GABA reuptake inhibitor explained

See main article: Reuptake inhibitor. A GABA reuptake inhibitor (GRI) is a type of drug which acts as a reuptake inhibitor for the neurotransmitter gamma-Aminobutyric acid (GABA) by blocking the action of the gamma-Aminobutyric acid transporters (GATs). This in turn leads to increased extracellular concentrations of GABA and therefore an increase in GABAergic neurotransmission.[1] Gamma-aminobutyric acid (GABA) is an amino acid that functions as the predominant inhibitory neurotransmitter within the central nervous system, playing a crucial role in modulating neuronal activity in both the brain and spinal cord. While GABA predominantly exerts inhibitory actions in the adult brain, it has an excitatory role during developmental stages. When the neuron receives the action potential, GABA is released from the pre-synaptic cell to the synaptic cleft. After the action potential transmission, GABA is detected on the dendritic side, where specific receptors collectively contribute to the inhibitory outcome by facilitating GABA transmitter uptake. Facilitated by specific enzymes, GABA binds to post-synaptic receptors, with GABAergic neurons playing a key role in system regulation.[2] The inhibitory effects of GABA diminish when presynaptic neurons reabsorb it from the synaptic cleft for recycling by GABA transporters (GATs). The reuptake mechanism is crucial for maintaining neurotransmitter levels and synaptic functioning.[3] Gamma-aminobutyric acid Reuptake Inhibitors (GRIs) hinder the functioning of GATs, preventing GABA reabsorption in the pre-synaptic cell. This results in increased GABA levels in the extracellular environment, leading to elevated GABA-mediated synaptic activity in the brain.[4] [5]

Gamma-aminobutyric acid (GABA), the brain's main inhibitory neurotransmitter, plays a crucial role in regulating neuronal activity by dampening down neuron firing. Disruptions in GABAergic neurotransmission, such as reduced synthesis, reuptake dysfunction, or receptor abnormalities, can lead to various pathologies in the central nervous system, including epilepsy, anxiety disorders, Parkinson's disease, and sleep disorders.[6] [7] [8] The inhibitory neurotransmitter GABA plays a complex role in modulating anxiety and stress, regulating sleep, circadian rhythms, mood, cognition, and perception. Low GABA levels are associated with emotional and behavioral disruptions, including short-term and/or long-term stress, anxiety disorders, and sleep disorders.[9]

Indications

GRIs may be used in the clinical treatment of seizures, convulsions, or epilepsy as anticonvulsants/antiepileptics, depression,[10] anxiety disorders[8] such as generalized anxiety disorder (GAD), social phobia (SP) also known as social anxiety disorder (SAD), and panic disorder (PD) as anxiolytics, insomnia as hypnotics, muscle tremors or spasms as muscle relaxants, and chronic pain as analgesics. They may also potentially be used as anesthetics in surgery.

Effects

GRIs can induce a wide range of psychological and physiological effects, including:

Many of these properties are dependent on whether the GRI in question is capable of crossing the blood-brain-barrier (BBB). Those that do not will only produce peripheral effects.

GRIs such as CI-966 have been characterized as hallucinogens with effects analogous to those of the GABAA receptor agonist muscimol (a constituent of Amanita muscaria (fly agaric) mushrooms) when administered at sufficient doses.[11]

Tiagabine is another GRI that selectively inhibits the action of GABA reuptake and its mechanism of action is the same as selective serotonin reuptake inhibitor (SSRI).[8] It is used as a treatment for partial seizures in adults and children over 12, and works by amplifying GABA's calming effects in the brain. This, however, comes with potential drawbacks. While generally well-tolerated, some users experience concentration issues, language difficulties, and even a higher risk of depression, hallucinations, and paranoia.[12]

Overdose

At very high doses characterized by overdose, a number of symptoms may come to prominence, including:

