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Mood & Behavior Support contains the supplement GABA (gamma-amino-butyric acid), which is an amino acid that functions as a major neurotransmitter in the brain and functions as an inhibitory neurotransmitter – meaning that it blocks nerve impulses.  

Neurotransmitters can either stimulate the brain or inhibit, and a proper balance must be maintained.  GABA assists in the inhibition process, meaning that it works to reduce restlessness, irritability, and insomnia, and to induce calmness and sleep.

GABA is concentrated in the hypo-thalamus region of the brain and is known to play a role in the overall functioning of the pituitary gland – which regulates growth hormone synthesis, sleep cycles, and body temperature.

In a study conducted at Yale University, patients suffering from depression were noted as having decreased levels of GABA.  In patients with schizophrenia, GABA supplementation resulted in increased cognitive ability and memory.  These signs indicate that for people suffering from mild psychological or cognitive disorders, GABA supplements may be beneficial.

Furthermore, serious illnesses such as Parkinson’s disease and Alzheimer’s disease are being linked with GABA depletion.  Maintaining sufficient levels of GABA in the brain may play a role in reducing the risk of acquiring these conditions.

 

(See Research Citations on GABA)

 

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REFERENCES:

Ebert MH, Schmidt DE, Thompson T et al: Elevated plasma gamma-aminobutyric acid (GABA) levels in individuals with either Prader-Willi syndrome or Angelman syndrome. J Neuropsychiatry Clin Neurosci 1997 Winter; 9(1):75-80.

Levy LJ & Losowsky MS: Plasma gamma aminobutyric acid concentrations provide evidence of different mechanisms in the pathogenesis of hepatic encephalopathy in acute and chronic liver disease.  hepatogastroenterology 1989 Dec; 36(6):494-498.

Plantey F. GHB and GABA. Am J Psychiatry. 1977 Sep;134(9):1045-6.

Prosser J, Hughes CW, Sheikha S et al: Plasma GABA in children and adolescents with mood, behavior, and comorbid mood and behavior disorders: a preliminary study. J Child Adolesc Psychopharmacol 1997; 7(3):181-199.

 

 

National Institutes of Health:

Cortical gamma-aminobutyric acid concentrations in depressed patients receiving cognitive behavioral therapy.

Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut, USA. gerard.sanacora@yale.edu

BACKGROUND: Reduced gamma-aminobutyric acid (GABA) concentrations have been reported in plasma, cerebrospinal fluid, and cortex of depressed subjects. Treatment with both electroconvulsive therapy (ECT) and selective serotonin reuptake inhibitors (SSRI) increased occipital cortex GABA concentrations in prior studies. The purpose of this study was to determine whether treatment of major depression with cognitive behavioral therapy (CBT) produces similar changes in cortical GABA concentrations. METHODS: Occipital cortex GABA concentrations were measured in eight subjects with Major Depressive Disorder prior to and after a course of CBT using proton magnetic resonance spectroscopy. RESULTS: The effect of CBT on occipital cortex GABA content was different than that seen for ECT and SSRI medication treatment of depressed patients. CONCLUSIONS: This preliminary finding suggests CBT has a less robust effect on cortical GABA content than ECT and SSRI treatments and might indicate a difference between the mechanisms of antidepressant action.

 

“Effects of  -Aminobutyric Acid–Modulating Drugs on Working Memory and Brain Function in Patients With Schizophrenia”

Lara Menzies, BA; Cinly Ooi, PhD; Shri Kamath, MB; John Suckling, PhD; Peter McKenna, MD; Paul Fletcher, MB; Ed Bullmore, MB, PhD; Caroline Stephenson, MB, PhD Arch Gen Psychiatry. 2007;64:156-167.

CONTEXT  Cognitive impairment causes morbidity in schizophrenia and could be due to abnormalities of cortical interneurons using the inhibitory neurotransmitter  -aminobutyric acid (GABA).

