Margaux M. Tolley
MSc (Neuroscience), PgDipSci (Neuroscience), BSc (Neuroscience)
There are hundreds of different neurotransmitters within the nervous system, each serving an important and distinct role. Some neurotransmitters have various functions which differ depending on where they are released, synthesized, and the pattern of their release.
Some of the neurotransmitters we discuss today are:
- Acetylcholine
- Dopamine
- Adrenaline (Epinephrine)
- Noradrenaline (Norepinephrine)
- Endorphin
- Glutamate
- Serotonin
- GABA
- Oxytocin
The following are brief introductions to common and well-known examples of neurotransmitters within the central nervous system.
Acetylcholine
Acetylcholine was the first neurotransmitter demonstrating chemical transmission within the central nervous system. Acetylcholine is generated from the precursor molecules, choline and acetyl-coA.
After binding to receptors, acetylcholine is broken down by the enzyme acetylcholinesterase back into choline and acetate. The choline is then taken back up and used to generate more acetylcholine within the cell.
Acetylcholine is an excitatory neurotransmitter which has numerous physiological roles within the body, most notably at the neuromuscular junction, where a neuron binds to a muscle cell.
Release of acetylcholine at the neuromuscular junction results in activation and contraction of the muscle.
Dopamine
Dopamine can be both a hormone and a neurotransmitter. As a neurotransmitter, dopamine is classed as a catecholamine under the monoamine neurotransmitter.
Dopamine is generated from the essential amino acid tyrosine and released from dopaminergic neurons located predominantly within the midbrain, in regions called the ventral tegmental area and the substantia nigra.
Dopaminergic projections are few in number but have powerful roles on four major pathways in the central nervous system: the mesolimbic pathway, nigrostriatal pathway, mesocortical pathway, and tuberoinfundibular pathway.[1]
These projections mean dopamine plays a role in
- motivation
- executive function
- behaviour
- motor function
Dopamine plays a key role in mood and motivation
Dopamine dysfunction is implicated in addiction disorders, Parkinson’s disease, mania and much more. Dopamine is also a precursor for norepinephrine (noradrenaline) and epinephrine (adrenaline).[2]
Adrenaline (Epinephrine)
Adrenaline is a monoamine neurotransmitter. It is an excitatory catecholamine involved in arousal levels and panic.
Adrenaline is associated with the sympathetic nervous system, better known for its role in the “fight-or-flight” response. The sympathetic nervous system ramps the body into action in stressful situations to promote survival.
Upon detection of perceived danger, adrenaline is released from neurons in the brainstem. Adrenaline binds locally to adrenergic receptors on postsynaptic neurons in the brainstem, amygdala, hypothalamus, prefrontal cortex, cerebellum and hippocampus.[3,4,5]
The combined effect of binding to these regions promotes
- alertness
- memory consolidation, and
- primes the body to move
Noradrenaline (Norepinephrine)
Noradrenaline is also a catecholamine neurotransmitter. Noradrenaline is primarily produced from the locus coeruleus in the brainstem and projects to numerous regions including the hippocampus, thalamus, amygdala, regions of the spinal cord and the cerebellum.[5,6]
Noradrenaline acts as a neuromodulator, also released upon sympathetic nervous system activity. Working with adrenaline, noradrenaline alters states of alertness and memory consolidation, especially emotional memories.
Noradrenaline is the precursor of adrenaline
Noradrenaline is also the precursor of adrenaline, implicating noradrenaline in the generation, activation, and effectiveness of adrenaline. Dysfunction of noradrenergic signaling has been linked to disorders such as PTSD, anxiety, depression and ADHD.
Endorphin
Endorphins can act as both neurotransmitters and hormones. As a neurotransmitter, they are neuropeptides and a part of the endogenous opioid system. There are three main types of endorphins. These are
- alpha-endorphin
- beta-endorphin
- gamma-endorphin
Endorphins are associated with easing pain and feeling good
Endorphin release is associated with easing pain and feeling good. The analgesic effects of endorphin release have been shown to be greater than morphine.
