Do all different types of neurons serve different roles?

Do all different types of neurons serve different roles?

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I know from my basic education in neurology that the brain has various sorts of neurons. These are usually bunched into 3 different categories (sensory, moto and interneurons).

I read in a recently published book, and papers on modern neuroscience that there have been thousands of different types of neurons identified in the brain. Does this mean that there are different types neurons each dedicated to a very specific task in the brain? If that is true, then what is each individual neuron's job (a few examples would be sufficient)?

Short answer
Neurons were (and still are) often identified based on their histological features (e.g., by Cajal). In turn, the structural hallmarks of neurons are often related to their specific functions.

The question is broad and difficult to answer without restricting to some example types of neurons. As you say, about 10,000 types of neurons have been identified. Their roles are often obscure. I will restrict the answer below to a few examples of neurons with relatively well characterized histological features and relatively established functionality.

Fig. 1. Examples of neuronal cell types. A. Purkinje cell B. Granule cell C. Motor neuron D. Tripolar neuron E. Pyramidal neuron F. Chandelier cell G. Spindle neuron H. Stellate cell.source: Ferris (2012)

The Purkinje cell (Fig. 1A) receives large amounts of input in the cerebellum, integrates it and sends it away to deeper layers. Hence, as an integrator, it has an elaborate input side (large dendritic tree) and a single output axon. The basic function is similar to the pyramidal cell in the cerebrum (Fig. 1E) and their appearance is hence similar.

On the other end of the spectrum is the spindle neuron (Von Economo neuron, Fig. 1G), which is believed to receive simple input and generate simple output and is built for speed. Less integration allows for faster responses. Hence, its dendritic tree is much less elaborated than the Purkinje cell (cf. fig. 1A) (Allman et al., 2011).

As a last example: the Chandelier cell (Fig. 1F); these neurons have axons that form elaborate collaterals that are believed to form local inhibitory connections in the cortex to keep (excessive) stimulation in check; hence their output is more elaborate, with relatively simple input. Dysfunction is believed to be associated to epilepsy (excessive stimulation) (Inan & Anderson, 2014).

- Allman et al., Ann N Y Acad Sci (2012), 1225: 59-71
- Inan & Anderson, Cur Opinion Neurobiol (2014), 26: 142-48
- Purves D et al. (eds.) Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001)

- Ferris, 2012, Sci Am blog

Do neurons regenerate?

Do neurons regenerate? The answer to this question is not simple and for years scientific studies have gone in the direction of affirming that neurogenesis or neuronal regeneration occurs from birth and throughout our lives.

However, the most recent research points in the opposite direction and suggests that neurogenesis does not occur in adult brains, or not in the way it was thought to.

In this article we explain what neurogenesis is, and we give you the keys to understanding the current controversy about whether or not neurons regenerate in adulthood.

According to Function

Neurons can also be classified based on their specific function. Sensory neurons are the neurons that harness information from the different sensory organs such as the eyes, nose, ears, tongue and skin. On the other hand, motor neurons transmit signals from the brain to the spinal cord to the muscles to initiate action or response to stimuli. Interneurons serves as connectors of neurons. Projection interneurons have long axons that join brain regions that are far from one another. Local interneurons feature shorter axons that create small circuits between near brain cells or regions.

Researchers also categorize neurons by function. Sensory neurons collect information from sensory organs—from the eyes, nose, tongue and skin, for example. Motor neurons carry signals from the brain and spinal cord to muscles. Interneurons connect one neuron to another: the long axons of projection interneuons link distant brain regions the shorter axons of local interneurons form smaller circuits between neighboring cells.

Nerve Cells

Although the nervous system is very complex, nervous tissue consists of just two basic types of nerve cells: neurons and glial cells. Neurons are the structural and functional units of the nervous system. They transmit electrical signals, called nerve impulses. Glial cells provide support for neurons. For example, they provide neurons with nutrients and other materials.

Neuron Structure

As shown in Figure below, a neuron consists of three basic parts: the cell body, dendrites, and axon.

  • The cell body contains the nucleus and other cell organelles.
  • Dendrites extend from the cell body and receive nerve impulses from other neurons.
  • The axon is a long extension of the cell body that transmits nerve impulses to other cells. The axon branches at the end, forming axon terminals. These are the points where the neuron communicates with other cells.

The structure of a neuron allows it to rapidly transmit nerve impulses to other cells.

