Commentary - Journal of Brain and Neurology (2025) Volume 8, Issue 1

Synaptic transmission: The foundation of neural communication

Synaptic transmission: The foundation of neural communication.^*

Department of Medical Laboratory Sciences, University of Sharjah, Japan

*Corresponding Author:

Brett Robinson
Department of Medical Laboratory Sciences
University of Sharjah,
Japan
E-mail: raquela@ucsf.edu.us

Received: 02-Feb-2025, Manuscript No. AAJBN-25-169531; Editor assigned: 03-Feb-2025, PreQC No. AAJBN-25-169531(PQ); Reviewed: 16-Feb-2025, QC No. AAJBN-25-169531; Revised: 20-Feb-2025, Manuscript No. AAJBN-25-169531(R); Published: 27-Feb-2025, DOI:10.35841/aajbn-8.1.182

Citation Robinson B. Synaptic transmission: The foundation of neural communication. J Brain Neurol. 2025;8(1):184

Introduction

Synaptic transmission is the fundamental process by which nerve cells, or neurons, communicate with each other and with target cells in the body. This highly specialized mechanism enables the brain to process information, control movement, regulate emotions, and maintain homeostasis. It occurs at the synapse, a junction between two neurons or between a neuron and another cell, such as a muscle or gland cell. Without effective synaptic transmission, the central and peripheral nervous systems would not be able to function properly, resulting in significant impairments in sensory perception, cognition, and motor control. [1].

In a typical synapse, the neuron sending the signal is referred to as the presynaptic neuron, while the neuron or cell receiving the signal is called the postsynaptic cell. The tiny gap between them, known as the synaptic cleft, plays a critical role in the process. Electrical impulses called action potentials travel down the presynaptic neuron to its terminal end, triggering the release of chemical messengers called neurotransmitters. These neurotransmitters cross the synaptic cleft and bind to receptors on the postsynaptic cell, initiating a new electrical signal or cellular response. [2].

The sequence of synaptic transmission begins when an action potential arrives at the presynaptic terminal, causing voltage-gated calcium channels to open. The influx of calcium ions triggers the synaptic vesicles—small membrane-bound sacs containing neurotransmitters—to fuse with the presynaptic membrane. This fusion results in the release of neurotransmitters into the synaptic cleft through a process called exocytosis. The rapid and precise nature of this process ensures that signals can be transmitted efficiently and repeatedly. Disruptions in synaptic transmission are linked to numerous neurological and psychiatric disorders. Conditions such as Alzheimer’s disease, Parkinson’s disease, epilepsy, depression, and schizophrenia often involve abnormalities in neurotransmitter production, release, or receptor function. For instance, the loss of dopamine-producing neurons in Parkinson’s disease impairs motor control, while reduced serotonin levels are associated with depression. Understanding these mechanisms has paved the way for developing targeted treatments, such as selective serotonin reuptake inhibitors (SSRIs) for depression or dopamine replacement therapies for Parkinson’s [3].

Once released, neurotransmitters diffuse across the synaptic cleft in a fraction of a second and bind to specialized receptor proteins on the postsynaptic membrane. These receptors can be ionotropic, which directly open ion channels to produce a rapid response, or metabotropic, which initiate a slower, more prolonged signaling cascade through second messengers. The type of receptor activated determines the nature of the postsynaptic response, which can be excitatory, promoting the generation of a new action potential, or inhibitory, reducing the likelihood of neuronal firing. Synaptic transmission is not only crucial for basic brain function but also plays a major role in learning and memory. Through a process called synaptic plasticity, the strength and efficiency of synaptic connections can change in response to repeated activity. Long-term potentiation (LTP) strengthens synapses, enhancing communication between neurons, while long-term depression (LTD) weakens them, allowing for adaptability and fine-tuning of neural networks. These changes form the basis for acquiring new skills, storing memories, and adapting to new experiences [4].

A key aspect of synaptic transmission is the termination of the signal, which ensures precise communication and prevents continuous stimulation. This can occur through enzymatic breakdown of neurotransmitters, reuptake into the presynaptic neuron, or diffusion away from the synaptic cleft. For example, the neurotransmitter acetylcholine is rapidly broken down by the enzyme acetylcholinesterase, while serotonin and dopamine are commonly reabsorbed by the presynaptic cell for reuse. This regulation maintains balance in the nervous system and prevents overstimulation that could damage neural circuits.[5].

Conclusion

Synaptic transmission is the cornerstone of neural communication, enabling the nervous system to coordinate thought, movement, sensation, and emotion. Its intricate steps, from neurotransmitter release to receptor activation and signal termination, ensure precise and adaptable information transfer. Disruptions in this process can lead to serious neurological conditions, making it a vital focus for research and medical intervention

References

1. Kim FJ, Maher CM. Sigma1 pharmacology in the context of cancer. Evolution of the Concept of Sigma Receptors. 2017:237-308.

Indexed at, Google Scholar

2. Checler F. p53 in neurodegenerative diseases and brain cancers. Clin Pharm Therap. 2014;142(1):99-113.

Indexed at, Google Scholar, Cross Ref

3. Dietrich J, Kesari S. Corticosteroids in brain cancer patients: benefits and pitfalls. Expert Rev Clin Pharmacol. 2011;4(2):233-42.

Indexed at, Google Scholar, Cross Ref

4. Parrasia S. Peptides as Pharmacological Carriers to the Brain: Promises, Shortcomings and Challenges. Mol Pharm. 2022;19(11):3700-29.

Indexed at, Google Scholar, Cross Ref

5. Pantic I. Cancer stem cell hypotheses: impact on modern molecular physiology and pharmacology research.J Biosci. 2011;36(5):957-61.

Indexed at, Google Scholar, Cross Ref