Neurotransmitter GABA

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A neuron, the fundamental unit of the nervous system, is structurally composed of a cell body, dendrites, and an axon. The cell body contains the nucleus and essential organelles. Dendrites, short and branched, receive signals from other neurons, while the axon, a long fiber, transmits signals away from the cell body.  

The nerve impulses are transmitted through neurons by two different mechanisms. From cell body along axons until it meets a synapse impulses are transmitted as an Action potential. At synapses that is converted into a Chemical gradient. These chemical molecules are called as “Neurotransmitters". Those can be Peptides, Amino acids or Monoamines. 

  • Amino Acids- Glutamate, GABA (Gamma-aminobutyric acid), Glycine 
  • Monoamines- Dopamine, Serotonin, Norepinephrine 
  • Peptides- Endorphins 


GABA (Gamma-aminobutyric acid) 

Basically, called as “The Hormone of Calmness”, 

GABA is the key inhibitory neurotransmitter of the brain. It reduces excitability of a neuron. It does this by binding to specific receptors, primarily GABA-A receptors, which then allow chloride ions to flow into the neuron. This influx of chloride ions hyperpolarizes the neuron, making it less likely to fire and transmit signals. Essentially, GABA acts as a brake on the nervous system, calming it down and preventing overexcitation.  

 It's secreted by GABAergic neurons in various brain regions. These include the amygdala, hippocampus, hypothalamus, prefrontal cortex, olfactory bulb, retina, and spinal cord. 

Here, we are going to discuss briefly the different relationships of GABA. 

 

GABA levels during sleep 

GABA levels are crucial for regulating sleep, and disruptions in GABA signaling can lead to sleep disorders like insomnia. Low GABA levels are associated with difficulty falling asleep, restless sleep, and decreased sleep quality. (Varinthra et al.) 

GABA in Depression 

 In fact, some studies suggest that GABA levels may be low or dysregulated in the brains of people with depression. Other research indicates that GABA levels can be elevated in certain brain regions after antidepressant treatment, potentially as a compensatory mechanism. (Lusher et al.) 

GABA levels in Meditation 

Meditation has been shown to increase GABA levels in the brain. GABA, a key inhibitory neurotransmitter, promotes calmness and reduces anxiety. 

Matt Dixon, a research scholar in Stanford’s psychology department, says meditation affects two main pathway changes in the brain. One is in the default mode network, the brain region involved in rumination and construction of thoughts about the past and future. (Hello, anxiety!) That network becomes less active in people who practice meditation. On the flip side, a part of the brain called the insula (responsible for body awareness, among other things) becomes more active in those who meditate, leading to increased awareness of their emotions and bodily sensations. “If you’re doing it right, you’re not thinking about yourself so much or judging yourself,” Dixon says. “You’re becoming more into the present moment.” 

GABA and Dopamine relationship 

GABA is the primary inhibitory neurotransmitter in the brain, and its activation in the ventral tegmental area (VTA), a brain region involved in dopamine production, leads to a suppression of dopamine neuron firing. However, it's important to note that the relationship is complex and can vary depending on the specific brain region and the context. Specifically, research has found that the release of VTA GABA significantly influences the activity of dopamine neurons. 

In mouse research, upon activation of GABA neurons in the VTA, a strong inhibitory effect was reported on the rate of firing in DA neurons.  In contrast, following GABA neuron inhibition, a disinhibition or increase of dopamine was witnessed. These findings indicate that firstly, GABA activation could be associated with dopamine suppression, and secondly, that GABA neurons in the VTA may have a direct connection with the synapses of local DA neurons. (Bennett) 

GABA relation to Melatonin 

The relationship between GABA and Melatonin is complicated. Melatonin, a hormone that regulates sleep-wake cycles, can enhance GABAergic transmission, suggesting a link between the two in promoting relaxation and sleep.  

The pineal hormone, melatonin, can exert sedative/hypnotic, anxiolytic and other neuropharmacological effects in experimental animals. There is evidence that flumazenil, a specific central-type BZ antagonist, can block some of these effects of melatonin. Therefore, it is thought that activation of central-type BZ receptors on the BZ-GABAA receptor complex, with consequent allosteric enhancement of GABAergic activity, is the primary mechanism underlying the neuropharmacological effects of melatonin. In addition, melatonin can interact with other BZ receptor subtypes to influence neurosteroidogenesis and cyclic AMP production, which can further modulate GABAergic activity in the CNS. (Niles) 

 

GABA relation with Exercise  

Research shows GABA production in your brain increases after an 8-20 minutes sessions of vigorous exercise. You can alternate vigorous exercise with moderate exercise to make it more doable. Specifically, intense exercise has been shown to increase both glutamate and GABA levels in the visual cortex. Furthermore, exercise can help restore GABA receptor function in key brain regions, like the paraventricular hypothalamic nucleus, which is involved in regulating the sympathetic nervous system.  (Novak et al.) 

GABA relation to Alcohol 

Alcohol increases GABA action, particularly on GABA-A receptors, leading to initial sedation and relaxation. This effect is mediated by alcohol binding to these receptors and enhancing their sensitivity to GABA, according to Ardu Recovery Center.  

 

References 

  1. Varinthra, Peeraporn, et al. “The Role of the GABAergic System on Insomnia.” Tzu Chi Medical Journal, vol. 36, no. 2, 1 June 2024, p. 103, journals.lww.com/tcmj/fulltext/2024/36020/the_role_of_the_gabaergic_system_on_insomnia.1.aspx, https://doi.org/10.4103/tcmj.tcmj_243_23. 

 

  1. Luscher, B, et al. “The GABAergic Deficit Hypothesis of Major Depressive Disorder.” Molecular Psychiatry, vol. 16, no. 4, 16 Nov. 2010, pp. 383–406, www.ncbi.nlm.nih.gov/pmc/articles/PMC3412149/, https://doi.org/10.1038/mp.2010.120. 

 

  1. magazine, STANFORD. “What Happens When You Meditate.” Stanfordmag.org, 13 Mar. 2023, stanfordmag.org/contents/what-happens-when-you-meditate. 

 

  1. Bennett, Chloe. “GABA Activation and Dopamine Suppression.” News-Medical.net, 18 July 2019, www.news-medical.net/health/GABA-Activation-and-Dopamine-Suppression.aspx. 

 

 

  1. Niles, Lennard P. “Melatonin Interaction with BZ-GabaA Receptors.” Springer EBooks, 1 Jan. 2006, pp. 95–99, link.springer.com/chapter/10.1007/0-387-27682-3_8, https://doi.org/10.1007/0-387-27682-3_8. Accessed 2 May 2025. 

 

  1. Novak, Tom S, et al. “GABA, Aging and Exercise: Functional and Intervention Considerations.” Neuroscience Insights, vol. 19, 1 Jan. 2024, pmc.ncbi.nlm.nih.gov/articles/PMC11457286/#fig1-26331055241285880, https://doi.org/10.1177/26331055241285880. Accessed 26 Mar. 2025. 

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