The axon of many neurons has an outer layer called a myelin sheath (see Figure above).Myelin is a lipid produced by a type of a glial cell known as a Schwann cell. The myelin sheath acts like a layer of insulation, similar to the plastic that encases an electrical cord. Regularly spaced nodes, or gaps, in the myelin sheath allow nerve impulses to skip along the axon very rapidly.

Types of Neurons

Neurons are classified based on the direction in which they carry nerve impulses.

  • Sensory neurons carry nerve impulses from tissues and organs to the spinal cord and brain.
  • Motor neurons carry nerve impulses from the brain and spinal cord to muscles and glands(see Figurebelow).
  • Interneurons carry nerve impulses back and forth between sensory and motor neurons.

This axon is part of a motor neuron. It transmits nerve impulses to a skeletal muscle, causing the muscle to contract.

Neurotransmitters and Withdrawal

At this point, you have developed a basic understanding of how neurotransmitters play a role in substance use, and have come to recognize the names of some of the key players. Let’s take a brief look at the other side of the coin: how neurotransmitters play a role in the experience of withdrawal from certain substances and why this might make a difference in keeping a person motivated to maintain a “quit” attempt after developing a substance use disorder. Here, we can draw from content presented in articles published by Koob and Simon (2009) and Trevisan et al (1998). They tell us that:

  • A decrease in dopamine or serotonin (as well as something called the opioid peptide) contributes to the experience of dysphoria. What is dysphoria? Dysphoria is the experience of a profound sense of unease, unhappiness, and general dissatisfaction, often associated with major depression and anxiety. [Your other readings also talked about the experience of anhedonia during recovery/prolonged withdrawal, as you may recall. The idea is the same: it is a punishing emotional/psychological experience.]
  • A decrease in GABA contributes to the experience of anxiety, even panic attacks, due to the resulting nervous system hyperactivity.
  • An increase in norepinephrine contributes to the experience of stress.
  • An increase in glutamate contributes to hyperexcitability.

Why does this matter? Because these negative emotional and psychological states make it difficult to sustain one’s motivation to avoid taking drugs and contribute to the pressure a person might feel to relapse back to using again. And, depending on the nature of the substances involved, withdrawal may lead to decreased dopamine, serotonin, or GABA, as well as increased norepinephrine or glutamate. Knowing about these links between neurotransmitter changes during prolonged withdrawal from using a substance has contributed to the development of several medications to help manage these negative experiences this, in turn, may help a person to sustain a quit attempt over time. (We will learn more about these medications in Module 13 when we study pharmacotherapy strategies.) Another reason why all of this matters: it helps us to understand the biology behind the frequently reported observation that, during withdrawal and early recovery from many types of substances, the risk for suicide is greater than in the general population.

Invertebrate Nervous Systems

Although the invertebrate nervous system is usually much simpler than the nervous systems found in vertebrates, there is still a broad range in complexity depending on the type of invertebrate.

The simplest type of nervous system is found in hydras and jellyfish (cnidarians) and is referred to as a "nerve net." Nerve nets do not have distinct central or peripheral regions, and lack anything that resembles a brain. Instead, the scattered nerve cells form loose networks in each cell layer of the body wall. Some of these neurons carry information from sensory organs that detect touch, light, or other changes in the environment. These neurons in turn contact neurons that control movement of the organism, such as swimming.

Unlike the hydras and jellyfish, invertebrates such as sea stars (echinoderms) display some centralized organization of the nervous system. A ring of neurons is located in the center of the sea star, and simple bundles of neurons called radial nerves extend from the ring to the tip of each arm. In each arm, extensions of the radial nerves form nerve nets as in the jellyfish. This arrangement permits coordinated movement of each arm and the tube feet located on the surface of the arm.

A distinct separation of peripheral and central nervous systems is found in invertebrates such as worms, insects, and mollusks, like the squid. Neuron cell bodies are grouped into clusters called ganglia , which are usually located along the animal's midline. The peripheral component of the nervous system is formed by the extensions of the cells in these ganglia some carry sensory information from the environment to the ganglia, while others carry signals from the ganglia to produce a response (such as movement). This type of organization permits segmentation, in which each ganglion responds to and controls an individual segment of the body. To coordinate the segments, these ganglia are connected to each other in a chainlike fashion by a nerve cord, which is a bundle of neurons that runs the length of

In many invertebrates, the nerve cord is enlarged at the anterior (or head) end of the organism. This enlargement can be considered a primitive brain, and together with the nerve cord comprises the central nervous system. Without any type of brain, the coordination between different segments of the organism is limited at best, and the nervous system primarily produces simple reflexive movements. The presence of a brain allows the organism to receive a wide array of information from the environment, analyze it, and generate a coordinated and complex response. For example, the large brain of a squid enables it to process visual information and rapidly generate coordinated responses to capture prey. In fact, this invertebrate nervous system is so specialized, it closely resembles some vertebrate nervous systems.


