Neurotensin increases endogenous glutamate release in rat cortical slices

In the present study, the effects of the tridecapeptide neurotensin [NT(1–13)] and its fragments, NT(1–7) and NT(8–13), on endogenous glutamate release from rat cortical slices, were evaluated. NT(1–13) (100–1000 nM) slightly increased spontaneous glutamate release, while it was ineffective at 1 and...

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Published in:	Life sciences (1973) 2000, Vol.66 (10), p.927-936
Main Authors:	Ferraro, L., Tomasini, M.C., Siniscalchi, A., Fuxe, K., Tanganelli, S., Antonelli, T.
Format:	Article
Language:	eng
Subjects:	Animals Cerebral Cortex - drug effects Cerebral Cortex - metabolism Glutamic Acid - metabolism In Vitro Techniques K +-evoked glutamate release Male Medicin och hälsovetenskap neurotensin Neurotensin - pharmacology neurotensin fragments Potassium - pharmacology Rats Rats, Sprague-Dawley SR48692
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Summary:	In the present study, the effects of the tridecapeptide neurotensin [NT(1–13)] and its fragments, NT(1–7) and NT(8–13), on endogenous glutamate release from rat cortical slices, were evaluated. NT(1–13) (100–1000 nM) slightly increased spontaneous glutamate release, while it was ineffective at 1 and 10 nM concentrations. Neither the biologically active NT fragment NT(8–13) nor the inactive one NT(1–7) affected basal glutamate release. NT(1–13) (1–1000 nM) enhanced potassium (35 mM)-evoked glutamate release displaying a bell-shaped concentration response curve. In addition NT(8–13) (10 nM) increased K +-evoked-glutamate release similarly to the parent peptide (10 nM), while the biologically inactive fragment NT(1–7) (10–100 nM) was ineffective. The effects of NT(1–13) and NT(8–13) were fully counteracted by the selective neurotensin receptor antagonist SR48692 (100 nM). These findings suggest that NT plays a role in regulating cortical glutamate transmission.
ISSN:	0024-3205 1879-0631