Anxiolytic-Like Effects of Bergamot Essential Oil Are Insensitive to Flumazenil in Rats

Anxiety disorders are one of the most common mental disorders, and benzodiazepines (BDZs), acting on gamma-aminobutyric acid type A (GABA-A) receptor complex, represent the most common antianxiety medications in the world. However, chronic BDZ use elicits several adverse reactions. Reportedly, aromatherapy is safer for the management of anxiety. Bergamot essential oil (BEO) extracted from Citrus bergamia Risso et Poiteau fruit, like other essential oils, is widely used in aromatherapy to relieve symptoms of stress-induced anxiety. Interestingly, preclinical data indicate that BEO induces anxiolytic-like/relaxant effects in animal behavioural tasks not superimposable to those of benzodiazepine diazepam. To better elucidate the involvement of GABAergic transmission, the present study examines the effects of pretreatment with flumazenil (FLZ), a benzodiazepine site antagonist, on BEO effects using open-field task (OFT) in rats. The data yielded show that FLZ does not significantly affect behavioural effects of the phytocomplex. These results demonstrate the lack of overlapping between BEO and BDZ behavioural effects, contributing to the characterization of the neurobiological profile of the essential oil for its rational use in aromatherapy.

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Gamma-Aminobutyric Acid Type-A (GABA-A) Receptors, Kinetic Models

Encyclopedia of Computational Neuroscience ◽

10.1007/978-1-4614-6675-8_348 ◽

2015 ◽

pp. 1258-1261

Author(s):

Mathew Jones

Keyword(s):

Kinetic Models ◽

Type A ◽

Aminobutyric Acid ◽

Gamma Aminobutyric Acid ◽

Gaba A ◽

Acid Type

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Design, synthesis and characterization of novel gamma‑aminobutyric acid type A receptor ligands

ARKIVOC ◽

10.24820/ark.5550190.p011.398 ◽

2020 ◽

Vol 2020 (7) ◽

pp. 242-256

Author(s):

Kamal P. Pandey ◽

Md Zubair Ahmed Khan ◽

Lalit K. Golani ◽

Prithu Mondal ◽

Md Yeunus Mian ◽

...

Keyword(s):

Type A ◽

Aminobutyric Acid ◽

Synthesis And Characterization ◽

Gamma Aminobutyric Acid ◽

Receptor Ligands ◽

Design Synthesis ◽

Acid Type

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Gamma-Aminobutyric Acid Type A Receptor Genes and Their Related Epilepsies

Journal of Pediatric Neurology ◽

10.1055/s-0041-1727269 ◽

2021 ◽

Author(s):

Viviana Brafa Musicoro ◽

Vincenzo Sortino ◽

Giulia Pecora ◽

Monica Tosto ◽

Manuela Lo Bianco ◽

...

Keyword(s):

Gaba Receptors ◽

Type A ◽

Autism Spectrum ◽

Aminobutyric Acid ◽

Gamma Aminobutyric Acid ◽

Phenotype Correlation ◽

Gaba A ◽

Genotype Phenotype Correlation ◽

Acid Type ◽

Neuropsychiatric Diseases

AbstractGamma-aminobutyric acid type A (GABA-A) receptor subunit gene mutations, which include GABRA1, GABRB3, GABRD, and GABRG2, are often involved in several genetic epilepsy syndromes and other neuropsychiatric diseases like autism spectrum disorder, schizophrenia, and anxiety. GABA-A are ligand-gated ionic channels, and are involved firstly in the fast inhibitory synaptic transmission of the central nervous system. The GABA receptors include the ionotropic GABA-A and GABA-C receptors and the metabotropic GABA-B receptors. According to the site in which mutations occur, they cause disorders in channel opening, “lock-and-pull” receptor system functioning, and capable of causing a specific epilepsy phenotype. The aim of this article is to summarize the most recent literature findings, considering genetic mutations, clinical features, genotype/phenotype correlation, and therapy about neurodevelopment diseases correlated to GABA receptors dysfunction, in particular epilepsy. According to our findings, we conclude that further mutation analysis could permit genotype–phenotype correlation and give more information about the best efficient treatment, even if—at present—more clinical and genetic studies are necessary.

