GABA ELISA Kit

Name: GABA ELISA Kit
SKU: DEIA05749
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

plasma, serum, urine.

Species Reactivity

Human

Intended Use

Enzyme Immunoassay for the quantitative determination of Gamma-aminobutyric acid (GABA) in human plasma, serum and urine.

Contents of Kit

1. Adhesive Foil - Ready to use
Adhesive Foils in a resealable pouch, 3 x 4 foils.
2. Macrotiter Plate - Ready to use
2 x 48 well plate, empty in a resealable pouch.
3. Extraction Plate - Ready to use
2 x 48 well plate, precoated with cation exchanger in a resealable pouch.
4. Wash Buffer Concentrate - Concentrated 50x
Buffer with a non-ionic detergent and physiological pH, 1 x 20 ml/vial, light purple cap.
5. Enzyme Conjugate - Ready to use
Goat anti-rabbit immunoglobulins conjugated with peroxidase, 1 x 12 ml/vial, red cap.
6. Substrate - Ready to use
Chromogenic substrate containing tetramethylbenzidine, substrate buffer and hydrogen peroxide, 1 x 12 ml/black vial, black cap.
7. Stop Solution - Ready to use
0.25 M sulfuric acid, 1 x 12 ml/vial, light grey cap.
8. GABA Microtiter Strips - Ready to use
1 x 96 well (12x8) antigen precoated microwell plate in a resealable foil pouch with desiccant.
9. GABA Antiserum - Ready to use
Rabbit anti- GABA antibody, blue coloured. 1 x 6 ml/vial, blue cap.
10. Standards and Controls - Ready to use

Conversion: GABA (ng/ml) x 9.7 = GABA (nmol/l)
Contents: Acidic buffer with non-mercury preservative, spiked with defined quantity of GABA
11. Assay Buffer - Ready to use
Buffer with non-mercury preservative, 1 x 20 ml/vial, yellow cap.
12. Equalizing Reagent - Lyophilized
Lyophilized protein, 1 vial, brown cap.
13. D-Reagent - Ready to use
Crosslinking agent in dimethylsulfoxide, 1 x 4 ml/vial, white cap.
14. Q-Buffer - Ready to use
TRIS buffer, 1 x 20 ml/vial, white cap.
15. I-Buffer - Konzentriert
Buffer with non-ionic detergent and non-mercury preservative, 1 x 4 ml/vial, light red cap.
16. Elution-Buffer - Ready to use
Buffer with citric acid, 1 x 50 ml/vial, dark green cap.
17. Diluent - Ready to use
Buffer with acidic pH, 2 x 20 ml/vial, blue cap.
18. NaOH - Ready to use
Sodium hydroxide solution, 1 x 2 ml/vial, purple cap.
* For the determination of serum and plasma, standards and controls should always be diluted 1:3 [e.g. 100 μl standard + 200 μl water (deionized, distilled, or ultra-pure)]. Do not forget to correct the result afterwards for the dilution. Urine values of GABA are higher than for serum and plasma. Dilution of the standards is to make sure sample is measured in linear part of standard curve.

Storage

Store the unopened reagents at 2 - 8°C until expiration date. Do not use components beyond the expiry date indicated on the kit labels. Once opened the reagents are stable for 1 month when stored at 2 - 8°C. Once the resealable pouch has been opened, care should be taken to close it tightly with desiccant again.

Precision

Sensitivity

Urine (spontaneous): 49 ng/ml

Standard Curve

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Treatment response after 6 and 26 weeks is related to baseline glutamate and GABA levels in antipsychotic-naive patients with psychosis

PSYCHOLOGICAL MEDICINE

Authors: Bojesen, Kirsten B.; Ebdrup, Bjorn H.; Jessen, Kasper; Sigvard, Anne; Tangmose, Karen; Edden, Richard A. E.; Larsson, Henrik B. W.; Rostrup, Egill; Broberg, Brian V.; Glenthoj, Birte Y.

Abstract

Background Poor response to dopaminergic antipsychotics constitutes a major challenge in the treatment of psychotic disorders and markers for non-response during first-episode are warranted. Previous studies have found increased levels of glutamate and gamma-aminobutyric acid (GABA) in non-responding first-episode patients compared to responders, but it is unknown if non-responders can be identified using reference levels from healthy controls (HCs). Methods Thirty-nine antipsychotic-naive patients with first-episode psychosis and 36 matched HCs underwent repeated assessments with the Positive and Negative Syndrome Scale and 3T magnetic resonance spectroscopy. Glutamate scaled to total creatine (/Cr) was measured in the anterior cingulate cortex (ACC) and left thalamus, and levels of GABA/Cr were measured in ACC. After 6 weeks, we re-examined 32 patients on aripiprazole monotherapy and 35 HCs, and after 26 weeks we re-examined 30 patients on naturalistic antipsychotic treatment and 32 HCs. The Andreasen criteria defined non-response. Results Before treatment, thalamic glutamate/Cr was higher in the whole group of patients but levels normalized after treatment. ACC levels of glutamate/Cr and GABA/Cr were lower at all assessments and unaffected by treatment. When compared with HCs, non-responders at week 6 (19 patients) and week 26 (16 patients) had higher baseline glutamate/Cr in the thalamus. Moreover, non-responders at 26 weeks had lower baseline GABA/Cr in ACC. Baseline levels in responders and HCs did not differ. Conclusion Glutamatergic and GABAergic abnormalities in antipsychotic-naive patients appear driven by non-responders to antipsychotic treatment. If replicated, normative reference levels for glutamate and GABA may aid estimation of clinical prognosis in first-episode psychosis patients.

Optical Control of GABA(A) Receptors with a Fulgimide-Based Potentiator

CHEMISTRY-A EUROPEAN JOURNAL

Authors: Rustler, Karin; Maleeva, Galyna; Gomila, Alexandre M. J.; Gorostiza, Pau; Bregestovski, Piotr; Koenig, Burkhard

Abstract

Optogenetic and photopharmacological tools to manipulate neuronal inhibition have limited efficacy and reversibility. We report the design, synthesis, and biological evaluation of Fulgazepam, a fulgimide derivative of benzodiazepine that behaves as a pure potentiator of ionotropic gamma-aminobutyric acid receptors (GABA(A)Rs) and displays full and reversible photoswitching in vitro and in vivo. The compound enables high-resolution studies of GABAergic neurotransmission, and phototherapies based on localized, acute, and reversible neuroinhibition.