NEUROTRANSMITTERS: THE CHEMISTRY OF EMOTIONS
- RAHUL K
- Aug 3
- 4 min read
Updated: Aug 14
Contents:
1)Abstract
2)Definition and function
3)Synthesis and storage in synapse
4)Mechanism of neurotransmitter release in synapse
5)Neurotransmitter Receptors
6)Neurotransmitter imbalances and diseases
7)Drugs affecting Neurotransmitters
Abstract:
Neurotransmitters are chemical messengers that play a critical role in the transmission of signals across synapses in the nervous system. They influence a wide range of functions, including mood, movement, cognition, and autonomic processes. Neurotransmitters can be classified as excitatory, inhibitory, or modulatory based on their effects on target neurons. Common examples include dopamine, serotonin, acetylcholine, glutamate, and GABA. Imbalances in neurotransmitter systems are associated with various neurological and psychiatric disorders, such as depression, Parkinson’s disease, and anxiety. Understanding neurotransmitter function is essential for the development of effective treatments for these conditions and for advancing knowledge in neuroscience and pharmacology.
Definition and function:
The nervous system processes sensory information and controls behavior by performing an enormous number of computations. These computations occur both within cells and between cells, but it is intercellular information processing, involving complex neural networks, that provides the nervous system with its remarkable functional capacity. The principal cells involved in information processing are neurons, of which there are hundreds, if not thousands of individual cell types based on morphology, location, connectivity and chemistry . In addition to neurons, the other major kind of cell in the nervous system is the glia, which play critical support roles, but which are increasingly seen to function in some aspects of information processing.
Neurotransmitters are chemical messengers that play a vital role in transmitting signals between nerve cells. They regulate a wide range of functions in the body, including mood, emotions, and the sleep-wake cycle. They also control muscle movement, influence heart rate and breathing, and support learning and memory. By enabling communication across synapses, neurotransmitters help maintain the proper functioning of the nervous system.

Synthesis and storage in synapse:
Neurotransmitters are synthesized within neurons, either in the cell body or the axon terminal, depending on their type. Small-molecule neurotransmitters, such as dopamine and acetylcholine, are typically synthesized in the axon terminal. The neuron takes in precursor molecules often derived from nutrients in the bloodstream and uses specific enzymes to convert them into active neurotransmitters. For example, dopamine is synthesized from the amino acid tyrosine. In contrast, neuropeptides, which are larger signaling molecules like endorphins, are synthesized in the cell body. These are produced in the endoplasmic reticulum, processed in the Golgi apparatus, and transported down the axon to the terminal using microtubules. Once synthesized, neurotransmitters are stored in synaptic vesicles and efficient communication between neurons.

Mechanism of transmitter release in synapse:
The release of neurotransmitters at a synapse is a carefully regulated process that begins when an electrical signal, known as an action potential, travels down the axon of a neuron and reaches the axon terminal. This electrical impulse causes voltage-gated calcium channels in the presynaptic membrane to open, allowing calcium ions (Ca²⁺) to flow into the neuron. The sudden influx of calcium acts as a signal that triggers synaptic vesicles—which store neurotransmitters—to move toward and fuse with the presynaptic membrane. This process, called exocytosis, involves specialized proteins like SNAREs that help the vesicle and cell membrane come together. Once fused, the vesicles release their neurotransmitter contents into the synaptic cleft (the gap between two neurons). The neurotransmitters then diffuse across the cleft and bind to specific receptors on the postsynaptic membrane of the adjacent neuron. This binding either excites or inhibits the receiving neuron, depending on the type of neurotransmitter and receptor involved. After their action, neurotransmitters are typically removed from the cleft through reuptake into the presynaptic neuron, enzymatic breakdown, or diffusion away from the synapse, ensuring the signal is brief and precise.

