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J Neurophysiol (March 12, 2008). doi:10.1152/jn.00890.2007
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Submitted on August 10, 2007
Accepted on March 8, 2008

Neurotensin Enhances GABAergic Activity in Rat Hippocampus CA1 Region by Modulating L-Type Calcium Channels

Shanshan Li1, Jonathan D. Geiger2*, and SAOBO LEI3

1 Pharmacology,Physiology and Therapeutics, University of North Dakota, Grand forks, North Dakota, United States
2 Pharmacology,Physiology and Therapeutics, University of North Dakota, Grand Forks, North Dakota, United States
3 Pharmacology, Physiology & Therapeutics, University of North Dakota, Grand Forks, North Dakota, United States

* To whom correspondence should be addressed. E-mail: jgeiger{at}medicine.nodak.edu.

Neurotensin (NT) is a tridecapeptide that interacts with three NT receptors, NTS1, NTS2 and NTS3. Whereas NT has been reported to modulate GABAergic activity in the brain, the underlying cellular and molecular mechanisms of NT are elusive. Here, we examined the effects of NT on GABAergic transmission and the involved cellular and signaling mechanisms of NT in the hippocampus. Application of NT dose-dependently increased the frequency of sIPSCs recorded from CA1 pyramidal neurons with no effects on the amplitude of sIPSCs. NT did not change either the frequency or the amplitude of mIPSCs recorded in the presence of tetrodotoxin. Triple immunofluorescent staining of recorded interneurons demonstrated the expression of NTS1 on GABAergic interneurons. NT increased action potential firing rate but decreased the afterhyperpolarization (AHP) amplitude in identified CA1 interneurons. Application of L-type calcium channel blockers (nimodipine and nifedipine) abolished NT-induced increases in action potential firing rate and sIPSC frequency and reduction in AHP amplitude suggesting that the effects of NT are mediated by interaction with L-type Ca2+ channels. NT-induced increase in sIPSC frequency was blocked by application of the specific NTS1 antagonist SR48692, the PLC inhibitor U73122, the IP3 receptor antagonist 2-APB, and the PKC inhibitor GF109203X suggesting that NT increases GABA release via a PLC pathway. Our results provide a cellular mechanism by which NT controls GABAergic neuronal activity in hippocampus.




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V. A. Mitchell, H. Kawahara, and C. W. Vaughan
Neurotensin inhibition of GABAergic transmission via mGluR-induced endocannabinoid signalling in rat periaqueductal grey
J. Physiol., June 1, 2009; 587(11): 2511 - 2520.
[Abstract] [Full Text] [PDF]


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