دورية أكاديمية

Caffeine regulates GABA transport via A 1 R blockade and cAMP signaling.

التفاصيل البيبلوغرافية
العنوان: Caffeine regulates GABA transport via A 1 R blockade and cAMP signaling.
المؤلفون: Borges-Martins VPP; Laboratório de Neurofarmacologia, Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Brazil. Electronic address: vladimirppbm@gmail.com., Ferreira DDP; Laboratório de Doenças Neurodegenerativas, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address: ferreiradanielle@id.uff.br., Souto AC; Laboratório de Neurofarmacologia, Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Brazil. Electronic address: arthursouto@id.uff.br., Oliveira Neto JG; Laboratório de Fisiologia Endócrina e Metabologia, Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Brazil. Electronic address: jgeisebel@gmail.com., Pereira-Figueiredo D; Laboratório de Neurobiologia da Retina, Departmento de Neurobiologia, Instituto de Biologia, Universidade Federal Fluminense, Niterói, Brazil. Electronic address: dannifigueiredo12@gmail.com., da Costa Calaza K; Laboratório de Neurobiologia da Retina, Departmento de Neurobiologia, Instituto de Biologia, Universidade Federal Fluminense, Niterói, Brazil. Electronic address: karincalaza@gmail.com., de Jesus Oliveira K; Laboratório de Fisiologia Endócrina e Metabologia, Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Brazil. Electronic address: karenoliveira@id.uff.br., Manhães AC; Laboratório de Neurofisiologia, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address: ac_manhaes@yahoo.com.br., de Melo Reis RA; Laboratório de Neuroquímica, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address: ramreis@biof.ufrj.br., Kubrusly RCC; Laboratório de Neurofarmacologia, Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Brazil. Electronic address: reginakubrusly1@gmail.com.br.
المصدر: Neurochemistry international [Neurochem Int] 2019 Dec; Vol. 131, pp. 104550. Date of Electronic Publication: 2019 Sep 26.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Pergamon Press Country of Publication: England NLM ID: 8006959 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1872-9754 (Electronic) Linking ISSN: 01970186 NLM ISO Abbreviation: Neurochem Int Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Oxford [Elmsford, N. Y.] Pergamon Press.
مواضيع طبية MeSH: Angiotensin II Type 1 Receptor Blockers/*pharmacology , Angiotensin Receptor Antagonists/*pharmacology , Caffeine/*pharmacology , Central Nervous System Stimulants/*pharmacology , Cyclic AMP/*physiology , gamma-Aminobutyric Acid/*metabolism, Adenosine/analogs & derivatives ; Adenosine/pharmacology ; Amacrine Cells/drug effects ; Amacrine Cells/metabolism ; Animals ; Caffeine/antagonists & inhibitors ; Chick Embryo ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; GABA Plasma Membrane Transport Proteins/metabolism ; Phenethylamines/pharmacology ; Receptor, Adenosine A1/drug effects ; Receptor, Adenosine A1/metabolism ; Receptor, Angiotensin, Type 1/drug effects ; Receptors, Adenosine A2/drug effects ; Receptors, Adenosine A2/metabolism ; Retina/drug effects ; Retina/embryology ; Retina/growth & development ; Signal Transduction/drug effects
مستخلص: Caffeine is the most consumed psychostimulant drug in the world, acting as a non-selective antagonist of adenosine receptors A 1 R and A 2A R, which are widely expressed in retinal layers. We have previously shown that caffeine, when administered acutely, acts on A 1 R to potentiate the NMDA receptor-induced GABA release. Now we asked if long-term caffeine exposure also modifies GABA uptake in the avian retina and which mechanisms are involved in this process. Chicken embryos aged E11 were injected with a single dose of caffeine (30 mg/kg) in the air chamber. Retinas were dissected on E15 for ex vivo neurochemical assays. Our results showed that [ 3 H]-GABA uptake was dependent on Na + and blocked at 4 °C or by NO-711 and caffeine. This decrease was observed after 60 min of [ 3 H]-GABA uptake assay at E15, which is accompanied by an increase in [ 3 H]-GABA release. Caffeine increased the protein levels of A 1 R without altering ADORA1 mRNA and was devoid of effects on A 2A R density or ADORA2A mRNA levels. The decrease of GABA uptake promoted by caffeine was reverted by A 1 R activation with N6-cyclohexyl adenosine (CHA) but not by A 2A R activation with CGS 21680. Caffeine exposure increased cAMP levels and GAT-1 protein levels, which was evenly expressed between E11-E15. As expected, we observed an increase of GABA containing amacrine cells and processes in the IPL, also, cAMP pathway blockage by H-89 decreased caffeine mediated [ 3 H]-GABA uptake. Our data support the idea that chronic injection of caffeine alters GABA transport via A 1 R during retinal development and that the cAMP/PKA pathway plays an important role in the regulation of GAT-1 function.
(Copyright © 2019 Elsevier Ltd. All rights reserved.)
فهرسة مساهمة: Keywords: A1R; Caffeine; Chick; Development; GAT; Retina
المشرفين على المادة: 0 (Angiotensin II Type 1 Receptor Blockers)
0 (Angiotensin Receptor Antagonists)
0 (Central Nervous System Stimulants)
0 (GABA Plasma Membrane Transport Proteins)
0 (Phenethylamines)
0 (Receptor, Adenosine A1)
0 (Receptor, Angiotensin, Type 1)
0 (Receptors, Adenosine A2)
120225-54-9 (2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine)
36396-99-3 (N(6)-cyclohexyladenosine)
3G6A5W338E (Caffeine)
56-12-2 (gamma-Aminobutyric Acid)
E0399OZS9N (Cyclic AMP)
EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
K72T3FS567 (Adenosine)
تواريخ الأحداث: Date Created: 20190930 Date Completed: 20200903 Latest Revision: 20200903
رمز التحديث: 20231215
DOI: 10.1016/j.neuint.2019.104550
PMID: 31563462
قاعدة البيانات: MEDLINE
الوصف
تدمد:1872-9754
DOI:10.1016/j.neuint.2019.104550