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Expression and presence of septal neurokinin‐2 receptors controlling hippocampal acetylcholine release during sensory stimulation in rat
Author(s) -
Steinberg R.,
Marco N.,
Voutsinos B.,
Bensaid M.,
Rodier D.,
Souilhac J.,
Alonso R.,
OuryDonat F.,
Fur G. Le,
Soubrie P.
Publication year - 1998
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1998.00244.x
Subject(s) - stimulation , acetylcholine , neuroscience , hippocampal formation , sensory system , receptor , acetylcholine receptor , endocrinology , medicine , chemistry , microbiology and biotechnology , psychology , biology
We examined the expression and presence of NK 2 receptors in the septal area of rat brain, and investigated their functional role in the regulation of the septohippocampal cholinergic system. Using reverse transcription‐polymerase chain reaction (RT‐PCR) analysis, we showed the presence of NK 2 receptor mRNA expression in the septal area, and detected septal NK 2 binding sites by using a fluorescent‐tagged neurokinin A (NKA) derivative. In vivo microdialysis was employed to explore the functional role of NK 2 receptors in the release of hippocampal acetylcholine evoked by tactile stimulation in freely moving rats. Two sessions of stroking of the neck and back of the rat for 30 min, at 90 min intervals, produced a marked and reproducible increase in hippocampal acetylcholine release. This effect was dose‐dependently prevented by intraperitoneal administration of the two selective non‐peptide tachykinin NK 2 receptor antagonists SR144190 (0.03–0.3 mg/kg, i.p.) and SR48968 (0.3 and 1 mg/kg, i.p.), but not by the inactive enantiomer of SR48968 (SR48965, 1 mg/kg) nor by the two non‐peptide NK 1 receptor antagonists SR140333 (3 mg/kg, i.p.) and GR205171 (1 mg/kg, i.p.). Furthermore, the intraseptal application of SR144190 (10 –8 m ) reduced the sensory response. Finally, intraseptal perfusion of neurokinin A (0.01–10 μ m ) in anaesthetized rats produced a concentration‐dependent increase in hippocampal acetylcholine release. The response to neurokinin A (0.1 μ m ) was prevented by SR144190 (0.03–0.3 mg/kg, i.p.) and SR48968 (0.3–1 mg/kg, i.p.). In conclusion, this study provides direct evidence for the role of endogenous NKA/substance P, through the activation of NK 2 receptors, in regulating the septohippocampal cholinergic function.

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