Chronic clozapine treatment improves prenatal infection-induced working memory deficits without influencing adult hippocampal neurogenesis

Meyer, Urs; Knuesel, Irène; Nyffeler, Myriel; Feldon, Joram

doi:10.1007/s00213-009-1754-6

Cited by 86 publications

(31 citation statements)

References 78 publications

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“…Studies on similar animal models have revealed that OLZ performs promitotic activity [29], increases the number of newly formed cells in the hippocampus and SVZ [28,39] and prevents neuronal loss in this region [37]. Similar neurogenic effects are reported for other atypic neuroleptics like clozapine and risperidon [28,38,40,50], as well as antidepressants, for example fluoxetine [39,41].…”

Section: Discussionmentioning

confidence: 60%

Effects of neuroleptics administration on adult neurogenesis in the rat hypothalamus

Rojczyk

Pałasz

Wiaderkiewicz

2015

Pharmacological Reports

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Section: Discussionmentioning

confidence: 60%

Effects of neuroleptics administration on adult neurogenesis in the rat hypothalamus

Rojczyk

Pałasz

Wiaderkiewicz

2015

Pharmacological Reports

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“…Since a role of PLs in axonal growth and sprouting is suggested by studies showing synthesis of PC, PE, and SM within axons (46,47), PL changes after injury in the hippocampi may be associated with self-reparative processes. As the hippocampus is a key site for neurogenesis (48,49), it is also possible that an increase in PLs within the hippocampi of injured mice is due to increased neurogenesis (50). Clearly, these Figure 9.…”

Section: Discussionmentioning

confidence: 99%

Lipidomic analyses identify injury‐specific phospholipid changes 3 mo after traumatic brain injury

et al. 2014

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Phospholipid (PL) abnormalities are observed in the cerebrospinal fluid of patients with traumatic brain injury (TBI), suggesting their role in TBI pathology. Therefore, PL levels were examined in a TBI mouse model that received 1.8 mm deep controlled cortical impact injury or craniectomy only (control). The rotarod and Barnes maze acquisition and probe tests were performed within 2 wk after injury, with another probe test performed 3 mo postinjury. Liquid chromatography/mass spectrometry analyses were performed on lipid extracts from several brain regions and plasma from injured and control mice collected at 3 mo postinjury. Compared to controls, injured mice with sensorimotor and learning deficits had decreased levels of cortical and cerebellar phosphatidylcholine (PC) and phosphatidylethanolamine (PE) levels, while hippocampal PC, sphingomyelin and PE levels were elevated. Ether PE levels were lower in the cortices and plasma of injured animals. Polyunsaturated fatty acid-containing PC and PE species, particularly ratios of docosahexaenoic acid (DHA) to arachidonic acid, were lower in the hippocampi and cortices and plasma of injured mice. Given the importance of DHA in maintaining neuronal function and resolving inflammation and of peroxisomes in synthesis of ether PLs, normalizing these PLs may be a useful strategy for treating the chronic pathology of TBI.-Abdullah, L., Evans, J. E., Ferguson, S., Mouzon, B., Montague, H., Reed, J., Crynen, G., Emmerich, T., Crocker, M., Pelot, R., Mullan, M., Crawford, F. Lipidomic analyses identify injury-specific phospholipid changes 3 months after traumatic brain injury. FASEB J. 28, 5311-5321 (2014). www.fasebj.org Key Words: controlled cortical impact ⅐ mass spectrometry ⅐ phosphatidylcholine ⅐ phosphatidylethanolamine ⅐ phosphatidylinositol ⅐ sphingomyelin Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in the United States among adults from both the civilian and military populations. Due to the improvements made in military body armor and combat helmets over the past 2 decades, the rate of severe TBI associated with Iraq and Afghanistan deployments has decreased to 1% of the total TBI sustained by military personnel, a rate that is lower than those reported for previous deployments (1-3). Estimates from the U.S. Centers for Disease Control and Prevention suggest that severe TBI remains an important issue in the civilian population. In 2010, 2.5 million admissions to emergency departments were due to TBI (4) contributing to about a third of injury related deaths in the United States. The annual U.S. costs associated with TBI are estimated to be $75 billion, largely attributed to medical care, loss of productivity, and long-term disability (5). Although mild TBI occurs more frequently than severe TBI, the latter has the largest adverse effect on the activities of daily living of injured individuals and accounts for 90% of the total TBI-related medical costs (5). The primary injury is caused by the immediate force of the trauma a...

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“…However haloperidol had no effect on neurogenesis in the adult dentate gyrus in several studies, using several doses and treatment regimens and examining long-term survival of new neurons as well as their generation (Halim et al, 2004;Malberg et al, 2000;Wakade et al, 2002;Wang et al, 2004). Similarly, atypical antipsychotics like olanzapine, risperidone, and clozapine were also ineffective at altering adult neurogenesis in several studies (Green et al, 2006;Meyer et al, 2010;Wakade et al, 2002;Wang et al, 2004). One study demonstrated an increase in proliferation with clozapine treatment, but the new cells were lost within 3 weeks, likely before becoming functional, despite ongoing clozapine treatment (Halim et al, 2004).…”

Section: Schizophreniamentioning

confidence: 99%

Adult Neurogenesis and Mental Illness

Schoenfeld

Cameron

2014

Neuropsychopharmacol

162

108

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Several lines of evidence suggest that adult neurogenesis, the production of new neurons in adulthood, may play a role in psychiatric disorders, including depression, anxiety, and schizophrenia. Medications and other treatments for mental disorders often promote the proliferation of new neurons; the time course for maturation and integration of new neurons in circuitry parallels the delayed efficacy of psychiatric therapies; adverse and beneficial experiences similarly affect development of mental illness and neurogenesis; and ablation of new neurons in adulthood alters the behavioral impact of drugs in animal models. At present, the links between adult neurogenesis and depression seem stronger than those suggesting a relationship between new neurons and anxiety or schizophrenia. Yet, even in the case of depression there is currently no direct evidence for a causative role. This article reviews the data relating adult neurogenesis to mental illness and discusses where research needs to head in the future.

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Chronic clozapine treatment improves prenatal infection-induced working memory deficits without influencing adult hippocampal neurogenesis

Cited by 86 publications

References 78 publications

Effects of neuroleptics administration on adult neurogenesis in the rat hypothalamus

Effects of neuroleptics administration on adult neurogenesis in the rat hypothalamus

Lipidomic analyses identify injury‐specific phospholipid changes 3 mo after traumatic brain injury

Adult Neurogenesis and Mental Illness

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