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Effects of chronic infusion of neurotensin and a neurotensin NT₁ selective analogue PD149163 on amphetamine-induced hyperlocomotion

¹ Division of Psychology, Nottingham Trent University, Burton Street, Nottingham, NG1 4BU UK.
² Institute of Neuroscience, University of Nottingham, Medical School, Queen's Medical Centre, Nottingham, NG7 2UH UK.
³ Johnson and Johnson Pharmaceutical R&D, Turnhoutseweg 30, B-2340, Beerse, Belgium
⁴ Institute of Neuroscience, University of Nottingham, Medical School, Queen's Medical Centre, Nottingham, NG7 2UH UK

^* To whom correspondence should be addressed.

	Abstract

Neurotensin has been proposed as an endogenous antipsychotic based in part on the similarity in behavioural effects to antipsychotic drugs, for example attenuation of both amphetamine-induced hyperlocomotion and amphetamine disrupted pre-pulse inhibition in the rat. However, there is some evidence that repeated administration of neurotensin or an analogue produces behavioural tolerance to such effects. The present experiments sought to confirm and extend these findings by testing the effects on amphetamine-induced hyperlocomotion of seven days central administration of neurotensin and the NT1 selective analogue PD 149163 and the effects of 21 days central administration of neurotensin. Neurotensin and PD149163 continuously administered for seven days produced no effect on amphetamine-induced hyperlocomotion (in contrast to attenuation with a single injection here and previously reported) while 21 days of neurotensin administration potentiated amphetamine-induced hyperlocomotion. Together these studies demonstrate that the effects of neurotensin or a neurotensin analogue on amphetamine-induced hyperlocomotion depend on the duration of administration of peptide. The results are discussed in comparison with the reported antipsychotic properties of acute administration of neurotensin and possible mechanisms involving NT1 receptors.

Key Words: antipsychotic, rat, chronic, schizophrenia, amphetamine, locomotion

First published on January 21, 2008, doi:10.1177/0269881107083838

Journal of Psychopharmacology 2008;22:300.

A more recent version of this article appeared on May 1, 2008


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