Among the three endorphins, beta-endorphins are the most understood. In response to pain or stressful situations, such as exercise, beta-endorphins are released and bind to opioid receptors which lower neuronal excitability resulting in analgesic effects.[7]
Glutamate
Glutamate is the primary excitatory neurotransmitter within the central nervous system. It is an amino acid neurotransmitter derived from glutamine supplied by surrounding cells and has roles in memory and long-term learning.
Glutamate has an important role in memory and long-term learning
Once released into the synapse and bound to the post-synaptic neuron, glutamate is taken up by the surrounding cells, converted into glutamine, which is then delivered back to the pre-synaptic neuron to generate more glutamate. Aberrant glutamate dysfunction has been implicated in many psychiatric disorders such as
RELATED — Introduction to: Depression
Glutamine is released from surrounding glial cells to the presynaptic neuron. Glutamine is then converted to glutamate which is stored in vesicles and the nerve ending. When the neuron is activated, glutamate is released and binds to receptors on the postsynaptic neuron.
Glutamate is either then taken up by the glial cells and broken back down into glutamine or taken and stored by the presynaptic neuron directly.[11]
Serotonin
Serotonin is another monoaminergic neurotransmitter. It gained popularity for its role in psychiatric disorders like depression and is also one of the main targets for antidepressants, like SSRIs.
Within the central nervous system, serotonin is generated by serotonergic neurons from the raphé nuclei located within the brain stem. Serotonin is generated from the essential amino acid tryptophan.
These neurons project to nearly every region of the brain, implicating serotonin in many cognitive functions like
- cognition
- mood
- appetite
- sleep
GABA
Gamma-aminobutyric acid, known as GABA, is an amino acid neurotransmitter. It is the primary inhibitory neurotransmitter demonstrated in the central nervous system in the 1950s.
There are three receptors in the central nervous system that bind GABA. These are
- GABA-A – densely expressed in the limbic system and rapidly inhibits the neuron by allowing chloride ions to enter the cell.[12]
- GABA-B – prevents calcium channels from opening and activating potassium channels, resulting in prolonged inhibition.[13]
- GABA-C – activation results in rapid, long-lasting inhibitory signals largely in the retina and all over the central nervous system.[14]
All receptors, after binding GABA, lower the likelihood of a neuron firing an action potential, slowing certain brain functions.
GABA is synthesized through decarboxylation of the excitatory neurotransmitter, glutamate, and stored at the end of the neuron, waiting to be signaled for release.
Imbalance of GABA functioning has been associated with schizophrenia, epilepsy, anxiety, and autism.
Oxytocin
Oxytocin, known as the “love hormone”, acts both as a hormone and a neurotransmitter. Oxytocin as a neurotransmitter is a neuropeptide and is implicated in:
- emotional
- social, and
- numerous cognitive processes
It is produced in the hypothalamus and binds to the oxytocin receptor which is widely expressed throughout the brain.
Oxytocin is a hormone involved in social bonding, reproduction and childbirth
The oxytocin receptor is densely expressed in the amygdala (which largely regulates fear recognition and response) reward centres like the ventral tegmental region and the nucleus accumbens, and the septum and the hypothalamus which integrates both social and stressful information.
There are numerous other regions that densely express the receptor and the density can change throughout our lifespan as we grow, learn, and have experiences.
Related Questions
1. How do I increase dopamine levels?
Eat foods rich in phenylalanine or tyrosine and exercise, specifically aerobic and resistance exercise, and try including rewarding activities, like listening to music.
2. What happens if noradrenaline is too high?
Noradrenergic neurons have wide connectivity throughout the brain, therefore excess noradrenaline can have major impacts.
Excess noradrenaline can cause anxiety symptoms, make us more agitated, increase distractability and cause insomnia.
3. What causes a lack of endorphins?
Sedentary behaviour, chronic stress, sleep deprivation, poor nutrition, or repeated intake of addictive substances like alcohol or opioids can all lead to reduced endorphin activity (synthesis, release, and signaling).
4. Does glutamate cause anxiety?
Numerous neurotransmitters are involved in anxiety, including excessive glutaminergic signaling.
Receptors are present throughout the brain, especially in the limbic system, specifically the amygdala, which is involved in our fear response.[17]
5. What causes a lack of serotonin?
Not ingesting enough tryptophan or having low levels of vitamin B6, which has a role in synthesis or serotonin, can result in diminished serotonin stores in the brain.