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What Is the Difference Between Afferent and Efferent Neurons?

Afferent neurons carry signals to the brain and spinal cord as sensory data, and efferent neurons send signals from the brain to the muscles, glands and organs of the body in response to sensory input.

What Are Neurons?

Within the body's nervous system, which controls and communicates the body's activities, the two main cell types are neuroglia and neurons. The latter is a specialized cell for functional purposes that may include responding to stimuli and transmitting messages around the body. Every neuron has a cell body, dendrites and an axon. Neurons are divided into three types: afferent neurons, efferent neurons and interneurons.

What Are Afferent Neurons?

Sensory information is carried from the body's periphery to a main organ, such as the brain. The sensory information includes neural pulses, which include how things that people hear, touch, see, taste and smell are transmitted from the sensory organs. Afferent neurons are also called sensory neurons, and it is these specialized cells that convey the nerve impulses from around the body directly to the central nervous system.

Physical stimuli, such as sound or light, activate afferent neurons into converting the modalities into nerve impulses. They do this using sensory receptors found in their cell membranes. The main cell bodies of afferent neurons are located near the brain and spinal column, which combine to form the central nervous system.

What Are Efferent Neurons?

Efferent neurons' cell bodies are located within the central nervous system and are also called motor neurons. Having received data from different neurons, which includes afferent neurons and interneurons, the efferent neurons take these signals from the central nervous system and transfer the nerve impulses to the peripheral nervous system, muscles and glands to initiate a response to stimulus.

How They Work Together

Afferent neurons usually have two axons, or terminals, that transmit electrochemical signals into the spinal column or the brain. Once there, the signal passes through a network of interneurons and through an efferent neuron. Afferent-efferent neuron pairs that travel through the spinal column govern reflexes, such as the knee-jerk response.

Afferent neurons are designed to respond to different stimuli. For example, an afferent neuron on a nerve ending designed to respond to heat detects excess heat and sends an impulse through the central nervous system. The efferent neuron then causes muscles to contract as a reflex to move the body away from the heat. Skin has sensory receptors for heat, cold, pleasure, pain and pressure, among others.

How They Differ

Afferent neurons have round and smooth cell bodies, while efferent neurons have satellite-shaped cell bodies. Afferent neurons are found in the peripheral nervous system, and efferent neurons are located in the central nervous system. The axons in afferent neurons move from the ganglia (a cluster of nerve cells that houses afferent and efferent neurons) to the spinal cord. A long axon is actually connected to an efferent neuron.

Afferent neurons have one long myelinated dendrite, whereas efferent neurons have shorter dendrites, and several of them. The dendrite in an afferent neuron is what is responsible for transferring nerve impulses from the receptors to the body of the cell, while in an efferent neuron the impulses pass through the dendrite and leave via a neuromuscular junction that is formed between the effectors and the axon.

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Action Potential V: Design and Analysis of Complex Neurons

  • This unit will provide you with the first opportunity to do a more extended analysis of a neural simulation.
  • Although it would be nice if this were ever true, it is never the case that biological neurons come with helpful, labeled parameter boxes that allow you to easily and quickly change their properties.
  • Instead, each neuron is a novel and unknown system.
  • Thanks to the evolutionary history of neurons, it is usually very likely that a novel neuron will have many of the conductances that are found in other neurons that have been studied previously, even in very different species, though of course there will be variations, and on occasion, you may find an entirely new type of ion channel.
  • The major tools at a neurophysiologist's disposal when studying a new neuron will be those you have learned about: current clamp, voltage clamp, and patch clamp.
  • In addition, he or she may have access to a range of pharmacological agents. These are generally drugs that have been found (or have been created) to block a specific ion channel.
    • For example, the cone snail injects its prey with a venom consisting of a variety of peptides (short sequences of amino acids), and many of these act to paralyze prey by binding to specific ion channels.
    • In particular, -conotoxin is known to bind to N-type calcium ion channels.
    • Thus, you will be provided with current clamp and voltage clamp simulations that include options for adding pharmacological agents. Using these simulations, you will be studying the properties of hypoglossal motor neurons in neonates (newly born rats) and in adult rats.
      • Using these tools, you will be asked to define how the neuron changes as an animal matures, and, in particular, to measure changes in the maximum conductance of the specific ion channels that are relevant to this difference.
      • It is intrinsically interesting to understand how the nervous system changes with development, since this clarifies the way in which it self-assembles.
      • It is also of considerable medical interest, since many diseases are the result of problems with the developmental processes. Understanding how a neonatal neuron differs from an adult neuron can be the basis for a rational therapy that allows a neuron that has not properly developed to be manipulated pharmacologically to act in ways that are more similar to an adult neuron, and also helps to pinpoint the genetic defect that caused the changes, which in turn could lead to a genetic therapy for the disease.

