Mapping of cholecystokinin transcription in transgenic mouse brain using <i>Escherichia coli β‐galactosidase</i> reporter gene

Itoh, Yoshio; Kozakai, Ikuo; Toyomizu, Masaaki; Ishibashi, Teru; Kuwano, Ryozo

doi:10.1046/j.1440-169x.1998.t01-2-00004.x

Cited by 7 publications

(3 citation statements)

References 39 publications

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“…Many regions known to express CCK mRNA and protein prenatally and postnatally (Cho et al, 1983;Itoh et al, 1998) were indeed positive at E14.5 and E17.5; hybridization signals were detected over cells in the hippocampus, forebrain, thalamus, ventromedial hypothalamic nucleus, and pituitary, and in the enteric nervous system (data not shown); however, no signal was detected in nasal regions. In taste receptors (Herness et al, 2002), robust CCK peptide expression has been documented, yet CCK mRNA expression levels were very low (detectable only after two rounds of RT-PCR).…”

Section: Cck Expression In the Developing Olfactory Systemmentioning

confidence: 90%

Cholecystokinin Modulates Migration of Gonadotropin-Releasing Hormone-1 Neurons

Giacobini

Kopin

Beart³

et al. 2004

J. Neurosci.

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Expression of the brain-gut peptide cholecystokinin (CCK) in the developing olfactory-gonadotropin-releasing hormone-1 (GnRH-1) neuroendocrine systems was characterized, and the function of CCK in these systems was analyzed both in vivo and in vitro. We present novel data demonstrating that CCK transcript and protein are expressed in sensory cells in the developing olfactory epithelium and vomeronasal organ, with both ligand and receptors (CCK-1R and CCK-2R) found on olfactory axons throughout prenatal development. In addition, migrating GnRH-1 neurons in nasal regions express CCK-1R but not CCK-2R receptors. The role of CCK in olfactory-GnRH-1 system development was evaluated using nasal explants, after assessing that the in vivo expression of both CCK and CCK receptors was mimicked in this in vitro model. Exogenous application of CCK (10-7 M) reduced both olfactory axon outgrowth and migration of GnRH-1 cells. This inhibition was mediated by CCK-1R receptors. Moreover, CCK-1R but not CCK-2R antagonism caused a shift in the location of GnRH-1 neurons, increasing the distance that the cells migrated. GnRH-1 neuronal migration in mice carrying a genetic deletion of either CCK-1R or CCK-2R receptor genes was also analyzed. At embryonic day 14.5, the total number of GnRH-1 cells was identical in wild-type and mutant mice; however, the number of GnRH-1 neurons within forebrain was significantly greater in CCK-1R Ϫ/Ϫ embryos, consistent with an accelerated migratory process. These results indicate that CCK provides an inhibitory influence on GnRH-1 neuronal migration, contributing to the appropriate entrance of these neuroendocrine cells into the brain, and thus represent the first report of a developmental role for CCK.

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Section: Cck Expression In the Developing Olfactory Systemmentioning

confidence: 90%

Cholecystokinin Modulates Migration of Gonadotropin-Releasing Hormone-1 Neurons

Giacobini

Kopin

Beart³

et al. 2004

J. Neurosci.

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“…In addition to rat, we have also observed taste receptor cells displaying cholecystokinin-like immunoreactivity in posterior fields of hamster and rabbit (our unpublished observations), suggesting that the distribution of the peptide may be common among mammalian taste buds. Interestingly, in a report of a transgenic mouse line produced using the CCK promoter with ␤-galactosidase as a reporter gene, a preliminary note of the expression of CCK-lacZ transgene in taste buds was mentioned (Itoh et al, 1998). In contrast, CCK immunoreactivity was observed in basal but not taste receptor cells in the mudpuppy (Welton et al, 1992).…”

Section: Expression Patterns Of Cck and Cck Mrnamentioning

confidence: 99%

Expression and Physiological Actions of Cholecystokinin in Rat Taste Receptor Cells

