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Principles of Neuroscience 101: Neurons - How the Nervous System Communicates


The nervous system is at the centre of who we are. Emotion, memory, consciousness, and the ability to move and regulate body functions are all controlled by the nervous system, whether we are aware of it or not. Neuroscience is the study of the structure and function of the nervous system. By studying neuroscience, we can gain an understanding of behaviour, movement and cognition, as well as a wide range of conditions that affect the nervous system, such as addiction, schizophrenia and neurodegenerative disorders. The Principles of Neuroscience 101 series delves into the structure and function of the nervous system and how the brain, spinal cord and peripheral neurons interact to regulate body functions and determine how we perceive the world. This article series aims to cover the story of the nervous system from the beginning: neural development from embryo into adulthood, and the anatomy and physiology of the brain and spinal cord to understand where signals come from in the nervous system. The role of neurons and neurotransmitters in transmitting electronic signals throughout the body will be detailed, and finally how all of these factors come together to allow the nervous system to process sensory inputs to help us perceive and understand the world around us.

This 101 series is divided into six articles including:

  1. Principles of Neuroscience 101: Neurons: How the Nervous System Communicates

  2. Principles of Neuroscience 101: Neurotransmitters: How to Get the Message Across

  3. Principles of Neuroscience 101: The Spinal Cord: Have Some Backbone

  4. Principles of Neuroscience 101: Sensory Neuroscience: How We Perceive the World

Principles of Neuroscience 101: Neurons - How the Nervous System Communicates

Neurons are the cells of the nervous system and are highly specialised to carry out nervous system functions and are structurally and functionally distinct from other animal body cells (Jan & Jan, 2003). The brain contains approximately 8.3 x 10^9 neurons that make approximately 6.7 x 10^13 connections (Sporns, 2002). Neurons, the cells that make up the nervous system, are distinct from other body cells as they also contain an axon and dendrites. These structures enable neurons to reach all over the body and form connections with neurons and other cells to perform the essential duty of neuronal cells: transmit signals (Goldberg, 2004; Stein et al., 2005). Neural connections are what distinguish one human brain from another. Neurons form huge numbers of connections, all determined by an individual’s unique experiences (Amaral, 2006).

Types of Neurons

There are different ways to classify neurons. Neurons can be distinguished as excitatory or inhibitory, afferent or efferent, or principal neurons and interneurons (Amaral, 2006). In the case of excitatory or inhibitory neurons, excitatory neurons usually function to integrate and transmit information signals through the nervous system. Nerve and muscle cells can be referred to as ‘excitable’ as they are subject to influence from an external stimulus. This causes the electrical potential of the cell membrane to change and cause an action potential. Inhibitory neurons, on the other hand, influence how excitatory neurons integrate signals. Unlike excitatory neurons, inhibitory neurons act in a context-specific and behaviour-specific manner. Together, excitatory and inhibitory neurons form complex interconnected neuronal circuits in the nervous system (Fletcher, 2019; Wood et al., 2017).

Figure 1: Neuron Excitation and Inhibition (Unknown, n.d.).

Another way to describe neurons is by functional class: principal neurons or interneurons. Principal, or projection, neurons include motor and sensory neurons that transmit information to the next stage in the neural pathway. Interneurons on the other hand only signal to local cells, within the interneuron’s own stage in the pathway (Amaral, 2006). Furthermore, principal neurons usually excite neurons they project to while interneurons are usually used to send local inhibitory signals to nearby neurons (Amaral, 2006). Interneurons are not solely inhibitory, however. They can also help control the output signals of principal cells and other interneurons. Another function of interneurons is in oscillatory rhythmic activity (e.g. brain waves). The intrinsic conduction, inhibitory synaptic transmission, and interneuronal gap junction connectivity of interneurons directly influence oscillatory activity in the brain (McBain & Fisahn, 2001).