Neurotransmitter Receptor:
Neurotransmitter receptors are specialized protein structures located on the postsynaptic membrane of neurons and other cell types. They mediate the physiological effects of neurotransmitters by initiating intracellular responses following ligand binding, thereby playing a pivotal role in synaptic transmission and the regulation of diverse neurobiological processes.
Ionotropic Receptors (ligand-gated ion channels) are fast-acting receptors that directly mediate the flow of ions across the neuronal membrane upon neurotransmitter binding. Activation of these receptors results in rapid changes in membrane potential, contributing to the immediate excitatory or inhibitory responses in the postsynaptic neuron. Prominent examples include the N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainate receptors for glutamate, as well as the receptor, which mediates inhibitory neurotransmission via chloride ion influx.
Metabotropic Receptors (G-protein-coupled receptors, GPCRs), in contrast, exert their effects through intracellular second messenger cascades. These receptors are involved in modulatory functions and often elicit slower but more prolonged changes in neuronal excitability and synaptic plasticity. Examples include dopamine receptors (D1–D5), serotonin receptors (e.g., 5-HT1A, 5-HT2A), muscarinic acetylcholine receptors, and GABAB receptors.
Neurotransmitter imbalances and diseases:
Disorder | Implicated Neurotransmitter(s) | Mechanism of Dysfunction |
Parkinson’s Disease | ↓ Dopamine | Nigrostriatal pathway degeneration |
Schizophrenia | ↑ Dopamine (mesolimbic), ↓ Glutamate | Dopaminergic hyperactivity; NMDA receptor hypofunction |
Major Depressive Disorder | ↓ Serotonin, ↓ Norepinephrine, ↓ Dopamine | Monoamine depletion hypothesis |
Anxiety Disorders | ↓ GABA, ↓ Serotonin | Reduced inhibition and impaired emotional regulation |
Alzheimer’s Disease | ↓ Acetylcholine | Loss of cholinergic neurons in the basal forebrain |
ADHD | ↓ Dopamine, ↓ Norepinephrine | Impaired prefrontal cortex signaling |
Epilepsy | ↓ GABA, ↑ Glutamate | Imbalance in excitatory/inhibitory tone |
Drugs affecting Neurotransmitters:
Drug Class | Target Neurotransmitter(s) | Mechanism of Action | Common Clinical Use |
Antidepressants (SSRIs, SNRIs, MAOIs, TCAs) | Serotonin, Norepinephrine, Dopamine | Block reuptake or degradation | Depression, anxiety, PTSD |
Antipsychotics (Typical, Atypical) | Dopamine (D2), Serotonin (5-HT2A) | Receptor antagonism | Schizophrenia, bipolar disorder |
Psychostimulants (e.g., Methylphenidate, Amphetamines) | Dopamine, Norepinephrine | Promote release or block reuptake | ADHD, narcolepsy |
Anxiolytics (Benzodiazepines) | GABA | GABA-A receptor agonists (positive allosteric modulators) | Anxiety, insomnia, seizures |
Antiepileptics | GABA, Glutamate | Enhance GABAergic inhibition or inhibit glutamate | Epilepsy |
References:
Kandel, E. R., Schwartz, J. H., Jessell, T. M., Siegelbaum, S. A., & Hudspeth, A. J.
Principles of Neural Science (5th ed.). McGraw-Hill Education, 2013.
– A foundational neuroscience textbook explaining neurotransmission and disorders.
Bear, M. F., Connors, B. W., & Paradiso, M. A.
Neuroscience: Exploring the Brain (4th ed.). Wolters Kluwer, 2015.
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Meyer, J. H., et al. (2006).
"Lower serotonin transporter binding potential in the human brain during major depressive episodes."
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– Demonstrates serotonin deficiency in depression using PET imaging.
Grace, A. A. (2016).
"Dopamine system dysregulation by the ventral subiculum as the common pathological mechanism in schizophrenia psychosis."
Schizophrenia Bulletin, 42(2), 247–254.
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