Distribution and local differentiation of mast cells in the parenchyma of the forebrain

Zhuang, Xiaoxi; Silverman, Ann‐Judith; Silver, Rae

doi:10.1002/(sici)1096-9861(19990614)408:4<477::aid-cne3>3.0.co;2-o

Cited by 47 publications

(36 citation statements)

References 71 publications

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“…Immature mast cells enter the tissues, where they differentiate, taking on phenotypic features (predominance of heparin-containing or serotoninergic granules, predominant expression of some proteases, etc.) dependent on tissue type (20). In aggregate, these data suggest that mast cells may mediate the deleterious effects of IL-9 on the neonatal brain.…”

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confidence: 64%

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Deleterious Effects of IL-9–Activated Mast Cells and Neuroprotection by Antihistamine Drugs in the Developing Mouse Brain

et al. 2001

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Elevated mean IL-9 serum levels have been observed in human neonates who will later develop cerebral palsy. In earlier studies, using a newborn mouse model of excitotoxic lesions mimicking those described in human cerebral palsy, we found that IL-9 pretreatment exacerbated brain damage produced by intracerebral injections of the glutamatergic analog ibotenate. Among its different cell targets, the Th2 cytokine IL-9 is a mast cell growth and differentiation factor that can cause mast cells to release various substances including histamine. In the present study, we sought to determine whether the deleterious effects of IL-9 in our mouse model were mediated by mast cells through histamine release. All mouse pups were pretreated with intraperitoneal injections of IL-9 or saline between postnatal days (P) P1 and P5. Immunohistochemistry for murine mast cell protease-1 performed on P5 showed an increased density of labeled cells in the neopallium of IL-9 -treated Swiss pups as compared with controls. Western blot analysis confirmed the increased murine mast cell protease-1 brain content of IL-9 -treated Swiss mice. IL-9 pretreatment had no significant effect on ibotenateinduced excitotoxic brain lesions in mast cell-deficient P5 pups (WBB6F1/J kit W/W-v ), whereas IL-9 exacerbated these lesions in the control littermates with normal mast cell populations. Finally, cromoglycate or antihistamine drugs significantly reduced ibotenate-induced brain lesions in IL-9 -treated Swiss pups. Taken together, these data suggest that recruitment of cerebral mast cells with histamine release may contribute to the exacerbation of neonatal excitotoxic brain lesions produced by IL-9. Neuroprotective strategies targeting mast cells may be useful in some neonates at risk for cerebral palsy. (1-7). Recent hypotheses have implicated multiple preconceptional and prenatal factors, such as hypoxiaperfusion failure, genetic factors, growth factor deficiency, and excess production of cytokines. In a striking retrospective study, mean levels of perinatal circulating cytokines-including IL-1␤, IL-6, IL-8, IL-9, and TNF-␣-were higher in patients with subsequent occurrence of cerebral palsy than in control subjects (8).In that study, although the numbers of included patients were limited, levels of proinflammatory cytokines (IL-1-␤, IL-6, IL-8, and TNF-␣) were associated with one another, but no correlation was detected between IL-9 levels and the levels of the other cytokines tested. Although further studies will be necessary to confirm this initial observation, these data could suggest the existence of a subpopulation of cerebral palsy patients characterized by increased levels of circulating IL-9 at birth. A better understanding of the mechanisms bridging IL-9 blood level elevation and brain damage might open up new therapeutic possibilities for preventing cerebral palsy in infants with high circulating IL-9 levels.Intracerebral injection of ibotenate, a glutamate analog, to newborn mice produces histologic lesions mimicking the brain lesions f...

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confidence: 64%

“…Mast cells are present in the brain, including the neopallium, where their numbers increase during early postnatal development (13)(14)(15)(16)(17). Mast cells are derived from the pluripotent hematopoietic stem cells in the bone marrow.…”

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confidence: 99%

Deleterious Effects of IL-9–Activated Mast Cells and Neuroprotection by Antihistamine Drugs in the Developing Mouse Brain

et al. 2001

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“…Cell birth and survival were determined by the number of BrdU-IR cells present in the GCL two hours or four weeks after BrdU injection, respectively. To control for bioavailability of BrdU between genotypes, BrdU-IR cells within the medial habenula, putatively dividing mast cells (Zhuang et al, 1999), were also quantified (Mandyam et al, 2004, Donovan et al, 2006, Lagace et al, 2006. The habenula is non-neurogenic, unlike more commonly used control regions (e.g.…”

