The effects of chronic administration of established and putative antipsychotics on natural prepulse inhibition deficits in Brattleboro rats

Feifel, David; Melendez, Gilia; Priebe, Kristianne; Shilling, Paul D.

doi:10.1016/j.bbr.2007.04.020

Cited by 42 publications

(51 citation statements)

References 75 publications

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“…Another highly used preclinical test of APD efficacy is facilitation of PPI. The lack of tolerance exhibited by PD149163 on amphetamine-induced locomotor activation is consistent with previous findings from our laboratory, in which the acute APD-like facilitation of naturally low PPI in Brattleboro rats by acute PD149163 persisted after sixteen consecutive daily administrations of PD149163 (Feifel et al 2007). Treatment of psychosis in most cases requires chronic daily use of APDs.…”

Section: Discussionsupporting

confidence: 91%

“…Acute systemic administration of PD149163 has produced robust APD-like effects in a number of preclinical predictive tests of APD efficacy including facilitation of PPI (Feifel et al 2003a;Feifel et al 1999). In a recent study, our laboratory found that the APD-like facilitation of the naturally low PPI in Brattleboro rats produced by acute administration of PD149163 persisted with no evidence of tolerance after consecutive daily subcutaneous administration of PD149163 for sixteen days (Feifel et al 2007). To further investigate whether the APD-like effects of PD149163 exhibit tolerance, we examined the effect of subchronic systemic injection of PD149163 on amphetamine-induced hyperlocomotion.…”

Section: Introductionmentioning

confidence: 95%

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The reversal of amphetamine-induced locomotor activation by a selective neurotensin-1 receptor agonist does not exhibit tolerance

et al. 2008

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Neurotensin-1 (NT1) receptor agonists have been proposed as putative antipsychotic drugs. Recently brain penetrating NT analogues produced by stability enhancing modification of the smallest NT fragment, , have demonstrated antipsychotic-like efficacy after acute systemic injection in several preclinical animal tests predictive for antipsychotic efficacy. However, the evidence regarding the persistence versus tolerance of these effects after repeated administration is ambiguous. Previous studies have used compounds that non-selectively activated both NT1 and NT2 receptors, a factor which may have contributed to the ambiguity in findings regarding the emergence of tolerance. In this study, we investigated the effects of subchronic systemic administration of PD149163, a brain penetrating NT analogue with selectivity for the NT1 receptor, on amphetamineinduced locomotor activation, a classic preclinical test of antipsychotic-efficacy. Sprague Dawley rats were pretreated with eight consecutive daily subcutaneous (SC) injections of PD149163 or saline. On the ninth day rats received a pair of SC injections consisting of PD149163 or saline, followed by amphetamine (0.5mg/kg) or saline. Locomotor activity was then measured in photobeam equipped cages. The results indicated that repeated daily administration of PD149163 was able to antagonize amphetamine's locomotor activating effect comparable to that of the first dose, despite that repeated administration of PD149163 produced an increase in baseline locomotor activity not seen after the first dose. The results do not support development of tolerance for the acute antipsychotic-like effect of NT1 agonists and thus lend support to the contention that NT1 agonists are viable candidates as putative novel antipsychotic drugs.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 95%

The reversal of amphetamine-induced locomotor activation by a selective neurotensin-1 receptor agonist does not exhibit tolerance

et al. 2008

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“…33 AVP-deficient Brattleboro rats also show several phenotypes of schizophrenia including sensorimotor gaiting and social cognitive deficits, some of which are reversed by antipsychotic drugs. [34][35][36] Fourth, postmortem AVP concentrations are reduced in the temporal cortex of schizophrenia patients. 37 Although OT and AVP have been implicated in schizophrenia, 14,38 the degree to which alterations in these hormone systems contribute to neurobehavioral deficits in schizophrenia and other psychotic disorders has not been systematically examined.…”

Section: Introductionmentioning

confidence: 99%

Reduced Levels of Vasopressin and Reduced Behavioral Modulation of Oxytocin in Psychotic Disorders

Rubin

Carter

Bishop

et al. 2014

Schizophrenia Bulletin

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Oxytocin (OT) and arginine vasopressin (AVP) exert robust influence on social affiliation and specific cognitive processes in healthy individuals. Abnormalities in these neuroendocrine systems have been observed in psychotic disorders, but their relation to impairments in behavioral domains that these endocrines modulate is not well understood. We compared abnormalities of OT and AVP serum concentrations in probands with schizophrenia (n = 57), schizoaffective disorder (n = 34), and psychotic bipolar disorder (n = 75); their first-degree relatives without a history of psychosis (n = 61, 43, 91, respectively); and healthy controls (n = 66) and examined their association with emotion processing and cognition. AVP levels were lower in schizophrenia (P = .002) and bipolar probands (P = .03) and in relatives of schizophrenia probands (P = .002) compared with controls. OT levels did not differ between groups. Familiality estimates were robust for OT (h 2 = 0.79, P = 3.97e−15) and AVP (h 2 = 0.78, P = 3.93e−11). Higher levels of OT were associated with better emotion recognition (β = 0.40, P < .001) and general neuropsychological function (β = 0.26, P = .04) in healthy controls as expected but not in any proband or relative group. In schizophrenia, higher OT levels were related to greater positive symptom severity. The dissociation of OT levels and behavioral function in all proband and relative groups suggests that risk and illness factors associated with psychotic disorders are not related to reduced OT levels but to a disruption in the ability of physiological levels of OT to modulate social cognition and neuropsychological function. Decreased AVP levels may be a marker of biological vulnerability in schizophrenia because alterations were seen in probands and relatives, and familiality was high.

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“…There is significant evidence implicating NTS1 in the sensorimotor gating mechanism of PPI (Binder et al, 2001;Caceda et al, 2005;Feifel et al, 2007;Feifel et al, 2004;Kinkead et al, 2005). Our results indicate that NTS1 is necessary for normal disruption of PPI by the indirect DA agonist d-amphetamine and the non-competitive NMDA receptor antagonist dizocilpine.…”

Section: Discussionmentioning

confidence: 63%

Sensorimotor gating in NTS1 and NTS2 null mice: effects of d-amphetamine, dizocilpine, clozapine and NT69L

Oliveros

Heckman

CORENA-Mcleod

et al. 2010

Journal of Experimental Biology

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SUMMARYPre-pulse inhibition (PPI) of the acoustic startle reflex is deficient in patients with schizophrenia. This deficiency is mimicked in mice by the use of the psychotomimetic drugs d-amphetamine and dizolcipine. Antipsychotic drugs such as clozapine are used to treat schizophrenic patients and are also administered to mice to prevent PPI disruption. Neurotensin (NT) produces antipsychotic-like effects when injected into rodent brain through its effects at NT subtype 1 (NTS1) and 2 (NTS2) receptors. We hypothesized that the NT receptor agonist (

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The effects of chronic administration of established and putative antipsychotics on natural prepulse inhibition deficits in Brattleboro rats

Cited by 42 publications

References 75 publications

The reversal of amphetamine-induced locomotor activation by a selective neurotensin-1 receptor agonist does not exhibit tolerance

The reversal of amphetamine-induced locomotor activation by a selective neurotensin-1 receptor agonist does not exhibit tolerance

Reduced Levels of Vasopressin and Reduced Behavioral Modulation of Oxytocin in Psychotic Disorders

Sensorimotor gating in NTS1 and NTS2 null mice: effects of d-amphetamine, dizocilpine, clozapine and NT69L

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