OBJECTIVES  To test the predictions that cognitive and brain functional responses to GABA-modulating drugs are correlated and abnormal in schizophrenia.

DESIGN  Pharmacological functional magnetic resonance imaging study of 2 groups, each undergoing scanning 3 times, using an N-back working memory task, after placebo, lorazepam, or flumazenil administration.

SETTING AND PARTICIPANTS  Eleven patients with chronic schizophrenia were recruited from a rehabilitation service, and 11 healthy volunteers matched for age, sex, and premorbid IQ were recruited from the local community.

INTERVENTION  Participants received 2 mg of oral lorazepam, a 0.9-mg intravenous flumazenil bolus followed by a flumazenil infusion of 0.0102 mg/min, or oral and intravenous placebo.

MAIN OUTCOME Measures  Working memory performance was summarized by the target discrimination index at several levels of difficulty. Increasing (or decreasing) brain functional activation in response to increasing task difficulty was summarized by the positive (or negative) load response.

RESULTS  Lorazepam impaired performance and flumazenil enhanced it; these cognitive effects were more salient in schizophrenic patients. Functional magnetic resonance imaging demonstrated positive load response in a frontoparietal system and negative load response in the temporal and posterior cingulate regions; activation of the frontoparietal cortex was positively correlated with deactivation of the temporocingulate cortex. After placebo administration, schizophrenic patients had abnormally attenuated activation of the frontoparietal cortex and deactivation of the temporocingulate cortex; this pattern was mimicked in healthy volunteers and exacerbated in schizophrenic patients by lorazepam. However, in schizophrenic patients, flumazenil enhanced deactivation of the temporocingulate and activation of the anterior cingulate cortices.

CONCLUSIONS  The GABA-modulating drugs differentially affect working memory performance and brain function in schizophrenia. Cognitive impairment in schizophrenia may reflect abnormal inhibitory function and could be treated by drugs targeting GABA neurotransmission.

AUTHOR AFFILIATIONS: Brain Mapping Unit, Department of Psychiatry, University of Cambridge, Addenbrooke's Hospital, Cambridge, England (Ms Menzies and Drs Ooi, Kamath, Suckling, Fletcher, Bullmore, and Stephenson); Cambridgeshire and Peterborough Mental Health Partnership National Health Service Trust, Huntingdon, England (Drs McKenna and Bullmore); and GlaxoSmithKline, Cambridge (Dr Bullmore).

 

“Enhancement of neuroprotection of mulberry leaves (Morus alba L.) prepared by the anaerobic treatment against ischemic damage.”

Kang,-T-H; Oh,-H-R; Jung,-S-M; Ryu,-J-H; Park,-M-W; Park,-Y-K; Kim,-S-Y Citation: Biol-Pharm-Bull. 2006 Feb; 29(2): 270-4

Abstract: Several neurological disorders such as Alzheimer's and Parkinson's diseases have been attributed to gamma-aminobutyric acid (GABA) depletion in the brain. In order to provide a pharmacological basis for the neuroprotective actions of the enhanced accumulation of GABA in mulberry leaves (ML) against cerebral ischemia in vitro and in vivo, a process was developed to enhance the accumulation of GABA in mulberry leaves (GAML) as a result of the various anaerobic treatments. The GABA concentrations were changed by N(2) gas purging, the reaction temperature, reaction time, pH and the leaf size. GABA enhanced the potential of neuroprotection in the PC12 cells damaged by H(2)O(2)-induced oxidation. GAML reduced the cytotoxicity in the PC12 cells against oxygen glucose deprivation-induced cerebral ischemic condition. The neuroprotective effect of GAML was further demonstrated in vivo using middle cerebral artery occlusion brain injury model. GAML significantly decreased the infarct volume of the brain compared with than control group. Overall, these results suggest that the anaerobic treatment of ML makes GAML enhance the neuroprotection effect against in vivo cerebral ischemia such as in vitro.

“GABA(A) receptor channel pharmacology.”

