produced at most synapses are usually well below the threshold for generating post-synaptic action potentials. How then can synapses transmit information if their postsynaptic potentials are subthreshold? Suppose that two excitatory endings are activated, causing local depolarizations of the cell body.
Taken alone, neither would be sufficient to trigger an action potential, but when combined, the two depolarizations sum to depolarize the membrane in the hillock region to threshold. When inhibitory synapses are active, the membrane potential tends to be stabilized below threshold because they induce hyperpolarizations or subthreshold depolarizations that cannot reach threshold. These postsynaptic effects also spread passively, dissipating as they travel. Because some potentials excite and others inhibit the hillock, these effects partially cancel out each other. Thus, the net effect is the difference between the two.
The neuron subtracts the IPSPs from the EPSPs. Post-synaptic effects that are not absolutely simultaneous can also be summed, because the post-synaptic potentials last a few milliseconds before fading away. The closer they are in time, the greater is the overlap and the more complete is the summation, which in this case is called temporal summation. The summation of potentials originating from different physical locations across the cell body is called spatial summation. Only if the overall sum of all the potentials, both EPSPs and IPSPs, is sufficient to depolarize the cell to threshold the axon hillock, is an action potential triggered.