Do neurotensin receptor agonists represent a novel class of antipsychotic drugs?

Ricardo Cáceda, Becky Kinkead, Charles Nemeroff

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Schizophrenia is one of the major psychiatric disorders for which effective pharmacotherapy has been available for approximately 50 years. Study of the mechanism of action of these antipsychotic drugs (APDs) has largely focused on the mesolimbic dopamine system and in the neurotransmitter systems that regulate it. Modulation of the neurotensin (NT) circuit in the mesolimbic system can underlie the mechanism of action of APDs. Several lines of evidence support this hypothesis, including: (1) association of NT with neural circuits relevant to the pathophysiology of schizophrenia and the therapeutic effects of APDs; (2) prediction of antipsychotic efficacy and side effect liability based on APD effects on the NT system; (3) low concentrations of NT in the cerebrospinal fluid of a subset of patients with schizophrenia and its normalization after associated clinical improvement with APDs; and (4) remarkable behavioral similarities between peripherally administered APDs and central NT administration. For these reasons, drugs that directly modify the activity of NT systems, particularly NT receptor agonists, could plausibly represent a novel class of APDs.

Original languageEnglish
Pages (from-to)94-108
Number of pages15
JournalSeminars in Clinical Neuropsychiatry
Volume8
Issue number2
DOIs
StatePublished - Apr 1 2003
Externally publishedYes

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Neurotensin Receptors
Antipsychotic Agents
Neurotensin
Schizophrenia
Therapeutic Uses
Neurotransmitter Agents
Psychiatry
Cerebrospinal Fluid
Dopamine

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology
  • Neuroscience(all)

Cite this

Do neurotensin receptor agonists represent a novel class of antipsychotic drugs? / Cáceda, Ricardo; Kinkead, Becky; Nemeroff, Charles.

In: Seminars in Clinical Neuropsychiatry, Vol. 8, No. 2, 01.04.2003, p. 94-108.

Research output: Contribution to journalArticle

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