List of GRIs

See also

References

Notes and References

  1. Bauer . Jürgen . Cooper-Mahkorn . Déirdre . 2008-08-08 . Tiagabine: efficacy and safety in partial seizures  - current status . Neuropsychiatric Disease and Treatment . English . 4 . 4 . 731–736 . 10.2147/NDT.S833 . free . 2536540 . 19043517.
  2. Gottlieb . David I. . 1988 . GABAergic Neurons . Scientific American . 258 . 2 . 82–89 . 10.1038/scientificamerican0288-82 . 24988982 . 2847312 . 1988SciAm.258b..82G . 0036-8733.
  3. Salters-Pedneault, K. (2023, June 13). How selective serotonin reuptake inhibitors (ssris) works. Verywell Mind.
  4. Zafar . Sadia . Jabeen . Ishrat . 2018 . Structure, Function, and Modulation of γ-Aminobutyric Acid Transporter 1 (GAT1) in Neurological Disorders: A Pharmacoinformatic Prospective . Frontiers in Chemistry . 6 . 397 . 10.3389/fchem.2018.00397 . free . 2296-2646 . 6141625 . 30255012. 2018FrCh....6..397Z .
  5. Niessen . W. M. A. . 2020-10-01 . Interpretation of tandem mass spectra of antiepileptic drugs using accurate-m/z data and m/z-shifts with stable-isotope labeled analogues . International Journal of Mass Spectrometry . 456 . 116409 . 10.1016/j.ijms.2020.116409 . 2020IJMSp.456k6409N . 224856466 . 1387-3806.
  6. Perucca . Emilio . Bialer . Meir . White . H. Steve . 2023-09-01 . New GABA-Targeting Therapies for the Treatment of Seizures and Epilepsy: I. Role of GABA as a Modulator of Seizure Activity and Recently Approved Medications Acting on the GABA System . CNS Drugs . en . 37 . 9 . 755–779 . 10.1007/s40263-023-01027-2 . 1179-1934 . 10501955 . 37603262.
  7. Motiwala . Zenia . Aduri . Nanda Gowtham . Shaye . Hamidreza . Han . Gye Won . Lam . Jordy Homing . Katritch . Vsevolod . Cherezov . Vadim . Gati . Cornelius . 2022. Structural basis of GABA reuptake inhibition . Nature . en . 606 . 7915 . 820–826 . 10.1038/s41586-022-04814-x . 1476-4687 . 9394549 . 35676483. 2022Natur.606..820M .
  8. Loughlin, K. R., Generali, J. A. (2006). The Guide to Off-label Prescription Drugs: New Uses for FDA-approved Prescription Drugs. United Kingdom: Free Press.
  9. Hepsomali . Piril . Groeger . John A. . Nishihira . Jun . Scholey . Andrew . 2020 . Effects of Oral Gamma-Aminobutyric Acid (GABA) Administration on Stress and Sleep in Humans: A Systematic Review . Frontiers in Neuroscience . 14 . 923 . 10.3389/fnins.2020.00923 . free . 1662-453X . 7527439 . 33041752.
  10. Zanoli . Paola . 2004. Role of Hyperforin in the Pharmacological Activities of St. John's Wort . CNS Drug Reviews . en . 10 . 3 . 203–218 . 10.1111/j.1527-3458.2004.tb00022.x . 1080-563X . 6741737 . 15492771.
  11. Hollister. Leo E.. New class of hallucinogens: GABA-enhancing agents. Drug Development Research. 21. 3. 1990. 253–256. 0272-4391. 10.1002/ddr.430210311. 143868762 .
  12. Cavanna, A. E., Ali, F., Rickards, H. E., & McCorry, D. (2010). Behavioral and cognitive effects of anti-epileptic drugs. Discovery medicine, 9(45), 138–144.
  13. 10.1016/0922-4106(94)90089-2 . Borden LA, Murali Dhar TG, Smith KE, Weinshank RL, Branchek TA, Gluchowski C . Tiagabine, SK&F 89976-A, CI-966, and NNC-711 are selective for the cloned GABA transporter GAT-1. . Eur J Pharmacol . 269 . 2 . 219–224 . 1994 . 7851497 .
  14. Wonnemann. M. Singer. A. Müller. WE. 10882845. Inhibition of Synaptosomal Uptake of 3H-L-glutamate and 3H-GABA by Hyperforin, a Major Constituent of St. John's Wort The Role of Amiloride Sensitive Sodium Conductive Pathways. Neuropsychopharmacology. August 2000. 23. 2. 188–197. 10.1016/S0893-133X(00)00102-0. free.