Sensory and motor neurons are the main type of neurons. They work in tandem: sensory neurons receive sensory information and motor neurons send signals to act on that sensory information. These two neuron types are different from each other as they are developed separately. During embryonic development of the nervous system, motor neurons develop from the neural tube, while sensory neurons develop from the neural plate border and neural crest (Cheah et al., 2017). Transcription factors, which regulate the expression of genes, play an important role in differentiating neurons by controlling the effect of extrinsic signals on the developing neurons. This is done by these cells regulating genes for molecules involved in axon guidance, ion channels, synapse formation, and neurotransmitter function. (Goulding, 1998). From these separate origins, motor and sensory neurons go on to have many differences as developed neurons. The structure, surrounding environment, response to injury, and growth requirements of motor and sensory neurons are vastly different (Cheah et al., 2017). There are different kinds of sensory and motor neurons. For example, dorsal root ganglion neurons are one type of sensory neuron. These are afferent neurons that relay sensory information from a peripheral stimulus to the CNS. Upper motor neurons are one type of motor neuron. The corticospinal tract is made of upper motor neurons that project from the sensorimotor cortex of the brain and has axons stretching the length of the spinal cord (Cheah et al., 2017).

Figure 2: Types of Neurons (Unknown, n.d.).

The nervous system affects muscles through motor neurons. By sending signals through motor neurons, the CNS can cause voluntary and involuntary movement. Motor neurons innervate muscle fibres, causing them to either relax or contract. Together, motor neurons and the muscle fibres they affect are referred to as the ‘motor unit’ (Amaral, 2006; McNeil et al., 2013). There are different sizes of motor neurons, and with these physical differences come functional differences. In larger motor neurons, a large soma (cell body) means the axonal diameter is also big. These larger axons conduct signals faster than smaller motor neurons. Furthermore, muscle fibres innervated by large motor neurons will contract faster than muscle fibres innervated by small motor neurons (McNeil et al., 2013). Motor neuron size has also been shown to determine when a motor neuron is recruited to the circuit. In a study by Henneman et al. (1965), it was shown that when an extensor muscle was stretched, the first motor neurons to fire and send their signals were alpha motor neurons, the smallest size. As the muscle was stretched further, other motor neurons were recruited in order of size, with the largest neurons firing when the muscle was at the greatest stretch. This suggests that the excitability of a motor neuron is governed by its size.

Neuronal Structure

Neurons are highly polarised and are made up of different subcellular compartments. For example, one compartment gives rise to at least one dendrite (but there can be many), and one axon extending from the cell body (Jan & Jan, 2003). Neurons are made up of three main structures: dendrites, cell body and an axon. Dendrites are thin fibres extending from the neuron. They receive signals, usually from other neurons. As in most body cells, the cell body performs basic cellular functions to maintain the cell, while the axon is a long, thin fibre that can stretch long distances to carry electrical signals and impulses. Neuronal signals need to be relayed over long distances in a very short time. If someone steps on something sharp, the sensory pain signal is transmitted from the foot to the brain. In response, the brain will send a signal to the muscles in the leg to contract and lift the foot. A neuronal circuit like this requires many neurons to work together, which requires a sophisticated and rapid signalling system between neurons (“The Principles of Nerve Cell Communication”, 1997). The function of neurons depends upon their structure. The branching of dendrites, the location of synapses, and any myelination (where axons are insulated by a fatty substance called myelin, which helps nerve impulses travel faster). of the axon determine the role played by an individual neuron. There are three levels of neuronal structure: ‘macroscopic’, ‘microscopic’, and ‘ultrastructural’. The macroscopic structure includes the neuron’s shape, the number of dendritic and axonal branches, and the location of the branches. The microscopic structure includes the shape, length, diameter, and branching points of the dendritic and axonal branches. Ultrastructure is the shape of the neurites near the synaptic connections, the ‘local’ contours, swellings, and dendritic spines (Miller & Jacobs, 1984).

Figure 3: Neuron (Unknown, n.d.).

