scholarly journals Malaria and Dengue Mosquito Vectors from Lao PDR Show a Lack of the rdl Mutant Allele Responsible for Cyclodiene Insecticide Resistance

2019 ◽  
Vol 57 (3) ◽  
pp. 815-823
Author(s):  
Sebastien Marcombe ◽  
Phoutmany Thammavong ◽  
Phonesavanh Luangamath ◽  
Somsanith Chonephetsarath ◽  
Nothasin Phommavanh ◽  
...  
Keyword(s):  
Gaba Receptor ◽  
Mutant Allele ◽  
Lao Pdr ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Mosquito Vectors ◽  
Health Concerns ◽  
Aedes Mosquitoes ◽  
Cyclodiene Insecticide ◽  
Potential Use

Abstract The gamma-aminobutyric acid (GABA) receptor, RDL, plays important roles in neuronal signaling and is the target of highly effective insecticides. A mutation in RDL, commonly A296S, underlies resistance to several insecticides such as cyclodienes. Even though the use of cyclodienes has been banned, the occurrence of mutations substituting A296 is notably high in mosquitoes from several countries. Here, we report a survey investigating the prevalence of the Rdl mutant allele in mosquitoes from Laos, a country where mosquito-borne diseases such as malaria and dengue fever are health concerns. Anopheles and Aedes mosquitoes were collected from 12 provinces in Laos. Adult bioassays on Aedes aegypti (Linnaeus) (Diptera: Culicidae) and Aedes albopictus (Skuse) (Diptera: Culicidae) showed that all the populations tested were susceptible to dieldrin (4%) following WHO protocols. Exon 7 from a total of 791 mosquitoes was sequenced to identify the amino acid encoded for at 296 of RDL. Only one of these mosquitoes, Anopheles maculatus rampae Harbach and Somboon (Diptera: Culicidae) from Attapeu, carried the mutant allele being heterozygous for A296S. We therefore found a general lack of the Rdl mutant allele indicating that mosquitoes from Laos are not exposed to insecticides that act on the GABA receptor compared to mosquitoes in several other countries. Identifying the prevalence of the Rdl mutation may help inform the potential use of alternative insecticides that act on the GABA receptor should there be a need to replace pyrethroids in order to prevent/manage resistance.

Molecular Targets of Cannabinoids Associated with Depression

2021 ◽  
Vol 28 ◽  
Author(s):  
Pradeep Paudel ◽  
Samir Ross ◽  
Xing-Cong Li
Keyword(s):  
Gaba Receptor ◽  
Rational Design ◽  
Cannabinoid Receptors ◽  
Molecular Targets ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Binding Modes ◽  
Novel Therapeutic Strategies ◽  
New Treatments ◽  
Synthetic Derivatives

: Novel therapeutic strategies are needed to address depression, a major neurological disorder affecting hundreds of millions of people worldwide. Cannabinoids and their synthetic derivatives have demonstrated numerous neurological activities and may potentially be developed into new treatments for depression. This review highlights cannabinoid (CB) receptors, monoamine oxidase (MAO), N-methyl-D-aspartate (NMDA) receptor, gamma-aminobutyric acid (GABA) receptor, and cholecystokinin (CCK) receptor as key molecular targets of cannabinoids that are associated with depression. The anti-depressant activity of cannabinoids and their binding modes with cannabinoid receptors are discussed, providing insights into rational design and discovery of new cannabinoids or cannabimimetic agents with improved druggable properties.

Gamma-aminobutyric acid (GABA) receptor binding selectively depleted by viral induced granule cell loss in hamster cerebellum

1976 ◽  
Vol 105 (2) ◽  
pp. 365-371 ◽  
Author(s):  
Rabi Simantov ◽  
Mary Lou Oster-Granite ◽  
Robert M. Herndon ◽  
Solomon H. Snyder
Keyword(s):  
Receptor Binding ◽  
Granule Cell ◽  
Gaba Receptor ◽  
Cell Loss ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid

A comparison of similar ionic responses to gamma-aminobutyric acid and acetylcholine

1978 ◽  
Vol 41 (3) ◽  
pp. 531-541 ◽  
Author(s):  
J. Yarowsky ◽  
D. O. Carpenter
Keyword(s):  
Gaba Receptor ◽  
Aminobutyric Acid ◽  
Identified Neurons ◽  
Ionic Conductance ◽  
Gamma Aminobutyric Acid ◽  
Gaba Antagonists ◽  
Conductance Increase ◽  
Alpha Bungarotoxin ◽  
Cl Conductance

1. Fast Na+-, Cl-, and K+-Conductance increase responses to gamma-aminobutyric acid (GABA) show times to peak similar to the comparable ionic responses to acetylcholine (ACh). 2. On some identified neurons, both putative transmitters elicit responses due to the same conductance change. For example, in cell R2 both substances cause an increase in Cl- conductance. Receptors for GABA and ACh on R2 do not cross desensitize and therefore are distinct. The ACh but not the GABA response is blocked by alpha-bungarotoxin and strychnine. 3. In R2 both responses reverse at -58 mV, and the Cl- ionophore (for both responses) appears to be partially permeant to propionate and isethionate, but impermeant to acetate, sulfate, and methylsulfate. 4. The Cl- responses but not the Na+ responses to both ACh and GABA are blocked by both picrotoxin and bicuculline, the classical GABA antagonists. 5. These results are compatible with the hypothesis that the ionophores associated with receptors to different neurotransmitters but mediating the same ionic conductance change have many common properties and may, in fact, be identical. Bicuculline and picrotoxin may be specific blockers of the Cl- ionophore, not the GABA receptor.

Respiratory depression produced by activation of GABA receptors in hindbrain of cat

1981 ◽  
Vol 51 (5) ◽  
pp. 1278-1286 ◽  
Author(s):  
K. A. Yamada ◽  
P. Hamosh ◽  
R. A. Gillis
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Respiratory Depression ◽  
Gaba Receptors ◽  
Gaba Receptor ◽  
Respiratory Activity ◽  
Aminobutyric Acid ◽  
Neural Pathways ◽  
Gamma Aminobutyric Acid ◽  
Respiratory Responses

Respiratory responses to activation of gamma-aminobutyric acid (GABA) receptors in the hindbrain were measured in chloralose-anesthetized cats using a Fleisch pneumotachograph. GABA receptors were activated by intracisternal injections of muscimol and GABA. Muscimol (0.05--6.65 micrograms) administered to seven animals caused a depression of respiratory activity with apnea occurring in each animal. Before apnea occurred, a decrease in tidal volume was observed (from 25.7 +/- 0.9 to 14.7 +/- 1.1 ml). Respiratory rate and inspiratory and expiratory durations were unchanged. GABA (0.05--12.15 mg) administered to five animals produced the same effect as muscimol on respiratory activity. Apnea produced by both agents was reversed by intracisternal administration of the GABA-receptor antagonist drug, bicuculline. Administration of bicuculline to four naive animals increased tidal volume (from 31.3 +/- 1.7 to 36.5 +/- 0.7 ml) but had no effect on either respiratory rate or inspiratory duration. These results indicate that activation of GABA receptors causes respiratory depression and suggest that GABA may be an important neurotransmitter in CNS neural pathways involved in regulating respiratory activity.

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