Brain-derived neurotrophic factor and neurotrophin 3 in schizophrenic psychoses

Durany, Núria; Michel, Tanja Maria; Zöchling, Robert; Boissl, Karl W.; Cruz-Sánchez, F. F.; Riederer, Peter; Thome, Johannes

doi:10.1016/s0920-9964(00)00084-0

Cited by 331 publications

(189 citation statements)

References 52 publications

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“…It is relevant, therefore, that accumulating preclinical and clinical data indicate a potential involvement of neurotrophins in the pathogenesis and therapy of schizophrenia (Buckley et al, 2007;Green et al, 2010;Shoval and Weizman, 2005). In fact, alterations in BDNF levels have been reported in PFC and CSF of schizophrenic patients, even in antipsychotic-naive firstepisode subjects (Durany et al, 2001;Hashimoto et al, 2005;Issa et al, 2010;Weickert et al, 2003). Thus, olanzapineinduced increases in DA turnover and BDNF levels may function individually or in concert to contribute to the effectiveness of olanzapine in reversing the enduring dystrophic changes in dendrites and asymmetric spine synapses seen following mesocortical lesions (Wang and Deutch, 2008) or chronic PCP treatment.…”

Section: Discussionmentioning

confidence: 99%

Phencyclidine-induced Loss of Asymmetric Spine Synapses in Rodent Prefrontal Cortex is Reversed by Acute and Chronic Treatment with Olanzapine

Elsworth

Morrow

Hajszán

et al. 2011

Neuropsychopharmacol

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Enduring cognitive deficits exist in schizophrenic patients, long-term abusers of phencyclidine (PCP), as well as in animal PCP models of schizophrenia. It has been suggested that cognitive performance and memory processes are coupled with remodeling of pyramidal dendritic spine synapses in prefrontal cortex (PFC), and that reduced spine density and number of spine synapses in the medial PFC of PCP-treated rats may potentially underlie, at least partially, the cognitive dysfunction previously observed in this animal model. The present data show that the decrease in number of asymmetric (excitatory) spine synapses in layer II/III of PFC, previously noted at 1-week post PCP treatment also occurs, to a lesser degree, in layer V. The decrease in the number of spine synapses in layer II/III was sustained and persisted for at least 4 weeks, paralleling the observed cognitive deficits. Both acute and chronic treatment with the atypical antipsychotic drug, olanzapine, starting at 1 week after PCP treatment at doses that restore cognitive function, reversed the asymmetric spine synapse loss in PFC of PCP-treated rats. Olanzapine had no significant effect on spine synapse number in saline-treated controls. These studies demonstrate that the effect of PCP on asymmetric spine synapse number in PFC lasts at least 4 weeks in this model. This spine synapse loss in PFC is reversed by acute treatment with olanzapine, and this reversal is maintained by chronic oral treatment, paralleling the time course of the restoration of the dopamine deficit, and normalization of cognitive function produced by olanzapine.

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Section: Discussionmentioning

confidence: 99%

Phencyclidine-induced Loss of Asymmetric Spine Synapses in Rodent Prefrontal Cortex is Reversed by Acute and Chronic Treatment with Olanzapine

Elsworth

Morrow

Hajszán

et al. 2011

Neuropsychopharmacol

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“…This hypothesis is supported by studies showing that NGF and BDNF are abnormally regulated in the CNS of animal models of schizophrenia, [53][54][55][56]13,57 and by the findings that schizophrenic patients have reduced number of TrkB and BDNF-positive neurons 5 and BDNF in the serum. 6 Results from studies on human post-mortem tissues from schizophrenic patients show a significant decrease in BDNF concentrations in cortical areas and the hippocampus, 4 whereas other authors have reported that BDNF protein is elevated in the anterior cingulated cortex and hippocampus of schizophrenics. 58 These data were taken as further evidence for the hypothesis that alterations in the expression of neurotrophins participate in the neural maldevelopment and the disturbed neural plasticity in schizophrenic patients.…”

Section: Animal Modelsmentioning

confidence: 99%

“…Studies on post-mortem Human Decreased BDNF concentrations in cortical areas and hippocampus of schizophrenic patients 4 Reduction of TrkB and BDNF-positive neurons in CNS 5 and BDNF in the serum 6 of schizophrenics Polymorphisms of BDNF gene associated with schizophrenia [7][8][9] Animal models…”

Section: Bdnf and Schizophreniamentioning

confidence: 99%

BDNF in schizophrenia, depression and corresponding animal models

2005

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Understanding the etiology and pathogenesis schizophrenia and depression is a major challenge facing psychiatry. One hypothesis is that these disorders are secondary to a malfunction of neurotrophic factors. Inappropriate neurotrophic support during brain development could lead to structural disorganisation in which neuronal networks are established in a nonoptimal manner. Inadequate neurotrophic support in adult individuals could ultimately be an underlying mechanism leading to decreased capacity of brain to adaptive changes and increased vulnerability to neurotoxic damage. Brain-derived neurotrophic factor (BDNF) is a mediator involved in neuronal survival and plasticity of dopaminergic, cholinergic, and serotonergic neurons in the central nervous system (CNS). In this review, we summarize findings regarding altered BDNF in schizophrenia and depression and animal models, as well as the effects of antipsychotic and antidepressive treatments on the expression of BDNF. Molecular Psychiatry (2005) 10, 345-352.

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“…One study finds decreased BDNF gene expression in the dorsolateral prefrontal cortex of subjects with schizophrenia compared with healthy subjects, 51 although other studies have contradictory findings. 52,53 Animal models suggest that antipsychotics may impact BDNF expression, 54 complicating the interpretation of these post-mortem studies.…”

Section: Expanding the 'Central Dogma' Do Perkins Et Almentioning

confidence: 99%