Neurons contain projections called axons which allow electrical signals to pass from one neuron to another and so are essential for neuronal cell communication (Jan & Jan, 2003). Neurons extend axons and branches of dendrites to reach all parts of the body and transmit signals to and from the central nervous system of the brain and spinal cord (Brodal, 2004; Goldberg, 2004). The axon is the longest part of the neuron and extends from the cell body. Axons can stretch for many meters, with the longest recorded axon in nature found in the spinal tract of the blue whale, stretching for over 30 meters. The longest axon in the human body reaches from the base of the spinal cord to the toes, with an average length of one meter. The long length of axons allows for long-distance communication. With long axons, signals from the cell body of neurons can reach far distances quickly, enabling rapid signal transduction essential for sensory reflexes and movement, as well as myriad other functions of the nervous system (Burdett & Freeman, 2014).

Although the long length of axons allows for long-distance signalling, there are complications associated with the elongated size of neurons. Cells contain mitochondria, organelles that produce energy. The central nervous system has a high demand for mitochondrial function as it has a very high metabolic rate compared to the rest of the body. Neuronal activity depends on the energy produced by mitochondria to maintain ionic gradients and neurotransmission of signals. Neuron mitochondria are located in the presynaptic and postsynaptic regions. However, as neurons are segmented into distinct subcellular compartments, each with its own functions and energy demands, there may be difficulties in adapting the cell’s energy supply locally. Therefore, neurons are extremely vulnerable to mitochondrial dysfunction (Kann & Kovacs, 2007). Similarly, the length of axons can also put lysosomal function at risk. Lysosomes are organelles that break down biomolecules and cellular debris as well as recycle nutrients. Due to functional compartmentalisation, lysosomes must be transported around the neuron to where they are needed, which is open to dysfunction. (Baker, 2014; Ferguson, 2019; Kann & Kovacs, 2007; Wartosch et al., 2015).


Dendrites have been called the ‘antennae of the neurons.’ These structures receive information in different ways. The dendrites of sensory neurons receive information from sensory receptors, while other CNS and PNS neurons receive information from synaptic connections with other neurons. Additionally, dendrites make, store and release neurotransmitter substances (Cuello, 1983; Jan, 2001). Dendritic spines are small projections found on dendrites. They are extremely plastic, meaning that the size, shape, and connections they form constantly change. Dendritic spines form connections with axons of other neurons in response to neuronal activity. The growth of these connections is associated with learning and memory. When these synapses are used more often, they are strengthened. However, in neurodegeneration and drug abuse, it has been observed that these connections reduce and deteriorate (Pchitskaya & Bezprozvanny, 2020).

Figure 4: Dendritic Spine (Unknown, n.d.).

The dendrite system of a neuron is referred to as a ‘dendritic tree’. As the name suggests, there can be many branches of dendrites belonging to one neuron. The pattern of dendritic branching pattern varies greatly in different types of neurons and every dendrite in the tree can form synapses with different neurons. As a result, a neuron can receive thousands of different inputs into its dendritic tree (Otopalik et al., 2017). Purkinje cells in the cerebrum can receive around 100,000 inputs, while hippocampal pyramidal cells can receive around 30,000 inputs (Spruston et al., 2008). Neurons must integrate or segregate these inputs in order to function efficiently. Integrating neuronal inputs is also essential as dendrites can be widely distributed, which would otherwise cause location-dependent variabilities in synaptic inputs to the cell. Neurons can perform a range of passive and active synaptic integration techniques on neuronal inputs, including changes in synaptic conductance, and linear encoding (Magee, 2000; Stuart & Spruston, 2015). Not all dendrites receive their inputs from other neurons, as many sensory neuron dendrites are sensory endings that receive signals from the environment, i.e. through mechanical stimuli like touch, which induce receptor potentials (Spruston et al., 2008).

Neuronal Communication

Neurons communicate through cell-to-cell signalling. With the exception of diffusible messengers, neurons must be in physical contact in order to communicate (Sporns, 2002). The point where two neurons meet is called a synapse. Synapses are formed when the axon of the neuron before the synapse (presynaptic neuron) is guided toward the dendrite of another neuron (postsynaptic neuron). The presynaptic neuron then sends signals across the synapse to a dendrite on the postsynaptic neuron in a one-directional signalling system (Jan & Jan, 2003; Ou & Shen, 2010). When forming a synapse, a variety of signalling cues cause an axon to extend from its cell body and stretch to its postsynaptic target. Some of these signals come from the target dendrite to guide the axon toward itself. The axon of a presynaptic neuron can elongate over distances of several feet to reach the dendrite of a postsynaptic neuron (Jan, 2001; Ou & Shen, 2010).