      Here is a voltage clamp simulation of the multi-conductance neuron that you studied in the previous class. The simulation is based on studies of neonatal rat hypoglossal motor neurons:

      Choose the Voltage clamp simulation with additional conductances. Set the Holding potential to -80 mV, the Step delay to 100 ms, the Step duration to 100 ms, and the Total duration to 300 ms. Looking at the graphs of the currents, conductance, and gates, please answer the following questions:

      • Question 1: What is the reason that the fast potassium current shuts off during the depolarizing pulse? What other current that you have learned about does this?
      • Question 2: What is the reason that the sag current does not return to its resting value after the depolarizing pulse?
      • Question 3: Please look at the Intracellular calcium concentration, and the Calcium Currents, Conductances and Gates. Note that the calcium concentration continues to increase after the depolarizing pulse. Explain.
      • Question 4: What is the reason that the calcium-dependent potassium current goes to zero after the depolarizing pulse ends, even though its conductance has not fallen to zero? Explain.

      You are now ready to start analyzing the differences that occur in hypoglossal motor neurons that arise over the course of development. Below, there is a link to a current clamp simulation that allows you to "toggle" between the adult and the neonatal hypoglossal motor neurons. You may want to open the simulation twice, in two different tabs or windows, and click on the button labeled "Adult simulation" in one of these windows (the default simulation is the "Neonatal simulation"). This way you can directly compare data from the two phases of development in two different windows.

      In this current clamp simulation, all of the cell parameters are hidden from you you are measuring only the membrane potential. For the following questions, you will make observations about the behavior of the neonatal and adult neurons, and develop hypotheses explaining your observations. Make sure to take snapshots of the data that you get, and to write down your hypotheses. You will test your hypotheses later, using voltage clamp.

      • Question 5: Compare the action potentials in the neonatal hypoglossal motor neuron to the action potentials in the adult hypoglossal motor neuron. How do they differ? Which of the different conductances you have previously studied could be responsible for this difference?
      • Question 6: Set the Total duration of the simulation to 150 ms, and set the Pulse duration to 100 ms. How do the responses of the two kinds of neurons differ from one another? Which of the different conductances could be responsible for this difference?
      • Question 7: Change the Stimulus current first pulse from 2 nA to -2 nA (i.e., inject hyperpolarizing current into both model neurons). How do the responses of the two kinds of neurons differ from one another? Pay attention to the scales on the plots. Which of the different conductances could be responsible for this difference?

      Given your results from Questions 5, 6, and 7, you are now ready to test your hypotheses about which currents may change during development from birth through adulthood. To test these hypotheses, you can use the simulation below, which provides you with voltage clamp tools and pharmacological agents that can specifically block different conductances. Unlike the previous voltage clamp simulations, all you will be shown is the total membrane current, which is equivalent to the sum of all the individual currents by using the drugs, you can dissect out the sources of this current (which is what you would do in a laboratory). Once again, you are encouraged to create two windows, one containing the "Adult simulation" and one containing the "Neonatal simulation" so that you can directly compare data from the two phases of development in two different windows. Again, make sure to take snapshots of the data that you get, and to write down your hypotheses prior to doing your experiments, and make sure to reflect on whether the data do or do not correspond to your hypotheses. Note that in these simulations, the capacitative current has been subtracted out to make your analysis easier.

      The different abbreviations used with each drug are the same that you saw in the multiple conductance simulations and are summarized here:

      K Delayed rectifier potassium conductance (this is the original Hodgkin-Huxley potassium conductance you first learned about)
      A Fast transient potassium conductance
      SK Calcium dependent potassium conductance
      Na Fast transient sodium conductance (this is the original Hodgkin-Huxley sodium conductance you first learned about)
      NaP Persistent sodium conductance
      H Sag conductance
      T, N, P Various calcium conductances

      You can assume that the differences you observe between the neonatal and adult neurons are caused by changes during development in the levels of expression of different types of ion channels. That is, the neonatal and adult neurons differ because some of the conductances strengthened or weakened as the animal matured. In Question 8, you will begin to determine how these conductances change by first determining the leak conductance.

