scholarly journals Gamma-Aminobutyric Acid (GABA) Promotes Growth in Zebrafish Larvae by Inducing IGF-1 Expression via GABAA and GABAB Receptors

2021 ◽  
Vol 22 (20) ◽  
pp. 11254
Author(s):  
Athapaththu Mudiyanselage Gihan Kavinda Athapaththu ◽  
Ilandarage Menu Neelaka Molagoda ◽  
Rajapaksha Gedara Prasad Tharanga Jayasooriya ◽  
Yung Hyun Choi ◽  
You-Jin Jeon ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Rate ◽  
Growth Performance ◽  
Total Body Length ◽  
Gabab Receptors ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Zebrafish Larvae ◽  
Gabaa And Gabab Receptors ◽  
Total Body

Insulin-like growth factor-1 (IGF-1) primarily increases the release of gamma-aminobutyric acid (GABA) in neurons; moreover, it is responsible for the promotion of longitudinal growth in children and adolescents. Therefore, in this study, we investigated whether exogenous GABA supplementation activates IGF-mediated growth performance. Zebrafish larvae treated with GABA at three days post fertilization (dpf) showed a significant increase in the total body length from 6 to 12 dpf through upregulation of growth-stimulating genes, including IGF-1, growth hormone-1 (GH-1), growth hormone receptor-1 (GHR-1), and cholecystokinin A (CCKA). In particular, at 9 dpf, GABA increased total body length from 3.60 ± 0.02 to 3.79 ± 0.03, 3.89 ± 0.02, and 3.92 ± 0.04 mm at concentrations of 6.25, 12.5, and 25 mM, and the effect of GABA at 25 mM was comparable to 4 mM β-glycerophosphate (GP)-treated larvae (3.98 ± 0.02 mm). Additionally, the highest concentration of GABA (50 mM) -induced death in 50% zebrafish larvae at 12 dpf. GABA also enhanced IGF-1 expression and secretion in preosteoblast MC3T3-E1 cells, concomitant with high levels of the IGF-1 receptor gene (IGF-1R). In zebrafish larvae, the GABA-induced growth rate was remarkably decreased in the presence of an IGF-1R inhibitor, picropodophyllin (PPP), which indicates that GABA-induced IGF-1 enhances growth rate via IGF-1R. Furthermore, we investigated the effect of GABA receptors on growth performance along with IGF-1 activation. Inhibitors of GABAA and GABAB receptors, namely bicuculline and CGP 46381, respectively, considerably inhibited GABA-induced growth rate in zebrafish larvae accompanied by a marked decrease in the expression of growth-stimulating genes, including IGF-1, GH-1, GHR-1, and CCKA, but not with an inhibitor of GABAC receptor, TPMPA. Additionally, IGF-1 and IGF-1R expression was impaired in bicuculline and CGP 46381-treated MC3T3-E1 cells, but not in the cells treated with TPMPA. Furthermore, treatment with bicuculline and CGP 46381 significantly downregulated GABA-induced IGF-1 release in MC3T3-E1 cells. These data indicate that GABA stimulates IGF-1 release via GABAA and GABAB receptors and leads to growth promotion performance via IGF-1R.

scholarly journals Gamma-Aminobutyric Acid (GABA) Inhibits α-Melanocyte-Stimulating Hormone-Induced Melanogenesis through GABAA and GABAB Receptors

2021 ◽  
Vol 22 (15) ◽  
pp. 8257
Author(s):  
Ilandarage Menu Neelaka Molagoda ◽  
Mirissa Hewage Dumindu Kavinda ◽  
Hyung Won Ryu ◽  
Yung Hyun Choi ◽  
Jin-Woo Jeong ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Melanoma Cells ◽  
Gabab Receptors ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
B16f10 Melanoma ◽  
Melanocyte Stimulating Hormone ◽  
Zebrafish Larvae ◽  
B16f10 Melanoma Cells ◽  
Gabaa And Gabab Receptors

