کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4320020 1613291 2008 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Neurotensin modulation of acetylcholine, GABA, and aspartate release from rat prefrontal cortex studied in vivo with microdialysis
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
Neurotensin modulation of acetylcholine, GABA, and aspartate release from rat prefrontal cortex studied in vivo with microdialysis
چکیده انگلیسی
The effects of the peptide transmitter neurotensin (NT) on the release of acetylcholine (ACh), γ-aminobutyric acid (GABA), glutamate (Glu), aspartate (Asp), and taurine from the prefrontal cortex (PFC) of freely moving rats were studied by transversal microdialysis. Neurotensin (0.2 and 1 μM) administered locally in the PFC produced a concentration-dependent increase in the extracellular levels of ACh, GABA, and Asp, but not of Glu or taurine. The increase produced by 1 μM NT reached a maximum of about 240% for ACh, 370% for GABA, and 380% for Asp. Lower doses of NT (0.05 μM) did not cause a significant change in ACh, GABA, or Asp output in the PFC. Higher concentrations of NT (2 μM) did not induce further increases in the level of neurotransmitters. A high-affinity selective neurotensin receptor (NTR1) antagonist SR 48692 (0.5 μM) perfused locally blocked neurotensin (1 μM)-evoked ACh, GABA, and Asp release. Local infusion of the sodium channel blocker tetrodotoxin (TTX) (1 μM) decreased the release of ACh, had no significant effect on GABA or Asp release, and prevented the 1 μM neurotensin-induced increase in ACh, GABA, and Asp output. Removal of calcium from the Ringer's solution prevented the peptide from having any effects on the neurotransmitters. Thus, in vivo NT plays a modulatory role in the PFC by interacting with cortical neurons releasing GABA and Asp and with ACh-containing neurons projecting to the PFC. The NT effects are of neural origin, as they are TTX-sensitive, and mediated by the NTR1 receptor, as they are antagonized by SR 48692.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research Bulletin - Volume 77, Issues 2–3, 30 September 2008, Pages 129-135
نویسندگان
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