Johnston,-G-A Citation: Curr-Pharm-Des. 2005; 11(15): 1867-85

Abstract: GABA(A) receptor channels are ubiquitous in the mammalian central nervous system mediating fast inhibitory neurotransmission by becoming permeant to chloride ions in response to GABA. The emphasis of this review is on the rich chemical diversity of ligands that influence GABA(A) receptor function. Such diversity provides many avenues for the design and development of new chemical entities acting on GABA(A) receptors. There is also a significant diversity of GABA(A) receptor subtypes composed of different protein subunits. The discovery of subtype specific agents is a major challenge in the continuing development of GABA(A) receptor pharmacology. Leads for the discovery of new chemical entities that influence GABA(A) receptors come from using recombinant GABA(A) receptors of known subunit composition as has been elegantly demonstrated by the refining of benzodiazepine actions with alpha1 subunit preferring agents showing sedative properties but not anxiolytic properties. The most recent advances in the therapeutic use of agents acting on GABA(A) receptors concern the promotion of sound sleep. Many herbal medicines are used to promote sleep and many of their active ingredients include flavonoids and terpenoids known to modulate GABA(A) receptor function.

 

“Chronic stimulation of GABAA receptor with muscimol reduces amyloid beta protein (25-35)-induced neurotoxicity in cultured rat cortical cells.”

Lee,-B-Y; Ban,-J-Y; Seong,-Y-H Citation: Neurosci-Res. 2005 Aug; 52(4): 347-56

 Abstract: The present study was performed to examine how the stimulation of gamma-aminobutyric acid (GABA) receptor affects amyloid beta protein (25-35) (Abeta (25-35)), a synthetic 25-35 amyloid peptide, -induced neurotoxicity using cultured rat cortical neurons. Abeta (25-35) produced a concentration-dependent reduction of cell viability, which was significantly reduced by (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine (MK-801), an N-methyl-d-aspartate (NMDA) receptor antagonist, verapamil, an L-type Ca(2+) channel blocker, and N(G)-nitro-l-arginine methyl ester (l-NAME), a nitric oxide synthase inhibitor. Pretreatment with muscimol, a GABAA receptor agonist, over a concentration range of 0.1-10microM 24h before the treatment with 10microM Abeta (25-35) showed concentration-dependent inhibition on the Abeta (25-35)-induced neuronal apoptotic death. However, baclofen (1 and 10microM), a GABAB receptor agonist, failed to inhibit the Abeta (25-35)-induced neuronal death. In addition, pretreatment with muscimol (1microM) for 24h inhibited the Abeta (25-35) (10microM)-induced elevation of cytosolic Ca(2+) concentration ([Ca(2+)]c) and glutamate release, generation of reactive oxygen species (ROS), and caspase-3 activity in cultured neurons. These neuroprotective effects of muscimol (1microM) were completely blocked by the simultaneous treatment with 10microM bicuculline, a GABAA receptor antagonist, indicating that the protective effects of muscimol were due to GABAA receptor stimulation. When, however, treated just 15min before the treatment with Abeta (25-35), muscimol (1microM) did not show any protective effect against Abeta (25-35) (10microM)-induced neurotoxicity in cultured neurons. These results suggest that the chronic activation of GABAA receptor may ameliorate Abeta-induced neurotoxicity by interfering with the increase of [Ca(2+)]c, and then by inhibiting glutamate release, generation of ROS and caspase-3 activity.

 

“Development of effective therapeutics targeting the GABAA receptor: naturally occurring alternatives.”