Figure 5: Neuronal Synapse (Pratt, 2023).

Neuronal signals are transmitted from one nerve cell to the next through a series of Action Potentials (AP). APs are fast, transient, electrical signals that are propagated along a neuron, carrying information (Bezanilla, 2006). These signals occurring in the pre-synaptic cell trigger biochemical and biophysical changes in the axon terminal of the presynaptic neuron. These changes prompt neurotransmitters to be released into the synaptic junction (where two neurons meet and transmit or receive signals) where they bind to receptors on the postsynaptic neuron. The postsynaptic neuron may then generate an output signal and transmit an AP along its own axon to the next synapse (Sporns, 2002). At rest, the transmembrane potential (difference in electrical potential between the internal and external environment of a cell) of a neuron is about −70 mV, relative to the extracellular matrix outside the cell. This is known as resting potential. When an AP occurs, transmembrane potential reverses and becomes less negative. This occurs in less than a millisecond, and within two milliseconds the transmembrane potential will have returned to its resting state (Bezanilla, 2006). The transmembrane potential of the AP moves quickly down the neuron from the point of initiation in the dendrites to the axon and on, to the axon terminal. APs can occur due to the activity of voltage-gated ion channels in the axon membrane (Barnett & Larkman, 2007). When the neuron cell membrane is polarised (at rest) voltage-gated ion channels are closed. When an AP causes the cell membrane to be depolarised these channels open quickly and the ions selective to this ion channel flow across the neuron cell membrane along their electrochemical gradients (i.e. from positive to negative) (Sands et al., 2005). The opening of these ion channels temporarily, and locally, changes the permeability of the axon membrane to specific ions, in this case, sodium (Na+) and potassium (K+) ions (Barnett & Larkman, 2007).

APs initiate in the axon initial segment (AIS) in the neurons of most vertebrates. The AIS is a highly plastic and specialised part of the axon which contains a high density of voltage-gated Na+ and K+ ion channels (Gulledge & Bravo, 2016). As the AP moves along the axon from the AIS, Na+ ion channels open and these positively charged ions flow into the negatively charged cell. These charged ions then make the membrane locally less negative, resulting in AP propagation. As Na+ ions make the membrane less negative, a positive feedback system is initiated that causes more Na+ ions to come into the cell and make the membrane even more charged (Bezanilla, 2006). When the AP reaches the axon terminal it causes voltage-sensitive Ca2+ ion channels to open. The cell becomes even less negative but the influx of Ca2+ also disrupts the positive feedback system by prompting K+ ion channels to open. These ion channels drive K+ ions in the opposite direction to Na+ ions: out of the cell. This Ca2+-driven loss of positively charged ions repolarises the membrane to its resting potential of −70 mV (Bezanilla, 2006; Bootman et al., 2001; Borst & Helmchen, 1998). APs are effective at signalling due to a few key features: highly selective ion channels in the axon membrane, voltage sensitivity and systems for rapid closure of ion channels once the AP has passed (ensures the AP will only move in one direction along the axon) and the action of Ca2+ to repolarise the cell membrane following an AP (Barnett & Larkman, 2007). Importantly, APs work on an “all or nothing” principle. This means that either an AP will occur as the result of electrical input, or it won’t. The strength of the initial stimulus doesn’t matter. There are no ‘weaker’ or ‘stronger’ APs (Fletcher, 2019).

