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Neural Signaling- Process and Characteristics

The specialized, specific cells in the body that receive and transmit information throughout the system are called neurons (Ciccarelli & Meyer, 2006). Neurons are the ones responsible for intracellular and extracellular signalling; for which their unique structure is capable (Levitan & Kaczmarek, 2015). This essay aims at highlighting the characteristics and the process of neural signalling.

Brain signalling entirely depends upon the ability of neurons to respond to even the smallest of stimuli with rapid changes in electrical signals (Koester & Siegelbaum, 2013). The part of the neuron that receives messages from other neurons is known as a dendrite. Dendrites are branch-like structures and are the cellular extensions of the neuron (Ciccarelli & Meyer, 2006). The dendrites receive numerous inputs from various synapses simultaneously and are integrated to form an articulate output response (Magee, 1999). These post-synaptic potentials can be excitatory (EPSP) or inhibitory (IPSP) (Fernster & Jagadeesh, 1992). Action potential (AP) is the primary method of cell-to-cell communication wherein membrane potential rapidly ascents and descents, causing the transfer of information from one neuron to the other (Hodgkin & Huxley, 1952). The process where information carried by PSPs, via increased or decreased probability of generating AP, is called synaptic integration (Palmer & Stuart, 2006). The blending of these inputs by spatial summation or temporal summation determines whether AP will be generated in the neuron or not (Kandel et al., 2013). Spatial summation, usually occurring on the dendrites, happens when impulses from multiple presynaptic neurons, are summed up to reach AP. Integrations of several EPSPs can lead to AP, whereas the integration of IPSPs can prevent the achievement of AP (Levin and Luders, 2000). Temporal potential ensues when high-frequency APs are received from the same presynaptic neuron continuously. The amplitude of each potential obtained is summed together to achieve AP (Carpenter & Reddi, 2012). The integrated potential, spatially or temporally, is transmitted to the axon hillock where AP is achieved (Kandel et al., 2013).

To respond to the rapid changes in the neuron, the cell membrane’s potential changes that lead to the firing of an AP. These membrane changes are mediated by ion channels that are specified to carry out responses to different parts of the nervous system. Ion channels can recognize and choose ions, and they open and close in response to specific electrical, chemical and mechanical changes; which is how they transfer ions through the cell membrane (Koester & Siegelbaum, 2013). These ions are shut when the cell is at resting potential (negative) and rapidly open once the AP threshold is achieved, releasing sodium and potassium ions into the cell (Barnett & Larkman, 2007).

The axon is that part of the neuron that specializes in transmission of intercellular information over long distances (Levitan & Kaczmarek, 2015). Axons are dependable and consistent transmission cables, and axonal dysfunction leads to several neurological disorders. Voltage-gates ion channels and axonal propagation together control the brain's signal processing, neuronal timing and efficiency of synapses (Debanne, Campanac, Bialowas, Carlier & Alcaraz, 2011). For the rapid proliferation of signals, the nodes of Ranvier are essential. They are intermittent and recurring interludes in myelination along the axon. These are clustered by v-gated sodium and potassium channels, thus minimizing ion loss in myelinated internodes, and AP is conducted fast and appropriately (Kole, 2011).

The AP rapidly causes the release of positively charged sodium ions that carry the message forward. This causes the cell body to become positively charged, and the extracellular region is negatively charged. After the AP has passed, the sodium ions become inactive and are pumped out by the ATPase pumps back into the extracellular region. After this, slower responding potassium channels open and potassium moves out of the neuron, hyperpolarizing it. The v-gated potassium channels close post this and the standard resting potential is achieved that keeps the neuron ready to fire again (Ciccarelli & Meyer, 2006; Kandel et al., 2013).

After the signal is promulgated to the axonal terminals, neurons communicate with one another at the synapse. Although synaptic transmission can happen electrically and chemically, most synapses are chemical. These synapses are dependent on the release of neurotransmitters across the synaptic cleft (Kandel et al., 2013). The neurotransmitters contained the synaptic vesicles of the presynaptic neuron are diffused when the AP releases calcium ions and triggers a process called exocytosis (Ciccarelli & Meyer, 2006; Kandel et al., 2013). These neurotransmitters bind to the post-synaptic receptors and alter its membrane potential that proceeds to carry the signal forward.

From the above discussion, we can see that reception, processing and transmission of neural signals are complex procedures that ride on several small elements to function accurately.


Barnett, M. W., & Larkman, P. M. (2007). The action potential. Practical neurology7(3), 192-197.

Carpenter, R., & Reddi, B. (2012). Neurophysiology: a conceptual approach. CRC Press.

Ciccarelli, S. K., & Meyer, G. E. (2006). Psychology, South Asia edition, Pearson Education, Inc. Copyright 2006.

Debanne, D., Campanac, E., Bialowas, A., Carlier, E., & Alcaraz, G. (2011). Axon physiology. Physiological reviews91(2), 555-602.

Ferster, D., & Jagadeesh, B. (1992). EPSP-IPSP interactions in cat visual cortex studied with in vivo whole-cell patch recording. Journal of Neuroscience12(4), 1262-1274.

Hodgkin, A. L., & Huxley, A. F. (1952). A quantitative description of membrane current and its application to conduction and excitation in nerve. The Journal of physiology117(4), 500-544.

Kandel, E. R., Schwartz, J. H., Jessell, T. M., Siegelbaum, S. A., Hudspeth, A. J., & Mack, S. (2013). From nerve cells to cognition: the internal representations of space and action. Principles of neural science, 370-391.

Koester, J., & Siegelbaum, S. A. (2013). Membrane potential and the passive electrical properties of the neuron. Principles of neural science, Ed5, 126-147.

Kole, M. H. (2011). First node of Ranvier facilitates high-frequency burst encoding. Neuron71(4), 671-682.

Levin, K. H., & Lüders, H. (2000). Comprehensive clinical neurophysiology. Saunders.

Levitan, I. B., & Kaczmarek, L. K. (2015). The neuron: cell and molecular biology. Oxford University Press, USA.

Magee, J. C. (1999). Dendritic I h normalizes temporal summation in hippocampal CA1 neurons. Nature neuroscience2(6), 508-514.

Palmer, L. M., & Stuart, G. J. (2006). Site of action potential initiation in layer 5 pyramidal neurons. Journal of Neuroscience26(6), 1854-1863.

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