Tsang,-S-Y; Xue,-H Citation: Curr-Pharm-Des. 2004; 10(9): 1035-44

Abstract: The enhancement of GABA-mediated synaptic transmission underlies the pharmacotherapy of various neurological diseases. GABAA receptors are thus targets for neuroactive drugs, including classical benzodiazepines, mediating their anxiolytic, hypnotic and anticonvulsant effects via the benzodiazepine site (BZS). Based on findings that low intrinsic efficacy and subtype selectivity can greatly improve the specificity of drugs targeting the BZS, recent research has identified possible drug leads with apparently little side effects. In particular, drug leads of natural sources have been identified as promising candidates. This review describes the advances in the design of effective therapeutics targeting the GABAA receptor, focusing on the more recent research on naturally occurring drug leads. This includes discussion on the isolation of neuroactive alkaloids and flavonoids from herbal medicines and their rational development based on structure-activity relationships studies. Interest in the development of effective therapeutics from natural sources is clear and awaits to be seen whether their medicinal potential can be fulfilled.

 

“Antihypertensive effect of gamma-amino butyric acid enriched soy products in spontaneously hypertensive rats.”

Shizuka,-F; Kido,-Y; Nakazawa,-T; Kitajima,-H; Aizawa,-C; Kayamura,-H; Ichijo,-N Citation: Biofactors. 2004; 22(1-4): 165-7

Abstract: The effect of gamma-amino butyric acid (GABA)-enriched soybean on blood pressure was investigated in male spontaneously hypertensive rats. Ten-week-old rats were given diets containing graded levels of GABA-enriched soybean powder for 8 weeks. The systolic blood pressure in rats fed 0.15% GABA diet was significantly lower at 1st week and maintained lower values for 4 weeks as compared with 0% GABA controls. No effect on blood pressure was found in those of 0.03 and 0.3% GABA. The results suggest that there exist appropriate dietary GABA level to get the blood pressure lowering effect.

“Functional coupling of gamma-aminobutyric acid receptors to chloride channels in brain membranes”

RA Harris and AM Allan

Gamma-Aminobutyric acid (GABA), the major inhibitory neurotransmitter in mammalian brain, is believed to act by increasing membrane conductance of chloride ions. In this study it was found that GABA agonists increased the uptake of chloride-36 by cell-free membrane preparations from mouse brain. This influx was rapid (less than 5 seconds), and 13 micromolar GABA produced a half-maximal effect. The GABA antagonists (bicuculline and picrotoxin) blocked the effect of GABA, whereas pentobarbital enhanced the action. This may be the first demonstration of functional coupling among GABA and barbiturate receptors and chloride channels in isolated membranes. The technique should facilitate biochemical and pharmacological studies of GABA receptor-effector coupling.

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:

Deletion of the fyn-Kinase Gene Alters Sensitivity to GABAergic Drugs: Dependence on {beta}2/{beta}3 GABAA Receptor Subunits.  S. L. Boehm II, L. Peden, R. A. Harris, and Y. A. Blednov (2004) J. Pharmacol. Exp. Ther. 309, 1154-1159    Abstract »    Full Text »    PDF »

Zinc Inhibition of gamma -Aminobutyric AcidA Receptor Function Is Decreased in the Cerebral Cortex during Pilocarpine-Induced Status Epilepticus.  P. K. Banerjee, R. W. Olsen, and O. C. Snead III (1999) J. Pharmacol. Exp. Ther. 291, 361-366    Abstract »    Full Text »

Role of brain allopregnanolone in the plasticity of gamma -aminobutyric acid type A receptor in rat brain during pregnancy and after delivery.  A. Concas, M. C. Mostallino, P. Porcu, P. Follesa, M. L. Barbaccia, M. Trabucchi, R. H. Purdy, P. Grisenti, and G. Biggio (1998) PNAS 95, 13284-13289    Abstract »    Full Text »    PDF »

Desensitization of a gamma -Aminobutyric Acid Type A Receptor in Rat Is Increased by Chronic Treatment with Chlordiazepoxide: A Molecular Mechanism of Dependence. D. J. Cash, P. Serfözö, and A. M. Allan (1997) J. Pharmacol. Exp. Ther. 283, 704-711    Abstract »    Full Text »

A selective imidazobenzodiazepine antagonist of ethanol in the rat. P. Suzdak, Glowa JR, J. Crawley, R. Schwartz, P Skolnick, and S. Paul (1986) Science 234, 1243-1247    Abstract »    PDF »