RELATED — Vitamin B6 (Pyridoxine)
6. What triggers the release of oxytocin?
Social interactions, including eye contact and physical touch, trigger release of oxytocin from limbic regions.
Other neurotransmitters, like noradrenaline or serotonin, modulate the release of oxytocin.
Margaux is a neuroscientist with a strong academic background and hands-on experience in research, specializing in muscle physiology, electrophoresis, and protein analysis. Her Master’s research focused on identifying key protein…
If you would like to learn more about Margaux, see Expert: Margaux M. Tolley.
References
(1) Costa, K. M., & Schoenbaum, G. (2022). Dopamine. Current Biology, 32(15), R817–R824.
(2) Khalil, B., Warrington, S. J., & Rosani, A. (2024, December 11). Physiology, Catecholamines.
(3) Stanford, S. C. (2013). Adrenaline and Noradrenaline: Introduction. In ELS, John Wiley & Sons, Ltd (Ed.).
(4) Shun Shimohama, Taniguchi, T., Fujiwara, M., & Masakuni Kameyama. (1986). Biochemical Characterization of α‐Adrenergic Receptors in Human Brain and Changes in Alzheimer‐Type Dementia. Journal of Neurochemistry, 47(4), 1294–1301.
(5) Perez, D. M. (2020). α1-Adrenergic Receptors in Neurotransmission, Synaptic Plasticity, and Cognition. Frontiers in Pharmacology, 11(581098).
(6) Arikuni, T., & Ban, T. (1978). Subcortical afferents to the prefrontal cortex in rabbits. Experimental Brain Research, 32(1).
(7) Pilozzi, A., Carro, C., & Huang, X. (2020). Roles of β-Endorphin in Stress, Behavior, Neuroinflammation, and Brain Energy Metabolism. International Journal of Molecular Sciences. https://www.mdpi.com/1422-0067/22/1/338
(8) Kruse, A. O., & Bustillo, J. R. (2022). Glutamatergic dysfunction in Schizophrenia. Translational Psychiatry, 12(1), 500. https://www.nature.com/articles/s41398-022-02253-w
(9) Lewerenz, J., & Maher, P. (2015). Chronic Glutamate Toxicity in Neurodegenerative Diseases—What is the Evidence? Frontiers in Neuroscience, 9. https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2015.00469/full
(10) Onaolapo, A. Y., & Onaolapo, O. J. (2021). Glutamate and depression: Reflecting a deepening knowledge of the gut and brain effects of a ubiquitous molecule. World Journal of Psychiatry, 11(7), 297–315.
(11) BioRender. (2025). Glutamate Synthesis and Cycling. https://app.biorender.com/biorender-templates/details/t-610aa2478308f200a1d89c57-glutamate-synthesis-and-cycling
(12) Sigel, E., & Steinmann, M. E. (2012). Structure, Function, and Modulation of GABAAReceptors. Journal of Biological Chemistry.
(13) Pirri, F., & McCormick, C. M. (2025). Oxytocin receptors within the caudal lateral septum regulate social approach-avoidance, long-term social discrimination, and anxiety-like behaviors in adult male and female rats. Neuropharmacology, 271, 110409.
(14) Zhang, D., Pan, Z.-H., Awobuluyi, M., & Lipton, S. A. (2001). Structure and function of GABAC receptors: a comparison of native versus recombinant receptors. Trends in Pharmacological Sciences.
(15) Foley, T. E., & Fleshner, M. (2008). Neuroplasticity of Dopamine Circuits After Exercise: Implications for Central Fatigue. NeuroMolecular Medicine.
(16) Salimpoor, V. N., Benovoy, M., Larcher, K., Dagher, A., & Zatorre, R. J. (2011). Anatomically distinct dopamine release during anticipation and experience of peak emotion to music. Nature Neuroscience.
(17) Krystal, J. H., D’Souza, D. C., Petrakis, I. L., Belger, A., Berman, R. M., Charney, D. S., Abi-Saab, W., Madonick, S. (1999). NMDA agonists and antagonists as probes of glutamatergic dysfunction and pharmacotherapies in neuropsychiatric disorders. Harvard Review of Psychiatry.
