Hippocampal volume and cell proliferation after acute and chronic clozapine or haloperidol treatment

Schmitt, Andrea; Weber, Silja; Jatzko, Alexander; Braus, Dieter F.; Henn, Fritz A.

doi:10.1007/s00702-003-0070-2

Cited by 52 publications

(37 citation statements)

References 47 publications

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“…In fact, such progenic effect was previously observed after only long-term (2 to 3 weeks) treatment with various ADs including fluoxetine (Malberg et al, 2000;Santarelli et al, 2003;Malberg and Duman, 2003;Mnie-Filali et al, 2007b). To our knowledge, only non-selective 5-HT 7 receptors antagonists (such as atypical neuroleptics risperidone or clozapine) were used to assess the effects on hippocampal cell proliferation but the results were not conclusive (Halim et al, 2004;Kodama et al, 2004;Schmitt et al, 2004). Also, Sarkisyan and Hedlund (2009) reported that the rate of cell proliferation in the DG was identical in 5-HT 7 receptor wild-type and knock-out mice even if such mice present antidepressant-like phenotypes (Guscott et al, 2005;Hedlund et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Pharmacological Blockade of 5-HT7 Receptors as a Putative Fast Acting Antidepressant Strategy

Mnie-Filali

Faure

Lambás‐Señas

et al. 2011

Neuropsychopharmacol

128

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Current antidepressants still display unsatisfactory efficacy and a delayed onset of therapeutic action. Here we show that the pharmacological blockade of serotonin 7 (5-HT 7 ) receptors produced a faster antidepressant-like response than the commonly prescribed antidepressant fluoxetine. In the rat, the selective 5-HT 7 receptor antagonist SB-269970 counteracted the anxiogenic-like effect of fluoxetine in the open field and exerted an antidepressant-like effect in the forced swim test. In vivo, 5-HT 7 receptors negatively regulate the firing activity of dorsal raphe 5-HT neurons and become desensitized after long-term administration of fluoxetine. In contrast with fluoxetine, a 1-week treatment with SB-269970 did not alter 5-HT firing activity but desensitized cell body 5-HT autoreceptors, enhanced the hippocampal cell proliferation, and counteracted the depressive-like behavior in olfactory bulbectomized rats. Finally, unlike fluoxetine, early-life administration of SB-269970, did not induce anxious/depressive-like behaviors in adulthood. Together, these findings indicate that the 5-HT 7 receptor antagonists may represent a new class of antidepressants with faster therapeutic action.

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Section: Discussionmentioning

confidence: 99%

Pharmacological Blockade of 5-HT7 Receptors as a Putative Fast Acting Antidepressant Strategy

Mnie-Filali

Faure

Lambás‐Señas

et al. 2011

Neuropsychopharmacol

128

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“…Animals were treated with daily intramuscular injections of haloperidol dissolved in Dimethyl sulfoxide (DMSO) (Fisher Scientific, Fair Lawn, NJ, USA) (1mg/kg/day, n=11), or vehicle (DMSO) (n=11) for 28 days (Halim et al, 2004, Schmitt et al, 2004, Spurney et al, 1999. Twenty-four hours after the last injection, the animals were sacrificed and brains were immediately removed, dissected, and frozen in isopentane.…”

Section: Acquisition and Processing Of Rodent Brain Tissuementioning

confidence: 99%

Cortical expression of glial fibrillary acidic protein and glutamine synthetase is decreased in schizophrenia

Steffek¹,

McCullumsmith²,

Haroutunian³

et al. 2008

Schizophrenia Research

110

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Altered expression of structural and functional molecules expressed by astrocytes may play a role in the pathophysiology of schizophrenia. We investigated the hypothesis that the astrocytic enzyme glutamine synthetase, involved in maintaining the glutamate-glutamine cycle, and the cytoskeletal molecule glial fibrillary acidic protein (GFAP) are abnormally expressed in schizophrenia. We used Western blot analysis to measure levels of glutamine synthetase and GFAP in several brain regions of subjects with schizophrenia and a comparison group. We found that glutamine synthetase protein expression was significantly decreased in the superior temporal gyrus, and both glutamine synthetase and GFAP were significantly reduced in the anterior cingulate cortex in schizophrenia. Neither molecule demonstrated altered expression in the dorsolateral prefrontal cortex, primary visual cortex, or hippocampus. Chronic treatment with haloperidol did not alter the expression of these molecules in the rat brain, suggesting that our findings are not due to a medication effect. These data support an astrocytic component to the pathophysiology of schizophrenia and suggest that astrocytic molecules involved in enzymatic activity and cytoskeletal integrity may have a role in disease-related abnormalities in this illness.

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“…Antidepressant drugs enhance neurogenesis in the adult rodent dentate gyrus of the hippocampus (Malberg et al, 2000;Duman et al, 2001;Santarelli et al, 2003), and animal models of depression are associated with decreased neurogenesis in the same brain structure (Malberg and Duman, 2003;Santarelli et al, 2003). Several studies have investigated the effects of antipsychotic drug on cell genesis in a number of brain regions; however, these studies have reported inconsistent findings (Dawirs et al, 1998;Wakade et al, 2002;Halim et al, 2004;Schmitt et al, 2004;Wang et al, 2004). This failure to establish a clear link between antipsychotic drug administration and cell genesis is likely attributable to not only administration of different antipsychotic drugs but also to the use of different protocols to detect cell genesis that are sensitive to mixed or different populations of proliferating and maturing cell types.…”

Section: Introductionmentioning

confidence: 98%

Dopamine Specifically Inhibits Forebrain Neural Stem Cell Proliferation, Suggesting a Novel Effect of Antipsychotic Drugs

Kippin

Kapur²,

Kooy³

2005

Journal of Neuroscience

188

129

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Neurogenesis has been implicated in antidepressant drug action and animal models of depression, suggesting that proliferating cells play a role in psychiatric disorders. Similar studies using antipsychotic drugs have yielded conflicting results, perhaps because of the lack of focus on specific cell types. We examine the effect of haloperidol on neural stem cells (NSCs), the ultimate precursors for adult cell genesis. We show that haloperidol increases NSC numbers, resulting in more progenitors and more new neurons and glia in the adult rat brain. The increase in NSCs by haloperidol is dependent on central dopamine D 2 receptors, and these receptors are expressed by NSCs. D 2 receptor stimulation in vitro inhibits NSC proliferation, which is reversed by haloperidol. Thus, haloperidol increases adult mammalian brain proliferation by antagonizing dopamine at D 2 receptors on NSCs. These findings demonstrate a direct link between neural activity and NSC proliferation and implicate cell genesis in antipsychotic drug effects.

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Hippocampal volume and cell proliferation after acute and chronic clozapine or haloperidol treatment

Cited by 52 publications

References 47 publications

Pharmacological Blockade of 5-HT7 Receptors as a Putative Fast Acting Antidepressant Strategy

Pharmacological Blockade of 5-HT7 Receptors as a Putative Fast Acting Antidepressant Strategy

Cortical expression of glial fibrillary acidic protein and glutamine synthetase is decreased in schizophrenia

Dopamine Specifically Inhibits Forebrain Neural Stem Cell Proliferation, Suggesting a Novel Effect of Antipsychotic Drugs

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