GABA receptor-mediated chloride transport in a "cell-free" membrane preparation from brain.  S. Paul, R. Schwartz, C. Creveling, E. Hollingsworth, J. Daly, and P Skolnick (1986) Science 233, 228-229 PDF »

Response: GABA Receptor--Mediated Chloride Transport in a "Cell-Free" Membrane Preparation from Brain. R. A. HARRIS and A. M. ALLAN (1986) Science 233, 229

GABA Supplement by Ray Sahelian, M.D. (Natural Medicine Comprehensive List)

GABA or gamma-aminobutyric acid, discovered in 1950, is the most important and widespread inhibitory neurotransmitter in the brain. Excitation in the brain must be balanced with inhibition. Too much excitation can lead to restlessness, irritability, insomnia, and even seizures. GABA is able to induce relaxation, analgesia, and sleep. Barbiturates and benzodiazepines are known to stimulate GABA receptors, and hence induce relaxation. Several neurological disorders, such as epilepsy, sleep disorders, and Parkinson’s disease are affected by this neurotransmitter.

GABA and Relaxation
Relaxation and immunity enhancement effects of gamma-aminobutyric acid (GABA) administration in humans.

Biofactors. 2006;26(3):201-8. Department of Research and Development, Pharma Foods International Co. Ltd., Kyoto, Japan.

The effect of orally administrated gamma-aminobutyric acid ( GABA ) on relaxation and immunity during stress has been investigated in humans. Two studies were conducted. The first evaluated the effect of GABA intake by 13 subjects on their brain waves.

 

Electroencephalograms (EEG) were obtained after 3 tests on each volunteer as follows: intake only water, GABA, or L-theanine. After 60 minutes of administration, GABA significantly increases alpha waves and decreases beta waves compared to water or L-theanine. These findings denote that GABA not only induces relaxation but also reduces anxiety. The second study was conducted to see the role of relaxant and anxiolytic effects of GABA intake on immunity in stressed volunteers. Eight acrophobic subjects were divided into 2 groups (placebo and GABA). All subjects were crossing a suspended bridge as a stressful stimulus. Immunoglobulin A (IgA) levels in their saliva were monitored during bridge crossing. Placebo group showed marked decrease of their IgA levels, while GABA group showed significantly higher levels. In conclusion, GABA could work effectively as a natural relaxant and its effects could be seen within 1 hour of its administration to induce relaxation and diminish anxiety. Moreover, GABA administration could enhance immunity under stress conditions.

 

GABA Research Update:

 

“Alcohol effects on gamma-aminobutyric acid type A receptors: are extrasynaptic receptors the answer?”

Life Sci. 2004 Nov 19;76(1):1-8.

GABA (A) receptors have long been implicated in mediating at least part of the actions of ethanol in mammalian brain. However, until very recently, reports of the actions of ethanol on recombinant receptors have required very high doses of ethanol and animals lacking receptor subunits shown to be important for ethanol actions in vitro did not support the view that these subunits are crucial in ethanol actions. Recombinant GABA (A) receptors are uniquely sensitive to ethanol, with a dose-response relationship mirroring the well known effects of alcohol consumption on the human brain. Receptors containing the delta subunit are thought to be located extrasynaptically and it will be important to determine if these extrasynaptic GABA (A) receptor subunit combinations mediate low dose alcohol effects in vivo.

 

“GABA inhibits T cell autoimmunity and the development of inflammatory responses in a mouse type 1 diabetes model.”

J Immunol. 2004 Oct 15;173(8):5298-304.