Ion Channels

The electrical activity that allows signals to be transmitted along neurons is enabled by ion channels in the axon membrane (Hucho & Weise, 2001). Ion channels are pores in cell membranes that allow specific ions to pass into and out of the cell. As ions are charged molecules, this movement of ions creates a charge in the cell and accounts for the electrical activity of cells. Ion channels are found in nearly all cells, including plant cells and even prokaryotes. Most ion channels are selective, meaning that a certain ion channel will only allow specific types of ions to pass through. Ion channels determine which ions can pass depending on ion size and whether the ion is positively or negatively charged. The opening of the ion channel then creates a pathway where ions can flow through. An ion channel may only open for a few seconds, with an opening only a few atoms wide, but in that time many thousands (in the order of 107 to 109 ) of ions per second can move in and out of the cell (Levitan, 1988; Unwin, 1993). The ion channels embedded in the cell membrane of axons also influence the neuron’s structure, function, and morphology (Otopalik et al., 2017). These ion channels also influence passive current flow and voltage propagation of signals and nerve impulses. This helps determine whether or not voltage signals from different dendritic locations are integrated. Therefore, the ion channels expressed on an axon drive the function of the neuron (Otopalik et al., 2017).

Figure 6: Types of Ion Channels (Lodish, 2001).

Some ion channels are gated, for example, ligand-gated and voltage-gated ion channels. Ligand-gated ion channels are closed until a ligand binds to it to prompt the channel to open (Hucho & Weise, 2001). Voltage-gated ion channels are found in the membranes of excitable cells, such as neurons. These ion channels are essential to the propagation of electrical signals along neurons. Voltage-gated ion channels open or close in response to changes in transmembrane voltage. In a polarised cell, voltage-gated ion channels will be closed, but when an electrical impulse occurs the voltage-gated ion channels open. This allows ions involved in propagating electrical signals, such as K+, Na+, and Ca2+ to flow across the cell membrane and aid in signal propagation (Sands et al., 2005).


Neurons are the link between the brain and the world, and so have a wide range of functions. From receiving sensory inputs, propagating signals, relaying information to and from the brain, and enabling movement and response by acting on muscles. These highly specialised and diverse cells are regarded separately from any other body cell type. Their distinctive shape, with a dendritic tree and long axon, set them apart, as well as their unique function in transmitting electrical signals. Neurons have developed systems that allow them to transmit signals over long distances in milliseconds and this efficiency is essential for nearly everything that happens in the body: breathing, movement, and heartbeat. These nervous system cells touch nearly every function in the body. Different types of neurons carry out specific roles in the neural circuit. Sensory neurons receive information from a receptor and relay that information to the CNS for processing. Motor neurons signal from CNS to cause muscles to move. Interneurons allow neurons to interact with each other and control local neuron signalling through inhibition. Neurons are involved in nearly every process in the body by receiving inputs and transmitting ‘messages’ through electric pulses, called action potentials, to other neurons to relay information throughout the body and cause an effect.

Bibliographical References

Amaral, D. (2006). The anatomical organization of the central nervous system. 4, 317-36.

Baker, M. R. (2014). ALS—dying forward, backward or outward? Nature Reviews Neurology, 10(11), 660.

Barnett, M., & Larkman, P. (2007). The Action Potential. Practical Neurology, 7, 192-197. ISBN 0-19-5165608.

Bezanilla, F. (2006). Voltage-Gated Ion Channels: Dynamics, Structure, and Applications. In Biological membrane ion channels (pp. 81–118). Springer.

Bootman, M. D., Lipp, P., & Berridge, M. J. (2001). The organisation and functions of local Ca2+ signals. Journal of Cell Science, 114(12), 2213–2222.

Borst, J., & Helmchen, F. (1998). [20] Calcium influx during an action potential. In Elsevier eBooks (pp. 352–371).

Brodal, P. (2004). The central nervous system: Structure and Function. (pp 3-47). Oxford University Press. ISBN 0-19-5165608.

Burdett, T. C., & Freeman, M. (2014). Astrocytes eyeball axonal mitochondria. Science, 345(6195), 385–386.

Cheah, M., Fawcett, J. W., & Haenzi, B. (2017). Differential regenerative ability of sensory and motor neurons. Neuroscience Letters, 652, 35–40.

Cuello, A. C. (1983). Dendrites as Sites of Storage and Release of Neurotransmitter Substances, an Extension of Dale’s Principle. In Dale’s Principle and Communication Between Neurones (pp. 69–82). Elsevier.