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Gamma-Aminobutyric Acid Type-A (GABA-A) Receptors, Kinetic Models

Encyclopedia of Computational Neuroscience ◽

10.1007/978-1-4614-7320-6_348-1 ◽

2014 ◽

pp. 1-4

Author(s):

Mathew Jones

Keyword(s):

Kinetic Models ◽

Type A ◽

Aminobutyric Acid ◽

Gamma Aminobutyric Acid ◽

Gaba A ◽

Acid Type

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CO 2 -induced ocean acidification increases anxiety in Rockfish via alteration of GABA A receptor functioning

Proceedings of The Royal Society B Biological Sciences ◽

10.1098/rspb.2013.2509 ◽

2014 ◽

Vol 281 (1775) ◽

pp. 20132509 ◽

Cited By ~ 124

Author(s):

Trevor James Hamilton ◽

Adam Holcombe ◽

Martin Tresguerres

Keyword(s):

Ocean Acidification ◽

Aminobutyric Acid ◽

Gamma Aminobutyric Acid ◽

Normal Behaviour ◽

Gaba A ◽

Exposed Fish ◽

Marine Life ◽

Acid Type ◽

Behavioural Tests ◽

Induced Changes

The average surface pH of the ocean is dropping at a rapid rate due to the dissolution of anthropogenic CO 2 , raising concerns for marine life. Additionally, some coastal areas periodically experience upwelling of CO 2 -enriched water with reduced pH. Previous research has demonstrated ocean acidification (OA)-induced changes in behavioural and sensory systems including olfaction, which is due to altered function of neural gamma-aminobutyric acid type A (GABA A ) receptors. Here, we used a camera-based tracking software system to examine whether OA-dependent changes in GABA A receptors affect anxiety in juvenile Californian rockfish ( Sebastes diploproa ). Anxiety was estimated using behavioural tests that measure light/dark preference (scototaxis) and proximity to an object. After one week in OA conditions projected for the next century in the California shore (1125 ± 100 µatm, pH 7.75), anxiety was significantly increased relative to controls (483 ± 40 µatm CO 2 , pH 8.1). The GABA A -receptor agonist muscimol, but not the antagonist gabazine, caused a significant increase in anxiety consistent with altered Cl − flux in OA-exposed fish. OA-exposed fish remained more anxious even after 7 days back in control seawater; however, they resumed their normal behaviour by day 12. These results show that OA could severely alter rockfish behaviour; however, this effect is reversible.

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Additive Effects of Sevoflurane and Propofol on γ-Aminobutyric Acid Receptor Function

Anesthesiology ◽

10.1097/00000542-200606000-00012 ◽

2006 ◽

Vol 104 (6) ◽

pp. 1176-1183 ◽

Cited By ~ 34

Author(s):

Luke E. Sebel ◽

James E. Richardson ◽

Sunil P. Singh ◽

Shannon V. Bell ◽

Andrew Jenkins

Keyword(s):

Gabaa Receptor ◽

Aminobutyric Acid ◽

Dependent Manner ◽

Gamma Aminobutyric Acid ◽

Receptor Function ◽

Human Embryonic Kidney Cells ◽

Gaba A ◽

Apparent Affinity ◽

Acid Type ◽

Transfection Method

Background Previous studies have shown that propofol and sevoflurane enhance the function of gamma-aminobutyric acid type A (GABAA) receptors. However, it is not known whether these two drugs modulate the same molecular pathways. In addition, little is known about receptor function in the presence of both propofol and sevoflurane. The aim of this study was to better understand the interactions of propofol and sevoflurane with the GABAA receptor. Methods Wild-type alpha1, beta(2), gamma(2s) GABA(A) receptor subunit complementary DNAs were transfected into human embryonic kidney cells grown on glass coverslips using a calcium phosphate transfection method. After transfection (36-72 h), cells were whole cell patch clamped and exposed to combinations of the following: 0.3-1,000 microm gamma-aminobutyric acid (GABA), 0-10 microm propofol, and 0-1,650 microm sevoflurane. Chemicals were delivered to the cells using two 10-channel infusion pumps and a rapid solution exchanger. Results Both propofol and sevoflurane alone enhanced the amplitude of GABA(A) receptor responses to submaximal concentrations of GABA in a dose-dependent manner. The enhancement was underpinned by an increase in the apparent affinity of the receptor for GABA. Coapplication of both anesthetics further enhanced the apparent affinity of the receptor for GABA. Conclusions Response surface modeling of the potentiation of GABA responses (0.3-1,000 microm) by sevoflurane and propofol revealed that the two anesthetics modulated receptor function in an additive manner. These results are consistent with recent mutagenesis studies, suggesting that these two drugs have separate binding sites and converging pathways of action on the GABAA receptor.

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