Gamma-aminobutyric acid ( GABA ) is both a major inhibitory neurotransmitter in the CNS and a product of beta cells of the peripheral islets. Our previous studies, and those of others, have shown that T cells express functional GABA A receptors. However, their subunit composition and physiological relevance are unknown. In this study, we show that a subset of GABA A receptor subunits are expressed by CD4+ T cells, including the delta subunit that confers high affinity for GABA and sensitivity to alcohol. GABA at relatively low concentrations down-regulated effector T cell responses to beta cell Ags ex vivo, and administration of GABA retarded the adoptive transfer of type 1 diabetes in mice. Furthermore, treatment with low dose of GABA dramatically inhibited the development of proinflammatory T cell responses and disease progression in diabetes-prone mice that already had established autoimmunity. Finally, GABA inhibited TCR-mediated T cell cycle progression in vitro, which may underlie GABA's therapeutic effects. The immunoinhibitory effects of GABA on T cells may contribute to the long prodomal period preceding the development of T1D, the immunological privilege of the CNS, and the regulatory effects of alcohol on immune responses. Potentially, pharmacological modulation of GABA A receptors on T cells may provide a new class of therapies for human diabetes as well as other inflammatory diseases.


“Effect of a gamma-aminobutyric acid-enriched dairy product on the blood pressure of spontaneously hypertensive and normotensive Wistar-Kyoto rats.”

Br J Nutr. 2004 Sep;92(3):411-7.

We investigated the blood-pressure-lowering effects of gamma-aminobutyric acid (GABA) and a GABA-enriched fermented milk product (FMG) by low-dose oral administration to spontaneously hypertensive (SHR/Izm) and normotensive Wistar-Kyoto (WKY/Izm) rats. FMG was a non-fat fermented milk product produced by lactic acid bacteria, and the GABA contained in FMG was made from the protein of the milk during fermentation. A single oral dose of GABA or FMG (5 ml/kg; 0.5 mg GABA/kg) significantly (P<0.05) decreased the blood pressure of SHR/Izm from 4 to 8 h after administration, but did not increase that of WKY/Izm rats. The hypotensive activity of GABA was dose-dependent from 0.05 to 5.00 mg/kg in SHR/Izm. During the chronic administration of experimental diets to SHR/Izm, a significantly slower increase in blood pressure with respect to the control group was observed at 1 or 2 weeks after the start of feeding with the GABA or FMG diet respectively (P<0.05) and this difference was maintained throughout the period of feeding. The time profile of blood-pressure change due to administration of FMG was similar to that of GABA. FMG did not inhibit angiotensin 1-converting enzyme. Furthermore, an FMG peptide-containing fraction from reverse-phase chromatography lacked a hypotensive effect in SHR/Izm rats. The present results suggest that low-dose oral GABA has a hypotensive effect in SHR/Izm and that the hypotensive effect of FMG is due to GABA.


“Molecular structure and physiological functions of GABA (B) receptors.”

Physiol Rev. 2004 Jul;84(3):835-67.

GABA (B) receptors are broadly expressed in the nervous system and have been implicated in a wide variety of neurological and psychiatric disorders. The cloning of the first GABA (B) receptor cDNAs in 1997 revived interest in these receptors and their potential as therapeutic targets. With the availability of molecular tools, rapid progress was made in our understanding of the GABA(B) system. This led to the surprising discovery that GABA (B) receptors need to assemble from distinct subunits to function and provided exciting new insights into the structure of G protein-coupled receptors (GPCRs) in general. As a consequence of this discovery, it is now widely accepted that GPCRs can exist as heterodimers. The cloning of GABA (B) receptors allowed some important questions in the field to be answered. It is now clear that molecular studies do not support the existence of pharmacologically distinct GABA (B) receptors, as predicted by work on native receptors. Advances were also made in clarifying the relationship between GABA (B) receptors and the receptors for gamma-hydroxybutyrate, an emerging drug of abuse. There are now the first indications linking GABA (B) receptor polymorphisms to epilepsy. Significantly, the cloning of GABA (B) receptors enabled identification of the first allosteric GABA (B) receptor compounds, which is expected to broaden the spectrum of therapeutic applications. Here we review current concepts on the molecular composition and function of GABA (B) receptors and discuss ongoing drug-discovery efforts.