Gamma-aminobutyric acid (GABA) is considered the primary inhibitory neurotransmitter in the human cortex. However, whether GABA regulates melanogenesis has not been comprehensively elucidated. In this study, we reveal that GABA (20 mM) significantly inhibited α-melanocyte-stimulating hormone (α-MSH)-induced extracellular (from 354.9% ± 28.4% to 126.5% ± 16.0%) and intracellular melanin contents (from 236.7% ± 11.1% to 102.7% ± 23.1%) in B16F10 melanoma cells, without inducing cytotoxicity. In addition, α-MSH-induced hyperpigmentation in zebrafish larvae was inhibited from 246.3% ± 5.4% to 116.3% ± 3.1% at 40 mM GABA, displaying no apparent cardiotoxicity. We also clarify that the GABA-mediated antimelanogenic properties were related to the direct inhibition of microphthalmia-associated transcription factor (MITF) and tyrosinase expression by inhibiting cyclic adenosine monophosphate (cAMP) and cAMP response element-binding protein (CREB). Furthermore, under α-MSH stimulation, GABA-related antimelanogenic effects were mediated through the GABAA and GABAB receptors, with subsequent inhibition of Ca2+ accumulation. In B16F10 melanoma cells and zebrafish larvae, pretreatment with bicuculline, a GABAA receptor antagonist, and CGP 46381, a GABAB receptor antagonist, reversed the antimelanogenic effect of GABA following α-MSH treatment by upregulating Ca2+ accumulation. In conclusion, our results indicate that GABA inhibits α-MSH-induced melanogenesis. Hence, in addition to the health benefits of GABA in the central nervous system, it could ameliorate hyperpigmentation disorders.

scholarly journals Axonal Modulation of Striatal Dopamine Release by Local γ-Aminobutyric Acid (GABA) Signalling

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 709
Author(s):  
Bradley M. Roberts ◽  
Emanuel F. Lopes ◽  
Stephanie J. Cragg
Keyword(s):  
Gabab Receptors ◽  
Striatal Dopamine ◽  
Aminobutyric Acid ◽  
Gaba Uptake ◽  
Short Term Plasticity ◽  
Psychomotor Disorders ◽  
Gabaa And Gabab Receptors ◽  
Uptake Transporters ◽  
Gabaergic Modulation ◽  
Da Release

Striatal dopamine (DA) release is critical for motivated actions and reinforcement learning, and is locally influenced at the level of DA axons by other striatal neurotransmitters. Here, we review a wealth of historical and more recently refined evidence indicating that DA output is inhibited by striatal γ-aminobutyric acid (GABA) acting via GABAA and GABAB receptors. We review evidence supporting the localisation of GABAA and GABAB receptors to DA axons, as well as the identity of the striatal sources of GABA that likely contribute to GABAergic modulation of DA release. We discuss emerging data outlining the mechanisms through which GABAA and GABAB receptors inhibit the amplitude as well as modulate the short-term plasticity of DA release. Furthermore, we highlight recent data showing that DA release is governed by plasma membrane GABA uptake transporters on striatal astrocytes, which determine ambient striatal GABA tone and, by extension, the tonic inhibition of DA release. Finally, we discuss how the regulation of striatal GABA-DA interactions represents an axis for dysfunction in psychomotor disorders associated with dysregulated DA signalling, including Parkinson’s disease, and could be a novel therapeutic target for drugs to modify striatal DA output.

scholarly journals Embryonic Thermal Manipulation and in ovo Gamma-Aminobutyric Acid Supplementation Regulating the Chick Weight and Stress-Related Genes at Hatch

2022 ◽  
Vol 8 ◽  
Author(s):  
Akshat Goel ◽  
Chris Major Ncho ◽  
Chae-Mi Jeong ◽  
Yang-Ho Choi
Keyword(s):  
Gene Expression ◽  
Growth Performance ◽  
Organ Weight ◽  
Aminobutyric Acid ◽  
Poultry Production ◽  
Gamma Aminobutyric Acid ◽  
Related Gene ◽  
In Ovo ◽  
Stress Related Genes ◽  
Thermal Manipulation

Chickens are exposed to numerous types of stress from hatching to shipping, influencing poultry production. Embryonic manipulation may develop resistance against several stressors. This study investigates the effects of thermoneutral temperature (T0; 37.8°C) with no injection (N0) (T0N0), T0 with 0.6 ml of 10% in ovo gamma-aminobutyric acid (GABA) supplementation (N1) at 17.5th embryonic day (ED) (T0N1), thermal manipulation (T1) at 39.6°C from the 10th to 18th ED (6 h/day) with N0 (T1N0), and T1 with N1 (T1N1) on hatchability parameters and hepatic expression of stress-related genes in day-old Arbor Acres chicks. The parameters determined were hatchability, body weight (BW), organ weight, hepatic malondialdehyde (MDA), and antioxidant-related gene expression. Percent hatchability was calculated on a fertile egg basis. Growth performance was analyzed using each chick as an experimental unit. Eight birds per group were used for organ weight. Two-way ANOVA was used taking temperature and GABA as the main effect for growth performance and gene expression studies. Analysis was performed using an IBM SPSS statistics software package 25.0 (IBM software, Chicago, IL, USA). Hatchability was similar in all the groups and was slightly lower in the T1N1. Higher BW was recorded in both T1 and N1. Intestinal weight and MDA were higher in T0N1 against T0N0 and T1N1, respectively. The expression of HSP70, HSP90, NOX1, and NOX4 genes was higher and SOD and CAT genes were lower in the T1 group. The present results show that T1 and N1 independently improve the BW of broiler chicks at hatch, but T1 strongly regulates stress-related gene expression and suggests that both T1 and N1 during incubation can improve performance and alleviate stress after hatch.

