Artículo

Goitia, B.; Rivero-Echeto, M.C.; Weisstaub, N.V.; Gingrich, J.A.; Garcia-Rill, E.; Bisagno, V.; Urbano, F.J. "Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors" (2016) Journal of Neurochemistry. 136(3):526-535
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Abstract:

Serotonin receptors are targets of drug therapies for a variety of neuropsychiatric and neurodegenerative disorders. Cocaine inhibits the re-uptake of serotonin (5-HT), dopamine, and noradrenaline, whereas caffeine blocks adenosine receptors and opens ryanodine receptors in the endoplasmic reticulum. We studied how 5-HT and adenosine affected spontaneous GABAergic transmission from thalamic reticular nucleus. We combined whole-cell patch clamp recordings of miniature inhibitory post-synaptic currents (mIPSCs) in ventrobasal thalamic neurons during local (puff) application of 5-HT in wild type (WT) or knockout mice lacking 5-HT 2A receptors (5-HT 2A -/-). Inhibition of mIPSCs frequency by low (10 μM) and high (100 μM) 5-HT concentrations was observed in ventrobasal neurons from 5-HT 2A -/- mice. In WT mice, only 100 μM 5-HT significantly reduced mIPSCs frequency. In 5-HT 2A -/- mice, NAN-190, a specific 5-HT 1A antagonist, prevented the 100 μM 5-HT inhibition while blocking H-currents that prolonged inhibition during post-puff periods. The inhibitory effects of 100 μM 5-HT were enhanced in cocaine binge-treated 5-HT 2A -/- mice. Caffeine binge treatment did not affect 5-HT-mediated inhibition. Our findings suggest that both 5-HT 1A and 5-HT 2A receptors are present in pre-synaptic thalamic reticular nucleus terminals. Serotonergic-mediated inhibition of GABA release could underlie aberrant thalamocortical physiology described after repetitive consumption of cocaine. Our findings suggest that both 5-HT 1A , 5-HT 2A and A1 receptors are present in pre-synaptic TRN terminals. 5-HT 1A and A1 receptors would down-regulate adenylate cyclase, whereas 5-HT 1A would also increase the probability of the opening of G-protein-activated inwardly rectifying K + channels (GIRK). Sustained opening of GIRK channels would hyperpolarize pre-synaptic terminals activating H-currents, resulting in less GABA release. 5-HT 2A -would activate PLC and IP 3 , increasing intracellular [Ca 2+ ] and thus facilitating GABA release. Our findings suggest that both 5-HT 1A , 5-HT 2A and A1 receptors are present in pre-synaptic TRN terminals. 5-HT 1A and A1 receptors would down-regulate adenylate cyclase, whereas 5-HT 1A would also increase the probability of the opening of G-protein-activated inwardly rectifying K + channels (GIRK). Sustained opening of GIRK channels would hyperpolarize pre-synaptic terminals activating H-currents, resulting in less GABA release. 5-HT 2A -would activate PLC and IP 3 , increasing intracellular [Ca 2+ ] and thus facilitating GABA release. © 2015 International Society for Neurochemistry.

Registro:

Documento: Artículo
Título:Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors
Autor:Goitia, B.; Rivero-Echeto, M.C.; Weisstaub, N.V.; Gingrich, J.A.; Garcia-Rill, E.; Bisagno, V.; Urbano, F.J.
Filiación:Departamento de Fisiología, Biología Molecular y Celular dr. Héctor Maldonado (DFBMC), Facultad de Ciencias Exactas y Naturales, Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-CONICET-UBA), Universidad de Buenos Aires, Ciudad Universitaria, Intendente Güiraldes 2160, Pabellón 2- Piso 2, Ciudad de Buenos Aires, C1428EGA, Argentina
Facultad de Farmacia y Bioquímica, Instituto de Investigaciones Farmacolõgicas (ININFA-UBA-CONICET), Universidad de Buenos Aires, Ciudad de Buenos Aires, Argentina
Department of Neurobiology and Developmental Sciences, Center for Translational Neuroscience, University of Arkansas for Medical Sciences, Little Rock, AR, United States
Grupo de Neurociencia de Sistemas, Departamento de Fisiología, Facultad de Medicina, Instituto de Fisiología y Biofísica (IFIBIO), UBA, Ciudad de Buenos Aires, Argentina
Division of Developmental Neuroscience, Columbia University, NYSPI Sackler Institute for Developmental Psychobiology, New York City, NY, United States
Palabras clave:caffeine; cocaine; GABA; serotonin; thalamic reticular nucleus; 1 (2 methoxyphenyl) 4 (4 phthalimidobutyl)piperazine; adenosine; caffeine; cocaine; serotonin; serotonin 1A receptor; serotonin 2A receptor; serotonin receptor; 4 aminobutyric acid; cadmium chloride; caffeine; cocaine; dopamine uptake inhibitor; inositol 1,4,5 trisphosphate; phosphodiesterase inhibitor; phospholipase C; serotonin; serotonin 2A receptor; serotonin receptor affecting agent; 4 aminobutyric acid release; animal experiment; animal tissue; Article; concentration (parameters); controlled study; excitatory postsynaptic potential; GABAergic transmission; inhibition kinetics; male; mouse; neuromodulation; nonhuman; pharmacological blocking; priority journal; serotoninergic system; thalamus reticular nucleus; thalamus ventral nucleus; whole cell patch clamp; action potential; animal; dose response; drug effects; genetics; in vitro study; knockout mouse; metabolism; patch clamp technique; thalamus nucleus; Action Potentials; Animals; Cadmium Chloride; Caffeine; Cocaine; Dopamine Uptake Inhibitors; Dose-Response Relationship, Drug; gamma-Aminobutyric Acid; In Vitro Techniques; Inositol 1,4,5-Trisphosphate; Male; Mice; Mice, Knockout; Patch-Clamp Techniques; Phosphodiesterase Inhibitors; Receptor, Serotonin, 5-HT2A; Serotonin; Serotonin Agents; Thalamic Nuclei; Type C Phospholipases
Año:2016
Volumen:136
Número:3
Página de inicio:526
Página de fin:535
DOI: http://dx.doi.org/10.1111/jnc.13398
Título revista:Journal of Neurochemistry
Título revista abreviado:J. Neurochem.
ISSN:00223042
CODEN:JONRA
CAS:1 (2 methoxyphenyl) 4 (4 phthalimidobutyl)piperazine, 115338-32-4; adenosine, 58-61-7; caffeine, 58-08-2; cocaine, 50-36-2, 53-21-4, 5937-29-1; serotonin, 50-67-9; 4 aminobutyric acid, 28805-76-7, 56-12-2; cadmium chloride, 10108-64-2; inositol 1,4,5 trisphosphate, 85166-31-0, 88269-39-0; phospholipase C, 9001-86-9; Cadmium Chloride; Caffeine; Cocaine; Dopamine Uptake Inhibitors; gamma-Aminobutyric Acid; Inositol 1,4,5-Trisphosphate; Phosphodiesterase Inhibitors; Receptor, Serotonin, 5-HT2A; Serotonin; Serotonin Agents; Type C Phospholipases
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00223042_v136_n3_p526_Goitia

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Citas:

---------- APA ----------
Goitia, B., Rivero-Echeto, M.C., Weisstaub, N.V., Gingrich, J.A., Garcia-Rill, E., Bisagno, V. & Urbano, F.J. (2016) . Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors. Journal of Neurochemistry, 136(3), 526-535.
http://dx.doi.org/10.1111/jnc.13398
---------- CHICAGO ----------
Goitia, B., Rivero-Echeto, M.C., Weisstaub, N.V., Gingrich, J.A., Garcia-Rill, E., Bisagno, V., et al. "Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors" . Journal of Neurochemistry 136, no. 3 (2016) : 526-535.
http://dx.doi.org/10.1111/jnc.13398
---------- MLA ----------
Goitia, B., Rivero-Echeto, M.C., Weisstaub, N.V., Gingrich, J.A., Garcia-Rill, E., Bisagno, V., et al. "Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors" . Journal of Neurochemistry, vol. 136, no. 3, 2016, pp. 526-535.
http://dx.doi.org/10.1111/jnc.13398
---------- VANCOUVER ----------
Goitia, B., Rivero-Echeto, M.C., Weisstaub, N.V., Gingrich, J.A., Garcia-Rill, E., Bisagno, V., et al. Modulation of GABA release from the thalamic reticular nucleus by cocaine and caffeine: Role of serotonin receptors. J. Neurochem. 2016;136(3):526-535.
http://dx.doi.org/10.1111/jnc.13398