Ferguson, S. M. (2019). Neuronal lysosomes. Neuroscience Letters, 697, 1–9.

Fletcher, A. (2019). Action potential: generation and propagation. Anaesthesia & Intensive Care Medicine, 20(4), 243–247.

Goldberg, J. L. (2004). Intrinsic neuronal regulation of axon and dendrite growth. Current Opinion in Neurobiology, 14(5), 551–557.

Goulding, M. (1998). Specifiying Motor Neurons and their Connections. Neuron, 21(5), 943–946.

Gulledge, A. T., & Bravo, J. J. (2016). Neuron morphology influences axon initial segment plasticity. ENeuro, 3(1).

Henneman, E., Somjen, G. G., & Carpenter, D. O. (1965). Excitability and Inhibitibility of Motoneurons of Different Sizes. Journal of Neurophysiology, 28(3), 599–620.

Hucho, F., & Weise, C. (2001). Ligand-Gated Ion Channels. Angewandte Chemie, 40(17).

Jan, Y. (2001). Dendrites. Genes & Development, 15(20), 2627–2641.

Jan, Y., & Jan, L. Y. (2003). The control of dendrite development. Neuron, 40(2), 229–242.

Kann, O., & Kovacs, R. J. (2007). Mitochondria and neuronal activity. American Journal of Physiology-cell Physiology, 292(2), C641–C657.

Levitan, I. B. (1988). Modulation of ION channels in neurons and other cells. Annual Review of Neuroscience, 11(1), 119–136.

Magee, J. C. (2000). Dendritic integration of excitatory synaptic input. Nature Reviews Neuroscience, 1(3), 181–190.

McBain, C. J., & Fisahn, A. (2001). Interneurons unbound. Nature Reviews Neuroscience, 2(1), 11–23.

McNeil, C. J., Butler, J. E., Taylor, J. L., & Gandevia, S. C. (2013). Testing the excitability of human motoneurons. Frontiers in Human Neuroscience, 7.

Miller, J. P., & Jacobs, G. A. (1984). Relationships between neuronal structure and function. The Journal of Experimental Biology, 112(1), 129–145.

Otopalik, A. G., Sutton, A. C., Banghart, M. R., & Marder, E. (2017). When complex neuronal structures may not matter. eLife, 6.

Ou, C., & Shen, K. (2010). Setting up presynaptic structures at specific positions. Current Opinion in Neurobiology, 20(4), 489–493.

Pchitskaya, E., & Bezprozvanny, I. (2020). Dendritic Spines Shape Analysis—Classification or Clusterization? Perspective. Frontiers in Synaptic Neuroscience, 12.

Sands, Z. A., Grottesi, A., & Sansom, M. S. (2005). Voltage-gated ion channels. Current Biology, 15(2), R44–R47.

Sporns, O. (2002). Network analysis, complexity, and brain function. Complexity, 8(1), 56–60.

Spruston, N., Stuart, G., & Häusser, M. (2008). Dendritic Integration. In Dendrites (2nd ed.). (pp.1-736). Oxford University Press.

Stein, R. B., Gossen, E. R., & Jones, K. E. (2005). Neuronal variability: noise or part of the signal? Nature Reviews Neuroscience, 6(5), 389–397.

Stille, D. R. (2006). Animal cells: Smallest Units of Life. (pp 1-48). Capstone.

Stuart, G. J., & Spruston, N. (2015). Dendritic integration: 60 years of progress. Nature Neuroscience, 18(12), 1713–1721.

The principles of nerve cell communication. (1997). Alcohol Health and Research World, 21(2), 107–108.

Unwin, N. (1993). Neurotransmitter action: Opening of ligand-gated ion channels. Cell, 72, 31–41.

Wartosch, L., Bright, N. A., & Luzio, J. P. (2015). Lysosomes. Current Biology, 25(8), R315–R316.

Wood, K. C., Blackwell, J. M., & Geffen, M. N. (2017). Cortical inhibitory interneurons control sensory processing. Current Opinion in Neurobiology, 46, 200–207.

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