Immunohistochemistry of CD38 in Different Cell Types in the Hypothalamus and Pituitary of Male Mice

Akimoto, Nozomi; Kamiyama, Yuko; Yamafuji, Megumi; Fujita, Kyota; Seike, Toshihiro; Kido, Mizuho A.; Yokoyama, Shigeru; Higashida, Haruhiro; Нода, Мами

doi:10.1166/msr.2013.1021

Cited by 8 publications

(8 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While we could not detect CD38 expression in microglia in the postnatal periods examined here, this is not surprising. CD38 is known to be induced in response to microglial activation in pathological conditions, such as brain inflammation, which may not be the case in the developing brain (Akimoto et al, ; Ma et al, ; Mayo et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…In the brain, CD38 expression has been observed not only in oxytocin neurons but also in glial cells, including astrocytes and microglia (Akimoto et al, ; Kou et al, ; Yamada, Mizuguchi, Otsuka, Ikeda, & Takahashi ). Ultrastructural analysis using adult rat brain demonstrated that CD38 immunoreactivity was found in a subset of pyramidal neurons and astrocytes, but not in microglia or oligodendrocytes (OLs) in the physiological condition (Yamada et al, ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

CD38 positively regulates postnatal development of astrocytes cell-autonomously and oligodendrocytes non-cell-autonomously

Hattori

Kaji

Ishii

et al. 2017

Glia

Self Cite

View full text Add to dashboard Cite

Glial development is critical for the function of the central nervous system. CD38 is a multifunctional molecule with ADP-ribosyl cyclase activity. While critical roles of CD38 in the adult brain such as oxytocin release and social behavior have been reported, those in the developing brain remain largely unknown. Here we demonstrate that deletion of Cd38 leads to impaired development of astrocytes and oligodendrocytes in mice. CD38 is highly expressed in the developing brains between postnatal day 14 (P14) and day 28 (P28). In situ hybridization and FACS analysis revealed that CD38 is expressed predominantly in astrocytes in these periods. Analyses of the cortex of Cd38 knockout (Cd38 ) mice revealed delayed development of astrocytes and subsequently delayed differentiation of oligodendrocytes (OLs) at postnatal stages. In vitro experiments using primary OL cultures, mixed glial cultures, and astrocytic conditioned medium showed that astrocytic CD38 regulates the development of astrocytes in a cell-autonomous manner and the differentiation of OLs in a non-cell-autonomous manner. Further experiments revealed that connexin43 (Cx43) in astrocytes plays a promotive role for CD38-mediated OL differentiation. Finally, increased levels of NAD , caused by CD38 deficiency, are likely to be responsible for the suppression of astrocytic Cx43 expression and OL differentiation. Our data indicate that CD38 is a positive regulator of astrocyte and OL development.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

CD38 positively regulates postnatal development of astrocytes cell-autonomously and oligodendrocytes non-cell-autonomously

Hattori

Kaji

Ishii

et al. 2017

Glia

Self Cite

View full text Add to dashboard Cite

show abstract

“…Subsequently, the sections were washed with PBS containing 0.3% TritonX-100 and coverslipped with anti-fade (Akimoto et al, 2013). Imaging was performed using an Olympus IX71 microscope.…”

Section: Methodsmentioning

confidence: 99%

Anxiety- and depression-like behavior in mice lacking the CD157/BST1 gene, a risk factor for Parkinson's disease

Lopatina

Yoshihara

Nishimura

et al. 2014

Front. Behav. Neurosci.

Self Cite

127

View full text Add to dashboard Cite

CD157, known as bone marrow stromal cell antigen-1, is a glycosylphosphatidylinositol-anchored ADP-ribosyl cyclase that supports the survival and function of B-lymphocytes and hematopoietic or intestinal stem cells. Although CD157/Bst1 is a risk locus in Parkinson's disease (PD), little is known about the function of CD157 in the nervous system and contribution to PD progression. Here, we show that no apparent motor dysfunction was observed in young knockout (CD157−/−) male mice under less aging-related effects on behaviors. CD157−/− mice exhibited anxiety-related and depression-like behaviors compared with wild-type mice. These behaviors were rescued through treatment with anti-psychiatric drugs and oxytocin. CD157 was weakly expressed in the amygdala and c-Fos immunoreactivity in the amygdala was less evident in CD157−/− mice than in wild-type mice. These results demonstrate for the first time that CD157 plays a role as a neuro-regulator and suggest a potential role in pre-motor symptoms in PD.

show abstract

“…In conclusion, it is clear that CD38 plays pivotal roles under neuronal physiological as well as pathophysiological conditions (Malavasi et al, 2008;Rah et al, 2012;Higashida, et al, 2012aAkimoto et al, 2013). DNA manipulation of CD38 and cADPR in the mAChR-signal cascade in NG108-15 cells revealed that CD38 has great impact on M-current inhibition.…”

Section: Discussionmentioning

confidence: 86%

Acetylcholine-Induced M/KCNQ Current Inhibition is Regulated by CD38 and A-Kinase Anchoring Protein in Neuroblastoma Cells

et al. 2013

Self Cite

View full text Add to dashboard Cite

The CD38 membrane protein exhibits multifunctional activities: ADP-ribosyl cyclase, cyclic ADP-ribose hydrolase, NAD + glycohydrolase, formation of nicotinic acid adenine dinucleotide phosphate (NAADP + by base exchange and degradation of NAADP + to 2 -phospho-ADP-ribose. The intermediate product of ADP-ribosyl cyclase of CD38 is cyclic ADP-ribose (cADPR). The role of cADPR as a second messenger in neurons is not completely understood. The present study was performed to determine whether cADPR plays a role as a second messenger as a downstream component of muscarinic acetylcholine receptor (mAChR) signaling in neuronal cells. We performed electrophysiology experiments on non-inactivating voltage-dependent potassium M-like currents, which are currently defined as currents due to KCNQ 2/3 or Kv 7.2/7.3 potassium channels. We first examined NG108-15 neuroblastoma × glioma hybrid cells expressing both m1 mAChRs and human CD38. ACh-evoked inhibition of the M-like current was significantly enhanced in CD38-transformed cells compared to control cells. ACh-induced inhibition was greater in the (KCNQ) components with faster kinetics in M-like currents than another (HERG) component with a slow decay time constant. The CD38-enhanced M-like current inhibition was decreased in the presence of 8-bromo-cADPR. Although overexpression of A-kinase anchoring protein (AKAP) did not interfere with AChinduced inhibition, alternative expression of mutant AKAP lacking the protein kinase C binding domain reduced ACh-induced M-like current inhibition in transformed NG108-15 cells with CD38 and mAChRs. These results indicate that overexpression and deletion of CD38 modulate M-current inhibition by ACh, and suggest that CD38 and cADPR are located downstream of mAChRs and upstream of AKAP-involved protein kinase C-induced inhibition of Kv 7.2 channels in the mAChR signaling cascade.

show abstract

Immunohistochemistry of CD38 in Different Cell Types in the Hypothalamus and Pituitary of Male Mice

Cited by 8 publications

References 54 publications

CD38 positively regulates postnatal development of astrocytes cell-autonomously and oligodendrocytes non-cell-autonomously

CD38 positively regulates postnatal development of astrocytes cell-autonomously and oligodendrocytes non-cell-autonomously

Anxiety- and depression-like behavior in mice lacking the CD157/BST1 gene, a risk factor for Parkinson's disease

Acetylcholine-Induced M/KCNQ Current Inhibition is Regulated by CD38 and A-Kinase Anchoring Protein in Neuroblastoma Cells

Contact Info

Product

Resources

About