Adulthood olanzapine treatment fails to alleviate decreases of ChAT and BDNF RNA expression in rats quinpirole-primed as neonates

Brown, Russell W.; Perna, Marla K.; Maple, Amanda M.; Wilson, Tracy D.; Miller, Barney E.

doi:10.1016/j.brainres.2008.01.041

Cited by 8 publications

(3 citation statements)

References 71 publications

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“…Pillai (2008) observed an increase in BDNF expression in the frontal cortex of rats after administration of olanzapine (10 mg/kg/day) for 45 days. In contrast, Brown et al (2008) observed no changes in BDNF levels in the frontal cortex of rats treated with a lower dose of olanzapine (5 mg/kg/day) for a shorter period of time (28 days). These findings suggest that higher doses of olanzapine and longer treatment periods may favor an increase in BDNF levels.…”

Section: Discussioncontrasting

confidence: 53%

“…Results from some of these studies have indicated that atypical antipsychotics enhance factors that promote cell survival, like BDNF, and may have differential effects from typical antipsychotics (like haloperidol), which reduce BDNF expression (Tohen et al, 2003;Thacker et al, 2006;Tan et al, 2007;Pillai, 2008). In contrast, other rodent studies have found no effect of antipsychotics on BDNF expression or levels in brain tissue (Brown et al, 2008, Valvassori et al, 2008.…”

Section: Introductionmentioning

confidence: 92%

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Increase in brain-derived neurotrophic factor in first episode psychotic patients after treatment with atypical antipsychotics

González-Pinto

Mosquera

Palomino

et al. 2010

International Clinical Psychopharmacology

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Some preclinical and postmortem studies suggest that the effects of atypical antipsychotics could be mediated by brain-derived neurotrophic factor (BDNF). Olanzapine is an atypical antipsychotic with shown efficacy in psychosis treatment. The aim of this study was to compare plasma BDNF levels at baseline and after 1 year of olanzapine treatment in 18 drug-naive patients who experienced a first psychotic episode with those of 18 healthy control participants matched by age, sex, and socioeconomic level. Plasma BDNF levels were measured in patients at the index episode and at 1, 6, and 12 months of follow-up using an enzyme-linked immunosorbent assay. Symptoms and functioning of patients and controls were assessed with the Positive and Negative Symptom Scale and Global Assessment of Function Scale. BDNF levels of patients at onset were significantly lower than controls but increased toward control values during olanzapine treatment. There was a significant positive correlation between BDNF levels and functioning (Global Assessment of Function Scale). BDNF levels were also negatively correlated with positive symptoms, but not with negative symptoms or general psychopathology. Results suggest that olanzapine can offset the low BDNF levels at the onset of first psychotic episodes, and improving psychotic symptoms. The increase in BDNF levels may be its mechanism of action in improving positive symptoms.

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Section: Discussioncontrasting

confidence: 53%

Section: Introductionmentioning

confidence: 92%

Increase in brain-derived neurotrophic factor in first episode psychotic patients after treatment with atypical antipsychotics

González-Pinto

Mosquera

Palomino

et al. 2010

International Clinical Psychopharmacology

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“…We have continued to expand this work investigating both behavioral and neurochemical mechanisms of this model [65,66,67,68,69,70,71]. The model is unique as no other models solely focus on increased sensitivity of the dopamine D 2 receptor.…”

Section: Findings From a Developmental Pharmacological Model Of Schizmentioning

confidence: 99%

Schizophrenia and Substance Abuse Comorbidity: Nicotine Addiction and the Neonatal Quinpirole Model

Brown¹,

Maple²,

Perna³

et al. 2012

Dev Neurosci

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This review focuses on nicotine comorbidity in schizophrenia, and the insight into this problem provided by rodent models of schizophrenia. A particular focus is on age differences in the response to nicotine, and how this relates to the development of the disease and difficulties in treatment. Schizophrenia is a particularly difficult disease to model in rodents due to the fact that it has a plethora of symptoms ranging from paranoia and delusions of grandeur to anhedonia and negative affect. The basis of these symptoms is believed to be due to neurochemical abnormalities and neuropathology in the brain, which most models have attempted to emulate. A brief review of findings regarding nicotine use and abuse in schizophrenics is presented, with findings using rodent models that have been able to provide insight into the mechanisms of addiction. A common clinical approach to the treatment of nicotine addiction in the schizophrenic population has been that these drugs are used for self-medication purposes, and it is clear that self-medication may actually be directed at several symptoms, including cognitive impairment and anhedonia. Finally, our laboratory has reported across a series of studies that neonatal treatment with the dopamine D₂/D₃ receptor agonist quinpirole results in long-term increases in dopamine-like receptor sensitivity, consistent with data reporting increases in dopamine D₂ receptor function in schizophrenia. Across these studies, we have reported several behavioral, neurochemical, and genetic consistencies with the disease, and present a hypothesis for what we believe to be the basis of psychostimulant addiction in schizophrenia.

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Applications of the Neonatal Quinpirole Model to Psychosis and Convergence upon the Dopamine D2 Receptor

Brown

Peterson

2015

Neurotoxin Modeling of Brain Disorders—Life-Long Outcomes in Behavioral Teratology

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This mini review focuses on the importance of the dopamine D-like receptor family and its importance in psychosis. Past findings from this laboratory along with collaborators have been that neonatal quinpirole (a dopamine D-like receptor agonist) results in increases in dopamine D receptor sensitivity that persists throughout the animal's lifetime. Findings from this model have been shown to have particular application and validity to schizophrenia, but may have broader implications toward other psychoses, which is reviewed in the present manuscript. In the present review, we also highlight other models of psychoses that have been centered on the subchronic administration of quinpirole to rats in order to model certain psychoses, which has uncovered some interesting and valid behavioral findings. This review highlights the importance of the combination of behavioral findings and neurobiological mechanisms focusing on neural plasticity in discovering underlying pathologies in these disorders that may lead to treatment discoveries, as well as the value of animal models across all psychoses.

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Adulthood olanzapine treatment fails to alleviate decreases of ChAT and BDNF RNA expression in rats quinpirole-primed as neonates

Cited by 8 publications

References 71 publications

Increase in brain-derived neurotrophic factor in first episode psychotic patients after treatment with atypical antipsychotics

Increase in brain-derived neurotrophic factor in first episode psychotic patients after treatment with atypical antipsychotics

Schizophrenia and Substance Abuse Comorbidity: Nicotine Addiction and the Neonatal Quinpirole Model

Applications of the Neonatal Quinpirole Model to Psychosis and Convergence upon the Dopamine D2 Receptor

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