Analysis of expression of cholecystokinin in dopamine cells in the ventral mesencephalon of several species and in humans with schizophrenia.

Schalling, Martin; Friberg, Kristina; Seroogy, Kim B.; Riederer, Peter; Bird, E. D.; Schiffmann, Serge N.; Mailleux, Pierre; Vanderhaeghen, Jean‐Jacques; Kuga, Shigeki; Goldstein, Menek

doi:10.1073/pnas.87.21.8427

Cited by 57 publications

(27 citation statements)

References 35 publications

(42 reference statements)

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“…The dopaminergic neurons induced by SDIA were CCK-negative (positive in A10 neuron; ref. 17) and GAD-negative (positive in olfactory bulb dopaminergic neurons; ref. 18) (Fig.…”

Section: Resultsmentioning

confidence: 99%

Generation of dopaminergic neurons and pigmented epithelia from primate ES cells by stromal cell-derived inducing activity

Kawasaki

Suemori

Mizuseki

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

445

302

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We previously identified a stromal cell-derived inducing activity (SDIA), which induces differentiation of neural cells, including midbrain tyrosine hydroxylase-positive (TH ؉ ) dopaminergic neurons, from mouse embryonic stem cells. We report here that SDIA induces efficient neural differentiation also in primate embryonic stem cells. Induced neurons contain TH ؉ neurons at a frequency of 35% and produce a significant amount of dopamine. Interestingly, differentiation of TH ؉ neurons from undifferentiated embryonic cells occurs much faster in vitro (10 days) than it does in the embryo (Ϸ5 weeks). In addition, 8% of the colonies contain large patches of Pax6 ؉ -pigmented epithelium of the retina. The SDIA method provides an unlimited source of primate cells for the study of pathogenesis, drug development, and transplantation in degenerative diseases such as Parkinson's disease and retinitis pigmentosa.

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“…The dopaminergic neurons induced by SDIA were CCK-negative (positive in A10 neuron; ref. 17) and GAD-negative (positive in olfactory bulb dopaminergic neurons; ref. 18) (Fig.…”

Section: Resultsmentioning

confidence: 99%

Generation of dopaminergic neurons and pigmented epithelia from primate ES cells by stromal cell-derived inducing activity

Kawasaki

Suemori

Mizuseki

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

445

302

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“…CCK ( The specificity of these oligonucleotides has been described in detail elsewhere (Kononen et al 1995;Schalling et al 1990). All in situ hybridization experiments were carried out as previously described in detail (Kresse et al 1995), and all sections were run in the same experiment under identical conditions.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

“…All brains were cut in five parallel series (20 m, coronal sections), with every fifth section being thawmounted on the same glass slide. Sections were stored at Ϫ 20 Њ C until use.The following oligonucleotide DNA probes were used for in situ hybridization.CCK ( The specificity of these oligonucleotides has been described in detail elsewhere (Kononen et al 1995;Schalling et al 1990). All in situ hybridization experiments were carried out as previously described in detail (Kresse et al 1995), and all sections were run in the same experiment under identical conditions.…”

mentioning

confidence: 99%

Long-Term Repetitive Transcranial Magnetic Stimulation Increases the Expression of Brain-Derived Neurotrophic Factor and Cholecystokinin mRNA, but not Neuropeptide Tyrosine mRNA in Specific Areas of Rat Brain

Müller

Toschi

Kresse

et al. 2000

Neuropsychopharmacology

252

107

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Repetitive transcranial magnetic stimulation (rTMS) is increasingly used as a therapeutic tool in various neurological and psychiatric disorders, and we recently found that it has a neuroprotective effect both in vitro andTranscranial magnetic stimulation (TMS), a technique in which a time-varying strong electric current is applied through a coil held in direct contact with the subject's head, was originally developed for diagnostic use in neurology (for review see Rossini and Rossi 1998). A possible effect of TMS on mood was first reported in 1987 (Bickford et al. 1987) and, although discussed controversially, to date several lines of evidence resulting from both preclinical (Fleischmann et al. 1995;Zyss et al. 1997) and clinical (e.g., Pascual-Leone et al. 1996) studies support the notion that repetitive TMS (rTMS) may have antidepressant properties: rTMS induces transient enhancement of mood in healthy subjects, and daily application alleviates symptoms in patients suffering from treatment-resistant major depression (for review see George et al. 1999).Although rTMS is currently being evaluated as a possible alternative or add-on therapy in the treatment of refractory depression, knowledge concerning its effects at the molecular and cellular level is still very limited. Recently, Ji et al. (1998) reported a specific activation of brain regions in terms of immediate early gene expression in rats in response to rTMS. In addition, we provided a first evidence for a neuroprotective effect of long-term rTMS in vivo and in vitro (Post et al. 1999). The in vitro studies showed that magnetic stimulation analogous to TMS increased the overall viability of mouse monoclonal hippocampal HT22 cells and had a neuroprotective effect against oxidative stressors such as amyloid beta (A ␤ ) and glutamate. Moreover, the treatment increased the release of the potentially neuroprotective secreted amyloid precursor protein (sAPP) into the supernatant of HT22 cells and into cerebrospinal fluid from rats. Accordingly, HT22 cells preincubated with cerebrospinal fluid from long-term rTMStreated rats were found to be protected against A ␤ (Post et al. 1999). However, the neurochemical mechanisms underlying these neuroprotective properties as well as the putative therapeutic effects of rTMS in neurological and psychiatric disorders still remain to be elucidated.Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family and is abundantly expressed in the adult brain. The neurotrophic and also neuroprotective effects of BDNF have been characterized extensively both in vitro and in vivo. In addition, upregulation of BDNF has been implicated in neuronal responses to various kinds of injuries, such as epileptic seizures, cerebral ischemia, and hypoglycemia (for review see Connor and Dragunow 1998). Recent work raised the possibility that one of the many long-term effects of antidepressant treatment may be regulation of neurotrophins: antidepressant drug treatment and electroconvulsive seizures (ECS) were shown to marke...

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“…This has led to speculation that CCK may play a role in the pathophysiology of schizophrenia (Nemeroff and Bissette 1992;Nair et al 1986). Support for this has come from studies showing significantly lower CCK levels in the cerebrospinal fluid (Beinfeld and Garver 1991;Verbanck et al 1984) and postmortem brains (Schalling et al 1990) of drugfree schizophrenia patients as compared to matched controls.…”

mentioning

confidence: 99%

Antipsychotic Potential of CCK-Based Treatments: An Assessment Using the Prepulse Inhibition Model of Psychosis

Feifel

Reza

Robeck

1999

Neuropsychopharmacology

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Analysis of expression of cholecystokinin in dopamine cells in the ventral mesencephalon of several species and in humans with schizophrenia.

Cited by 57 publications

References 35 publications

Generation of dopaminergic neurons and pigmented epithelia from primate ES cells by stromal cell-derived inducing activity

Generation of dopaminergic neurons and pigmented epithelia from primate ES cells by stromal cell-derived inducing activity

Long-Term Repetitive Transcranial Magnetic Stimulation Increases the Expression of Brain-Derived Neurotrophic Factor and Cholecystokinin mRNA, but not Neuropeptide Tyrosine mRNA in Specific Areas of Rat Brain

Antipsychotic Potential of CCK-Based Treatments: An Assessment Using the Prepulse Inhibition Model of Psychosis

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