Herness

Zhao²,

Lu³

et al. 2002

J. Neurosci.

105

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Gustatory perception arises not only from intracellular transduction cascades within taste receptor cells but also from cell-to-cell communication among the cells of the taste bud. This study presents novel data demonstrating that the brain-gut peptide cholecystokinin (CCK) is expressed in subsets of taste receptor cells, and that it may play a signaling role unknown previously within the taste bud. Immunocytochemistry revealed positively stained subsets of cells within taste buds throughout the oral cavity. These cells typically displayed round nuclei with full processes, similar to those classified as light cells. Peptide expression was verified using nested PCR on template cDNA derived from mRNA extracted from isolated posterior taste buds. Multiple physiological actions of cholecystokinin on taste receptor cells were observed. An outward potassium current, recorded with the patch-clamp technique, was inhibited by exogenous application of sulfated cholecystokinin octapeptide in a reversible and concentration-dependent manner. Pharmacological analysis suggests that this inhibition is mediated by CCK-A receptors and involves PKC phosphorylation. An inwardly rectifying potassium current, typically invariant to stimulation, was also inhibited by cholecystokinin. Additionally, exogenous cholecystokinin was effective in elevating intracellular calcium as measured by ratiometric techniques with the calcium-sensitive dye fura-2. Pharmacology similarly demonstrated that these calcium elevations were mediated by CCK-A receptors and were dependent on intracellular calcium stores. Collectively, these observations suggest a newly discovered role for peptide neuromodulation in the peripheral processing of taste information.

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“…Before 2019, Escherichia coli (E. coli) among the intestinal flora was a hot research topic in the field. In 1998, researchers used the E. coli β-galactosidase reporter gene to localize cholecystokinin transcripts in the brains of transgenic TBI mice (Itoh et al, 1998), and this was the first time E. coli entered the arena of TBI-related research as a primary subject of study. In the following 20 years, studies on the relationship between TBI and E. coli gradually increased, mainly focusing on the pathogenic mechanism of E. coli in TBI (Unzicker et al, 2011), the regulatory effect of interventions on E. coli in individuals with TBI (Watanabe et al, 2004), and the changes of E. coli after TBI (Patel et al, 2016).…”

Section: Research Trends and Hot Spots Of "Intestinal Microbiota And ...mentioning

confidence: 99%

Emerging trends and focus of research on the relationship between traumatic brain injury and gut microbiota: a visualized study

Du,

Li,

Liao

et al. 2023

Front. Microbiol.

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BackgroundTraumatic brain injury (TBI) is one of the most serious types of trauma and imposes a heavy social and economic burden on healthcare systems worldwide. The development of emerging biotechnologies is uncovering the relationship between TBI and gut flora, and gut flora as a potential intervention target is of increasing interest to researchers. Nevertheless, there is a paucity of research employing bibliometric methodologies to scrutinize the interrelation between these two. Therefore, this study visualized the relationship between TBI and gut flora based on bibliometric methods to reveal research trends and hotspots in the field. The ultimate objective is to catalyze progress in the preclinical and clinical evolution of strategies for treating and managing TBI.MethodsTerms related to TBI and gut microbiota were combined to search the Scopus database for relevant documents from inception to February 2023. Visual analysis was performed using CiteSpace and VOSviewer.ResultsFrom September 1972 to February 2023, 2,957 documents published from 98 countries or regions were analyzed. The number of published studies on the relationship between TBI and gut flora has risen exponentially, with the United States, China, and the United Kingdom being representative of countries publishing in related fields. Research has formed strong collaborations around highly productive authors, but there is a relative lack of international cooperation. Research in this area is mainly published in high-impact journals in the field of neurology. The “intestinal microbiota and its metabolites,” “interventions,” “mechanism of action” and “other diseases associated with traumatic brain injury” are the most promising and valuable research sites. Targeting the gut flora to elucidate the mechanisms for the development of the course of TBI and to develop precisely targeted interventions and clinical management of TBI comorbidities are of great significant research direction and of interest to researchers.ConclusionThe findings suggest that close attention should be paid to the relationship between gut microbiota and TBI, especially the interaction, potential mechanisms, development of emerging interventions, and treatment of TBI comorbidities. Further investigation is needed to understand the causal relationship between gut flora and TBI and its specific mechanisms, especially the “brain-gut microbial axis.”

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Mapping of cholecystokinin transcription in transgenic mouse brain using Escherichia coli β‐galactosidase reporter gene

Cited by 7 publications

References 39 publications

Cholecystokinin Modulates Migration of Gonadotropin-Releasing Hormone-1 Neurons

Cholecystokinin Modulates Migration of Gonadotropin-Releasing Hormone-1 Neurons

Expression and Physiological Actions of Cholecystokinin in Rat Taste Receptor Cells

Emerging trends and focus of research on the relationship between traumatic brain injury and gut microbiota: a visualized study

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