Neonatal Damage of the Ventral Hippocampus Impairs Working Memory in the Rat

Lipska, Barbara K.; Aultman, Julie M.; Verma, Anita; Weinberger, Daniel R.; Moghaddam, Bita

doi:10.1016/s0893-133x(02)00282-8

Cited by 195 publications

(122 citation statements)

References 45 publications

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“…[63][64][65][66] For example, neonatal damage of the ventral hippocampus or amygdala, [67][68][69] administration of amphetamine 70 inducing disruption (and probably blocking) of latent inhibition, or phencyclidine 71 inducing changes in the startle response provided productive animal models with construct, face, and predictive validity for schizophrenia. It has been shown 72,73 that interference with neurogenesis in the mediotemporal allocortex of rat embryos, during the earliest stages of cortical proliferation, results not only in a thickness reduction of the adult entorhinal cortex and hippocampus 55,73 but also in other morphological characteristics resembling those observed in patients with schizophrenia.…”

Section: Bdnf and Animal Models Of 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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Section: Bdnf and Animal Models Of Schizophreniamentioning

confidence: 99%

BDNF in schizophrenia, depression and corresponding animal models

2005

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“…Another recently developed nonpharmacological model, which also exhibits a fair degree of validity to several aspects of schizophrenia, is the 'neonatal ventral hippocampal (NVH) lesion-induced deficits' model proposed by Lipska and co-workers as offering a valid simulation of psychosis disorders (Lipska et al, 2002(Lipska et al, , 1993Lipska and Weinberger, 2000). Indeed, NVH-lesioned rats showed behavioral deficits resembling several aspects of schizophrenia.…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, NVH-lesioned rats showed behavioral deficits resembling several aspects of schizophrenia. For instance, NVH-lesioned rats showed hyperactivity, PPI deficits, disruption of social interaction, and cognitive deficits (Becker and Grecksch, 2000;Becker et al, 1999;Lipska et al, 2002Lipska et al, , 1995Sams-Dodd et al, 1997), resembling positive, negative, and cognitive symptoms of schizophrenia, respectively. The onset of the schizophrenic symptoms typically appears in early adulthood, and the NVH lesion-induced behavioral abnormality in rats also appeared only after puberty (Lipska et al, 1993(Lipska et al, , 1995.…”

Section: Introductionmentioning

confidence: 99%

Effect of Dopamine D3 Antagonists on PPI in DBA/2J Mice or PPI Deficit Induced by Neonatal Ventral Hippocampal Lesions in Rats

Zhang

Ballard

Kohlhaas

et al. 2005

Neuropsychopharmacol

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Schizophrenic patients typically exhibit impairment of sensorimotor gating, which can be modeled in animal models such as the test of prepulse inhibition of startle response (PPI) in rodents. It has been found that antipsychotics enhanced PPI in DBA mice and reversed the PPI deficit induced by neonatal ventral hippocampal (NVH) lesions in rats. However, the relative involvement of D 3 and D 2 receptors in these effects is unknown since all antipsychotics are D 2 /D 3 antagonists with limited binding preference at D 2 receptors. Therefore, in the current study, we investigated the influence of several dopamine antagonists with higher selectivity at D 3 vs D 2 receptors on PPI in DBA/ 2J mice and in NVH-lesioned rats. The PPI in DBA/2J mice was enhanced by the nonselective D 2 /D 3 antagonists, haloperidol at 0.3-3 mg/ kg, or risperidone at 0.3-1 mg/kg, while PPI-enhancing effects were observed after the administration of higher doses of the preferential D 3 /D 2 antagonist, BP 897 at 8 mg/kg, and the selective D 3 antagonists, SB 277011 at 30 mg/kg and A-437203 at 30 mg/kg. No effect was observed following the treatment with the selective D 3 antagonist, AVE 5997 up to 30 mg/kg. The PPI deficits induced by NVH lesions were reversed by haloperidol but not by the more selective D 3 antagonists, A-437203 and AVE 5997. BP 897 enhanced PPI nonselectivity, that is, in both lesioned and nonlesioned rats. In summary, the present study indicates that PPI-enhancing effects induced by antipsychotics in DBA/2J mice and in NVH-lesioned rats are unlikely to be mediated by D 3 receptors.

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“…NVHL animals (Becker et al 1999;Le Pen et al 2000;Lipska et al 1993Lipska et al , 2002, and most of these alterations become evident only after puberty Weinberger 1998, 2000). Treatment with classical and atypical antipsychotic drugs has been shown to reverse many of the abnormal behavioral and physiological changes associated with the NVHL (Goto and O'Donnell 2002;Le Pen and Moreau 2002;Lipska and Weinberger 1994), strengthening the notion that neural alterations in this model are relevant to schizophrenia pathophysiology.…”

mentioning

confidence: 99%

Post-Pubertal Disruption of Medial Prefrontal Cortical Dopamine–Glutamate Interactions in a Developmental Animal Model of Schizophrenia

Tseng

Lewis

Lipska³

et al. 2007

Biological Psychiatry

116

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Background-A neonatal ventral hippocampal lesion (NVHL) induces behavioral and physiological anomalies mimicking pathophysiological changes of schizophrenia. Because prefrontal cortical (PFC) pyramidal neurons recorded from adult NVHL rats exhibit abnormal responses to activation of the mesocortical dopaminergic (DA) system, we explored whether these changes are due to an altered DA modulation of pyramidal neurons.

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Neonatal Damage of the Ventral Hippocampus Impairs Working Memory in the Rat

Abstract: We investigated if a developmental lesion of the ventral

Cited by 195 publications

References 45 publications

BDNF in schizophrenia, depression and corresponding animal models

BDNF in schizophrenia, depression and corresponding animal models

Effect of Dopamine D3 Antagonists on PPI in DBA/2J Mice or PPI Deficit Induced by Neonatal Ventral Hippocampal Lesions in Rats

Post-Pubertal Disruption of Medial Prefrontal Cortical Dopamine–Glutamate Interactions in a Developmental Animal Model of Schizophrenia

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