General Information: Because gamma-aminobutyric acid (GABA) is a neurotransmitter widely distributed in the brain, the role of which is to inhibit or reduce the excitement and activity of the neurons (nerve cells) to which it binds to in the brain by regulating communication between them.1
What is a neurotransmitter? The nervous system is composed of specialized, individual cells; neurons.
These cells function as the body's wiring, with nerve signals (electrical impulses) that are being transmitted through the length of the neuron. Once a nerve signal reaches the end of a neuron, it is able to jump over to the next neuron by using various chemical messengers. These chemical messengers are called neurotransmitters.2
In the body’s central nervous system (CNS), which is composed of the brain and spinal cord, the neurotransmitters travel from neuron to neuron.3 But, in the peripheral nervous system, which is composed of the nerves that extend from the central nervous system to the rest of the body; the chemical signals must pass between a neuron and a nearby muscle or gland cell.45
GABA is one of the most abundant neurotransmitters in the entire central nervous system and is especially abundant in the cerebral cortex, where thoughts are generated, and sensory data are interpreted.6
At the end of each neuron, neurotransmitters are stored in small sacs (storage vesicles). When a nerve impulse reaches the end of a cell - it triggers these sacs to release neurotransmitters into the spaces that separate one neuron from another.7 These gaps are called synapses. The various neurotransmitters migrate across the synapse, and when they reach a neighboring neuron, they fit into specialized receptor sites the same way that a key will fit into a lock.8
When sufficient neurotransmitter chemicals attach to a receptor site, the neuron will ‘fire,’ transmitting an electrical impulse down its length to repeat the process at the next synapse.
What is GABA used for? GABA plays a critical role in:
GABA is synthesized in the body from Glutamate, an excitatory neurotransmitter that is essential for healthy brain function. Essentially, GABA counterbalances the level of excitement in neurons caused by excitatory neurotransmitters (like Glutamate), helping to prevent becoming too anxious or over-stimulated.912
GABA’s numerous benefits originate from this effect; ranging from improved mood, ability to focus, increased relaxation, and helping to reduce perceived stress levels.
Recently conducted research suggests that GABA can significantly help to control the fear and anxiety that may occur when neurons become overexcited.13
Certain scientific studies have also shown that lower than normal levels of GABA in the human brain may be linked to depression, anxiety, sleep disorders, and schizophrenia, among many other symptoms.14
Who shouldn’t take this supplement? GABA should not be taken by people with bipolar or unipolar depressive disorders.15 GABA can also cause drowsiness, so you shouldn’t drive or operate heavy machinery after taking GABA.12
What are the precautions when taking this medicine? You should also exercise caution if taking GABA with any drug that may affect the GABA pathway in the brain. Drugs that that may affect the GABA pathway include,19 but are certainly not limited to:
- Benzodiazepines (like Xanax and Valium)
Pregnant or lactating women, children, and people who suffer from liver or kidney disease should not take GABA due to an absence of research into the potential side effects in these groups.
What are some possible side effects of this medicine? While GABA is a safe and natural substance, users may still experience side effects.
Common side effects can include; a sore throat, throat burning, a skin burning sensation, headache, and dizziness.20 Patients may experience some irritation at the injection site.
Storage: Store this medication at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond use date. Do not flush unused medications or pour down a sink or drain.
- 1. GABA and Glutamate in the Human Brain. Ognen A. C. Petroff. The Neuroscientist Vol 8, Issue 6, pp. 562 – 573. First published date: June-29-2016
- 2. Cold Spring Harb Perspect Biol. 2011 Jun 1;3(6). pii: a001727. doi: 0.1101/cshperspect.a001727. Mechanisms and molecules of neuronal wiring: a primer. Kolodkin AL1, Tessier-Lavigne M.
- 3. https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0024269/
- 4. https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0024269/
- 5. Lodish H, Berk A, Zipursky SL, et al. Molecular Cell Biology. 4th edition. New York: W. H. Freeman; 2000. Section 21.4, Neurotransmitters, Synapses, and Impulse Transmission.
- 6. Y. ZhouN. C. Danbolt. Journal of Neural Transmission. August 2014, Volume 121, Issue 8, pp 799–817
- 7. Principles of Psychopharmacology for Mental Health Professionals By Jeffrey E. Kelsey, Charles B. Nemeroff, D. Jeffrey Newport. Pages 16-17.
- 8. The Molecular Basis of Communication between Cells. Solomon H. Snyder. Scientific American Vol. 253, No. 4 (October 1985), pp. 132-141.
- 9. Bravo-Rivera, Christian et al. “Long-Range GABAergic Neurons in the Prefrontal Cortex Modulate Behavior.” Journal of Neurophysiology 114.3 (2015): 1357–1359. PMC. Web. 11 Sept. 2017.
- 10. PONTES, Adalto, Yonggang ZHANG, and Wenhui HU. “Novel Functions of GABA Signaling in Adult Neurogenesis.” Frontiers in biology 8.5 (2013): 10.1007/s11515–013–1270–2. PMC. Web. 11 Sept. 2017.
- 11. Smith, Sean M., and Wylie W. Vale. “The Role of the Hypothalamic-Pituitary-Adrenal Axis in Neuroendocrine Responses to Stress.” Dialogues in Clinical Neuroscience 8.4 (2006): 383–395. Print.
- 12. J.C.Reub. Comparative study of the release of glutamate and GABA, newly synthesized from glutamine, in various regions of the central nervous system. Neuroscience, Volume 5, Issue 12, December 1980, Pages 2145-2150
- 13. Lakhan, Shaheen E, and Karen F Vieira. “Nutritional and Herbal Supplements for Anxiety and Anxiety-Related Disorders: Systematic Review.” Nutrition Journal 9 (2010): 42. PMC. Web. 11 Sept. 2017.
- 14. Martin, Elizabeth I. et al. “The Neurobiology of Anxiety Disorders: Brain Imaging, Genetics, and Psychoneuroendocrinology.” The Psychiatric clinics of North America 32.3 (2009): 549–575. PMC. Web. 11 Sept. 2017.
- 15. Cuellar, Amy K., Sheri L. Johnson, and Ray Winters. “Distinctions between Bipolar and Unipolar Depression.” Clinical psychology review 25.3 (2005): 307–339. PMC. Web. 11 Sept. 2017.
- 16. Dagli AI, Mueller J, Williams CA. Angelman Syndrome. 1998 Sep 15 [Updated 2015 May 14]. In: Pagon RA, Adam MP, Ardinger HH, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2017.
- 17. Jones EA, Weissenborn K. Neurology and the liver. Journal of Neurology, Neurosurgery & Psychiatry 1997;63:279-293.
- 18. neuro.psychiatryonline.org/doi/pdf/10.1176/jnp.9.1.75
- 19. Linnoila M. Benzodiazepines and alcohol. J Psychiatr Res. 1990;24 Suppl 2:121-7.
- 20. Li, Junfeng et al. “Study of GABA in Healthy Volunteers: Pharmacokinetics and Pharmacodynamics.” Frontiers in Pharmacology 6 (2015): 260. PMC. Web. 11 Sept. 2017.