کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4341182 1295826 2007 13 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Influence of glial cells in the dopamine releasing effect resulting from the stimulation of striatal δ-opioid receptors
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
Influence of glial cells in the dopamine releasing effect resulting from the stimulation of striatal δ-opioid receptors
چکیده انگلیسی

Recent data indicate that striatal dopamine release induced by stimulation of δ-opioid receptors is a consequence of glutamate release. However, glial cells, which mainly support glutamate uptake and are involved in glutamate signaling and potentially express δ-opioid receptors, could participate to this effect. The present study investigates the contribution of glial cells in the releasing effects of [d-Pen2, d-Pen5]-enkephalin (DPDPE) by using the gliotoxin l-α-aminoadipate (l-αAA). Initially, we evaluated the early influence of l-αAA local infusion (10 μg/μL) on dialysate levels of glutamate and dopamine under basal or DPDPE treatment conditions. l-αAA produced a significant increase of glutamate and dopamine in dialysates (+76% and +50% respectively) and the concomitant infusion of DPDPE (10 μM) significantly enhanced this effect in an additive manner (+110% and +44% respectively). Secondly, we assessed the DPDPE effects on striatal glutamate and dopamine dialysate levels, 2 days after an intra-striatal injection of l-αAA which produced destruction of glial cells. This lesion, decreasing the basal glutamate dialysate level as well as its tissue content (by 55% and 36% respectively), prevented the increase in glutamate and dopamine extracellular levels induced by DPDPE. This result confirmed that the DPDPE-induced dopamine release requires an initial glutamate release. However, this effect could reflect a major disruption of glutamatergic transmission caused by the toxin, as suggested by the local infusion of glutamine (2.5 mM) which, in lesioned rats, prevented the decrease in the basal extracellular content of glutamate and restored the DPDPE-induced increase in glutamate and dopamine dialysate levels. Therefore, these results indicate that, although glial cells are essential to maintain functional glutamatergic neurotransmission, they are not directly involved in the process by which stimulation of striatal δ-opioid receptors induces extracellular glutamate release and, consecutively, dopamine release.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 150, Issue 1, 30 November 2007, Pages 131–143
نویسندگان
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