“Acupuncture-mediated inhibition of ethanol-induced dopamine release in the rat nucleus accumbens through the GABA B receptor.”

Neurosci Lett. 2004 Oct 21;369(3):234-8.

Clinical trials are currently underway to determine the effectiveness of acupuncture in the treatment of drug abuse. However, there are still many unanswered questions about the basic mechanisms of acupuncture. Studies have shown that the GABA (B) receptor system may play a significant modulatory role in the mesolimbic system in drug abuse, including ethanol. The in vivo microdialysis study was designed to investigate the effect of acupuncture on acute ethanol-induced dopamine release in the nucleus accumbens and the potential role of the GABA (B) receptor system in acupuncture. Male Sprague-Dawley rats were administered with the highly selective GABA (B) antagonist SCH 50911 (3 mg/kg, i.p.) 1h prior to an intraperitoneal injection of ethanol (1 g/kg). Immediately after ethanol treatment, acupuncture was given at bilateral Shenmen (HT7) points for 1min. Acupuncture at the specific acupoint HT7, but not at control points (PC6 or tail) significantly decreased dopamine release in the nucleus accumbens. Inhibition of dopamine release by acupuncture was completely prevented by SCH 50911. These results suggest that stimulation of specific acupoints inhibits ethanol-induced dopamine release by modulating GABA (B) activity and imply that acupuncture may be
effective in blocking the reinforcing effects of ethanol.

“GABA pharmacology-what prospects for the future?”

Biochem Pharmacol. 2004 Oct 15;68(8):1537-40.

Following the recognition of GABA as an inhibitory neurotransmitter, the discovery of high affinity GABA uptake, and the characterisation of GABA receptors great progress has been made in developing GABA pharmacology. Tiagabide, the first marketed GABA uptake inhibitor may be followed by new and more selective uptake inhibitors. Knowledge of the molecular pharmacology of GABA-A receptors, both synaptic and non-synaptic, may lead to improved anti-anxiety/anticonvulsant agents devoid of the sedative and dependence liabilities of earlier compounds and new hypnotics. Gaboxadol (THIP) is an example of a novel hypnotic that acts on GABA-A receptors by a non-benzodiazepine mechanism. Exploiting neurosteroid interactions with GABAergic mechanisms also holds much future promise.


“A role for GABA mechanisms in the motivational effects of alcohol.”

Biochem Pharmacol. 2004 Oct 15;68(8):1515-25.

Low doses of ethanol have been hypothesized to act directly via proteins that form ligand-gated receptor channels, such as the gamma-aminobutyric acid (GABA) receptor complex, to allosterically alter function, particularly in specific brain areas such as those hypothesized to be involved in ethanol reinforcement. At the pharmacological level, one can antagonize the effects of ethanol with GABA antagonists, particularly its sedative, anxiolytic-like and acute reinforcing actions. Brain sites involved in the GABA ergic component of ethanol reinforcement include the ventral tegmental area, elements of the extended amygdala (including the central nucleus of the amygdala), and the globus pallidus. Chronic administration of ethanol sufficient to produce dependence and increased ethanol intake are associated with increased GABA release in the amygdala and increased sensitivity to GABA agonists. A hypothesis is proposed that GABA ergic interactions with the brain stress neurotransmitter corticotropin-releasing factor in specific elements of the extended amygdala may be an important component for the motivation for excessive drinking associated with the transition from social drinking to addiction.


“Comparative study of the effect of picamilone and piracetam on learning in rats in a radial maze”

Farmakol Toksikol. 1989 Jul-Aug;52(4):14-7.

During four weeks rats were learned to visit consequently 4 baited arms in the 8-armed radial maze. Picamilone ( nicotinoyl- GABA ) in a dose of 10 mg/kg daily accelerated rats to reach 80% level of learning (to 20-28 trials). After picamilone injections rats obtained the maximal level of short-term memory as just 3-5 trials. Piracetam in a dose of 200 mg/kg daily exerted no effects on long-term and short-term memory of rats in the radial maze.

 

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