Arturo Gálvez-Rosas1, Alberto Avila-Luna1, Margarita Valdés-Flores2, Sergio Montes3, Antonio Bueno-Nava4. 1. Lab. Neurofisiología Química de la Discapacidad, División de Neurociencias, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, SSa, Calz. México-Xochimilco 289, Col. Arenal de Guadalupe, 14389, Mexico City, Mexico. 2. Departamento de Genética y Medicina Genómica, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, SSa, Calz. México-Xochimilco 289, Col. Arenal de Guadalupe, 14389, Mexico City, Mexico. 3. Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, SSa, Insurgentes Sur 3877, 14269, Mexico City, Mexico. 4. Lab. Neurofisiología Química de la Discapacidad, División de Neurociencias, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, SSa, Calz. México-Xochimilco 289, Col. Arenal de Guadalupe, 14389, Mexico City, Mexico. abueno@inr.gob.mx.
Abstract
RATIONALE: The sensorimotor cortex and the striatum are interconnected by the corticostriatal pathway, suggesting that cortical injury alters the striatal function, which may be modulated by dopamine. OBJECTIVES: We studied whether the activation of dopamine D1 receptors (D1Rs) modulates the γ-aminobutyric acid (GABA) and glutamate levels in the striatum of recovered rats at 192 h after cortical injury. METHODS: The D1R agonist SKF-38393 (0, 2, 3, or 4 mg/kg) was administered at 24, 48, 96, and 192 h post-injury, and then rats were decapitated to determine GABA and glutamate levels and the levels of D1R mRNA on both sides of the striatum. RESULTS: GABAergic imbalance in the striatum contralateral to the injury site was normalized by the administration of the D1R agonist, but this treatment did not produce a significant effect on glutamate levels, suggesting that glutamate was metabolized into GABA. The administration of SKF-38393 (2 mg/kg) decreased the levels of D1R mRNA in the striatum contralateral to the injury, and this effect was blocked by the coadministration of the D1R antagonist SCH-23390 (2 mg/kg). In the striatum ipsilateral to the injury, the D1R agonist increased the D1R mRNA levels, an effect that was blocked by SCH-23390. CONCLUSION: The reversal of the GABAergic imbalance in the striatum contralateral to the cortical injury can be modulated by extrastriatal D1R activation, and the D1R agonist-induced increases in the D1R mRNA levels in the striatum ipsilateral to the injury suggest that the striatum may be necessary to achieve functional recovery.
RATIONALE: The sensorimotor cortex and the striatum are interconnected by the corticostriatal pathway, suggesting that cortical injury alters the striatal function, which may be modulated by dopamine. OBJECTIVES: We studied whether the activation of dopamine D1 receptors (D1Rs) modulates the γ-aminobutyric acid (GABA) and glutamate levels in the striatum of recovered rats at 192 h after cortical injury. METHODS: The D1R agonist SKF-38393 (0, 2, 3, or 4 mg/kg) was administered at 24, 48, 96, and 192 h post-injury, and then rats were decapitated to determine GABA and glutamate levels and the levels of D1R mRNA on both sides of the striatum. RESULTS: GABAergic imbalance in the striatum contralateral to the injury site was normalized by the administration of the D1R agonist, but this treatment did not produce a significant effect on glutamate levels, suggesting that glutamate was metabolized into GABA. The administration of SKF-38393 (2 mg/kg) decreased the levels of D1R mRNA in the striatum contralateral to the injury, and this effect was blocked by the coadministration of the D1R antagonist SCH-23390 (2 mg/kg). In the striatum ipsilateral to the injury, the D1R agonist increased the D1R mRNA levels, an effect that was blocked by SCH-23390. CONCLUSION: The reversal of the GABAergic imbalance in the striatum contralateral to the cortical injury can be modulated by extrastriatal D1R activation, and the D1R agonist-induced increases in the D1R mRNA levels in the striatum ipsilateral to the injury suggest that the striatum may be necessary to achieve functional recovery.
Authors: A K Wagner; J E Sokoloski; D Ren; X Chen; A S Khan; R D Zafonte; A C Michael; C E Dixon Journal: J Neurochem Date: 2005-10 Impact factor: 5.372
Authors: Zafiris J Daskalakis; Guillermo O Paradiso; Bruce K Christensen; Paul B Fitzgerald; Carolyn Gunraj; Robert Chen Journal: J Physiol Date: 2004-03-26 Impact factor: 5.182
Authors: Antonio Verduzco-Mendoza; Paul Carrillo-Mora; Alberto Avila-Luna; Arturo Gálvez-Rosas; Adriana Olmos-Hernández; Daniel Mota-Rojas; Antonio Bueno-Nava Journal: Front Neurosci Date: 2021-06-24 Impact factor: 4.677