Dietary gamma-aminobutyric acid ameliorates growth impairment and intestine dysfunction in turbot (Scophthalmus maximus L.) fed a high soybean meal diet.

2021 ◽  
Author(s):  
Chaoqun Li ◽  
Yuan Tian ◽  
Qinyuan Ma ◽  
Beili Zhang
Keyword(s):  
Growth Performance ◽  
Soybean Meal ◽  
Scophthalmus Maximus ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Growth Impairment ◽  
Turbot Scophthalmus Maximus

Over-substitution of fishmeal with soybean meal (SBM) commonly leads to inferior growth performance and intestinal dysfunction in fish. This study aims to evaluate whether dietary gamma-aminobutyric acid (GABA) could ameliorate...

Effects of dietary gamma-aminobutyric acid supplementation on the intestinal functions in weaning piglets

2019 ◽  
Vol 10 (1) ◽  
pp. 366-378 ◽  
Author(s):  
Shuai Chen ◽  
Bie Tan ◽  
Yaoyao Xia ◽  
Simeng Liao ◽  
Meiwei Wang ◽  
...  
Keyword(s):  
Amino Acid ◽  
Growth Performance ◽  
Aminobutyric Acid ◽  
Gut Microflora ◽  
Gamma Aminobutyric Acid ◽  
Intestinal Immunity ◽  
Weaned Piglets ◽  
Amino Acid Profiles ◽  
Intestinal Functions ◽  
Weaning Piglets

This study aims to investigate the effects of dietary gamma-aminobutyric acid (GABA) supplementation on the growth performance, intestinal immunity, intestinal GABAergic system, amino acid profiles and gut microflora of the weaned piglets.

scholarly journals Propofol Requirement in Patients with Growth Hormone-Secreting Pituitary Tumors Undergoing Transsphenoidal Surgery

2019 ◽  
Vol 8 (5) ◽  
pp. 571
Author(s):  
Seung Hyun Kim ◽  
Namo Kim ◽  
Eui Hyun Kim ◽  
Sungmin Suh ◽  
Seung Ho Choi
Keyword(s):  
Growth Hormone ◽  
General Anesthesia ◽  
Transsphenoidal Surgery ◽  
Pituitary Tumors ◽  
Aminobutyric Acid ◽  
Loss Of Consciousness ◽  
Gamma Aminobutyric Acid ◽  
Gh Secretion ◽  
Effect Site ◽  
Effect Site Concentration

Growth hormone (GH) secretion is regulated by various hormones or neurotransmitters, including gamma-aminobutyric acid. The aim of this study was to determine the propofol requirement in patients with GH-secreting pituitary tumors undergoing transsphenoidal surgery. General anesthesia was induced in 60 patients with GH-secreting tumors (GH group, n = 30) or nonfunctioning pituitary tumors (NF group, n = 30) using an effect-site target-controlled intravenous propofol infusion. The effect-site concentrations were recorded at both a loss of consciousness and a bispectral index (BIS) of 40, along with the effect-site concentration after extubation, during emergence from the anesthesia. The effect-site concentration of propofol was higher in the GH group than in the NF group at a loss of consciousness and a BIS of 40 (4.09 ± 0.81 vs. 3.58 ± 0.67, p = 0.009 and 6.23 ± 1.29 vs. 5.50 ± 1.13, p = 0.025, respectively) and immediately after extubation (1.60 ± 0.27 vs. 1.40 ± 0.41, p = 0.046). The total doses of propofol and remifentanil during anesthesia were comparable between the groups (127.56 ± 29.25 vs. 108.64 ± 43.16 µg/kg/min, p = 0.052 and 6.67 ± 2.89 vs. 7.05 ± 1.96 µg/kg/h, p = 0.550, respectively). The propofol requirement for the induction of a loss of consciousness and the achievement of a BIS of 40 is increased during the induction of general anesthesia in patients with GH-secreting tumors.

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