Neurotensin receptors in the rat striatum: lesion studies

Goedert, Michel; Pittaway, K.; Emson, Piers C.

doi:10.1016/0006-8993(84)90801-1

Cited by 64 publications

(15 citation statements)

References 21 publications

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“…The results of this study are similar to those reported for SR 48692 indicating that disruption of NT 1 receptor mediated transmission is crucial for the observed reduction in haloperidol-induced Fos expression in the CPU and that there is no additional contribution of NT 2 . The documented enhanced NT release in this brain region following haloperidol administration (Huang and Hanson, 1997;Radke et al, 1998) may thus partially mediate haloperidolinduced Fos expression, by direct activation of NT1 in striatal neurons (Ehlers et al, 1998;Lambert et al, 1996;Portier et al, 1998) or by acting on NT 1 receptors located on glutamatergic corticostriatal projections or dopaminergic projections (Boudin et al, 1996;Goedert et al, 1984). Pretreatment with the NTR antagonist SR 142948A increased Fos expression in the dorsomedial and dorsolateral CPu in combination with olanzapine, but had no effect by itself in these brain regions.…”

Section: Discussionmentioning

confidence: 93%

Neurotensin Receptor Antagonist SR 142948A Alters Fos Expression and Extrapyramidal Side Effect Profile of Typical and Atypical Antipsychotic Drugs

Binder

Kinkead

Owens

et al. 2004

Neuropsychopharmacol

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Antipsychotic drugs (APDs) have previously been shown to alter Fos expression in a regionally specific manner. Increases in Fos expression in the nucleus accumbens (NAcc) are common to all clinically effective APDs. In contrast, APD-induced Fos expression increases in the caudate-putamen (CPu) and prefrontal cortex (PFC) are associated with the extrapyramidal side effect liability of typical APDs or the effectiveness against negative symptoms of atypical APDs, respectively. Considerable evidence suggests that the neuropeptide neurotensin (NT) mediates some of the effects of APDs. To determine whether NT neurotransmission is also involved in APD-induced Fos expression in brain regions relevant for therapeutic efficacy, the NT receptor antagonist SR 142948A (10 or 100 mg/ kg i.p.) was coadministered with APDs (haloperidol (2.0 mg/kg s.c.), olanzapine (5 mg/kg i.p.), or clozapine (20 mg/kg s.c.)). Fos expression was evaluated in the PFC, NAcc shell, dorsomedial, and dorsolateral CPu and the lateral septum. SR 142948A attenuated haloperidolinduced Fos expression in the CPu but, in contrast, increased olanzapine-induced Fos expression in this brain region. The effects of the NT receptor antagonist were paralleled by its effects on catalepsy in olanzapineFbut not haloperidolFtreated animals.

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Section: Discussionmentioning

confidence: 93%

Neurotensin Receptor Antagonist SR 142948A Alters Fos Expression and Extrapyramidal Side Effect Profile of Typical and Atypical Antipsychotic Drugs

Binder

Kinkead

Owens

et al. 2004

Neuropsychopharmacol

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“…First, the neural signal from the NT-sensitive neurons may be transmitted through catecholaminergic synapses to LHRH neurons. It has been re ported that NT could bind with its receptors on dopaminergic cells [24] and terminals [12,26], The peptide stimulates activi ties of dopaminergic neurons [25] and increases the release of dopamine from the brain tissue [7,28], Increases in the turnover rates o f dopamine and norepinephrine by NT in the rat brain [ 111 further support this possibility.…”

Section: Discussionmentioning

confidence: 78%

Inhibition by Catecholaminergic Blockers of the Neurotensin-Induced Enhancement of Luteinizing Hormone Secretion in the Ovariectomized Estrogen-Primed Rat

Akema

Kimura

1989

Neuroendocrinology

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We have shown that the injection of neurotensin (NT) in the medial preoptic area significantly enhanced the estrogen-induced circadian secretion of luteinizing hormone (LH) in the ovariectomized rat. Unaltered timing of the LH secretion, despite the increased magnitude of its secretion, after the peptide injection has suggested a certain relationship between NT and other neurotransmitter systems which are involved in regulating LH secretion. The present study was undertaken to examine whether the activity of brain catecholaminergic systems are necessary for the manifestation of the peptide effect. The medial preoptic injection of NT elevated the peak value of the estrogen-induced LH secretion in vehicle-treated ovariectomized rats. Pretreatment of the animal with either α-methyl-p-tyrosine, pimozide or phenoxybenzamine delayed the timing or reduced the peak value of the LH surge. In these drug-treated animals, the preoptic NT injection failed to induce a change in serum LH levels. It is concluded that dopaminergic and α-adrenergic systems are required to be intact for the manifestation of the peptide effect on LH secretion.

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“…2) [90][91][92][93]. APDevoked Fos activation involves both dopamine D 2 receptor blockade and glutamate signaling through N-methyl-Daspartate (NMDA) receptors [94][95][96].…”

Section: Nt Is Required For Certain Antipsychotic Drug Actionsmentioning

confidence: 99%

Multitasking with neurotensin in the central nervous system

Dobner

2005

Cell. Mol. Life Sci.

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The 13-amino acid peptide neurotensin (NT) was discovered over 30 years ago and has been implicated in a wide variety of neurotransmitter and endocrine functions. This review focuses on four areas where there has been substantial recent progress in understanding NT signaling and several functions of the endogenous peptide. The first area concerns the functional activation of the high-affinity NT receptor, NTR-1, including the delineation of the NT binding pocket and receptor domains involved in functional coupling to intracellular signaling pathways. The development of NT receptor antagonists and the application of genetic and molecular genetic approaches have accelerated progress in understanding NT function in several areas, including the involvement of NT in antipsychotic drug actions, psychostimulant sensitization and the modulation of pain, and these are reviewed in that order. There is now substantial evidence indicating that NT is required for certain antipsychotic drug actions and that the peptide plays a key role in stress-induced analgesia.

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Neurotensin receptors in the rat striatum: lesion studies

Cited by 64 publications

References 21 publications

Neurotensin Receptor Antagonist SR 142948A Alters Fos Expression and Extrapyramidal Side Effect Profile of Typical and Atypical Antipsychotic Drugs

Neurotensin Receptor Antagonist SR 142948A Alters Fos Expression and Extrapyramidal Side Effect Profile of Typical and Atypical Antipsychotic Drugs

Inhibition by Catecholaminergic Blockers of the Neurotensin-Induced Enhancement of Luteinizing Hormone Secretion in the Ovariectomized Estrogen-Primed Rat

Multitasking with neurotensin in the central nervous system

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