      • Question 8: To begin to assess the source of the differences between the neurons at the different developmental stages, it is useful to see if they can be made more similar to one another if the voltage-dependent conductances are removed. Change the First step potential to -90 mV, and apply all the drugs to the Neonatal simulation (by checking all the boxes) and to the Adult simulation (by checking all the boxes).
        • What is the response of the total membrane current to the hyperpolarizing voltage step?
        • Calculate the conductance of the membrane for both the neonatal and adult from these data. To do this, use the change in total membrane current and the change in membrane potential with Ohm's law to find the total membrane conductance, Since all other conductances are blocked, the total membrane conductance must be equal to the leak conductance, i.e., .
        • What can you say about the conductance of the leak current in the neonatal and in the adult based on this calculation? Is it the same or different?
        • Question 9: You will now begin to analyze the voltage-dependent conductances one at a time. You will design voltage clamp protocols that allow you to estimate the maximum conductance for each voltage-gated current in both the neonatal neurons and the adult neurons.
          • Create a table in your lab notebook for organizing your data. Click this link, and copy the table template into your notebook. For all your measurements and calculations, always include appropriate units!
          • For each of the nine voltage-gated conductances, do the following:
            • Using the pharmacological agents provided, block all conductances except the one you are currently studying.
            • Find a voltage clamp protocol that strongly activates the conductance. That is, find a holding potential, a step potential, and a step duration that results in a total membrane current that is significantly different from the leak current alone. Once you have done so, record the holding and step potentials in your table, and compute and record the step size (). Remember to include the right units! Here are some things to keep in mind:
              • Both the current you are interested in and the leak current are summed together in the plotted membrane current, so you need to elicit a large current in addition to the leak current.
              • Since some conductances are activated by depolarizations and others by hyperpolarizations, you should try both to see which works best. Your previous experiences studying these conductances should help you get started.
              • Extreme steps in voltage can damage cells, so you should avoid clamping the membrane potential far outside its normal range.
              • Since some conductances take a long time to activate, you may need to significantly extend the duration of the step (and the simulation) to see the maximum current. In some cases, this may take hundreds of milliseconds.
              • If you note that a current takes a long time to activate, you may want to measure the conductance using a tail current protocol:
                • When a conductance takes a long time to activate, this means that several gates must open. Thus, at the end of a long hyperpolarizing or depolarizing pulse, the conductance reaches its maximum value.
                • However, it only takes one gate closing to stop the current, and this usually happens with very little delay.
                • Thus, if you measure the maximum current through a specific channel near the end of a long hyperpolarizing or depolarizing pulse, and then find the minimum value of the current after the pulse ends, the difference in these two current values can be used as a fairly accurate measure of the peak channel conductance.
                • For the calcium-dependent potassium (SK) conductance, you will additionally need to subtract out the conductance of the calcium current you have enabled (which you will need to find independently using the same voltage clamp protocol and measurement timing that you are using for the SK conductance).
                • Question 10: Your table should now summarize the differences between the adult and the neonatal neurons.
                  • Which conductances are unchanged during development?
                  • Which conductances differ between adult and neonatal neurons?
                  • Do these data support the hypotheses you formulated in Questions 5, 6, and 7?
                  • As a final test, open the Current clamp simulation with additional conductances used in the previous class. This model is identical to the current clamp model of the neonatal neuron you were working with earlier. For each conductance that varies between neonatal and adult neurons, change the maximum conductances using the ratios you computed in Question 9 as scaling factors. Do this for all the differing conductances simultaneously so that you can reconstruct the adult neuron. (You may notice that some of the maximum conductances shown in this simulation are larger than the maximum conductances you measured for the neonatal neurons. This may be because your voltage clamp protocol did not fully activate the conductance. This is why you should use the ratio to scale the conductances in this simulation, rather than use the maximum conductances you found for the adult simulation.)
                    • Repeat the measurements done in Questions 5, 6 and 7 above using your reconstructed adult neuron. (You will need to increase the Stimulus current first pulse to 2 nA so that this simulation matches the simulation you used in those questions.) Do you obtain the same results? Include pictures in your notebook.