Section: Quantification Of Immunoreactive (Ir) and Apoptotic Cellsmentioning

confidence: 99%

Knockout of the mu opioid receptor enhances the survival of adult-generated hippocampal granule cell neurons

Harburg¹,

Hall²,

Harrist³

et al. 2007

Neuroscience

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Recent evidence suggests that mu opioid receptors (MOR) are key regulators of hippocampal structure and function. For example, exogenous MOR agonists morphine and heroin negatively impact hippocampal function and decrease adult hippocampal neurogenesis. Here we explored the role of MOR in the birth and survival of hippocampal progenitor cells by examining adult neurogenesis in mice that lack MOR. Adult male mice lacking exon 1 of MOR were injected with the S phase marker bromodeoxyuridine (BrdU) and sacrificed either two hours or four weeks later to evaluate proliferating and surviving BrdU-immunoreactive (IR) cells, respectively, in the adult hippocampal granule cell layer. WT, heterozygote, and homozygote mice did not differ in the number of BrdU-IR cells at a proliferation time point. However, four weeks after BrdU injection, heterozygote and homozygote mice had 57% and 54% more surviving BrdU-IR cells in the hippocampal granule cell layer as compared to WT mice. A decrease in apoptosis in the heterozygote and homozygote mice did not account for the difference in number of surviving BrdU-IR cells since there were no alterations in number of pyknotic, TUNEL-positive, or activated caspase 3-IR cells compared to WT. In concordance with the increased numbers of granule cells maturing into neurons, heterozygote and homozygote mice had larger hippocampal granule cell layers and increased numbers of granule cells. These findings indicate that MOR may play a role in regulating progenitor cell survival and more generally encourage further exploration of how MOR activation can influence hippocampal structure and function.

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“…This is a technique previously used by us and others, in both rats and doves, which ensures proper detection of mast cells in the brain (Zhuang, Silverman, and Silver, 1999;Wilhelm et al, 2000;Florenzano and Bentivoglio, 2000).…”

Section: Mechanisms For Increases In Thalamic Mast Cell Numbermentioning

confidence: 99%

Stimuli from Conspecifics Influence Brain Mast Cell Population in Male Rats

Asarian

Yousefzadeh

Silverman

et al. 2002

Hormones and Behavior

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It is well established that mast cells occur within the brain of many species, and that the brain mast cell population is not static, but changes with the behavioral and physiological state of the animal.In this study, we tested whether exposure to conspecifics alters the number of brain mast cells in male rats, and then investigated the nature of stimuli influencing the changes observed in the number and localization of brain mast cells. Five days of cohabitation with an ovariectomized, estrogen-progesterone (OVX + EP)-treated female resulted in the largest number of thalamic mast cells, while pairing with such a female physically separated by a wire mesh or with a novel male produced a smaller, but significant increase over other pairings (OVX females for 5 days, OVX and OVX + EP females for 1 day, familiar or isolated males for 5 days). In all groups, mast cells were localized within specific dorsal thalamic nuclei, including the paraventricular nucleus, anterior nuclear group, or mediodorsal, ventroposterior, or medial geniculate nuclei. The results suggest that the behavioral and/or endocrine factors associated with cohabitation with conspecifics are sufficient to alter the number of brain mast cell-specific nuclei in the thalami of male rats and thus can provide targeted delivery of neuromodulators to specific regions of the brain that process information concerning the normal physiological state of the animal. Keywordsfemale; thalamus; mating; aggressive; endocrine; immune; stress Although mast cells are well known in their role as effectors of IgE-mediated allergic reactions, their physiological function(s) remains poorly understood (Wedemeyer, Tsai, and Galli, 2000; Forsberg, Pejler, Ringwall, Lunderius, Tomasini-Johansson, Kusche-Gullberg, Eriksson, Ledin, Hellman, and Kjellen, 1999;Echtenacher, Mannel, and Hultner, 1996;Malaviya, Ikeda, Ross, and Abraham, 1996). Recent evidence indicates that bacterial recognition followed by endocytosis, processing and presentation of bacterial antigen, immune cell recruitment, and elimination of parasites number among these functions (McLachlan and Abraham, 2001;Vincent-Schneider, Thery, Mazzeo, Tenza, Raposo, and Bonnerot, 2001;Abraham and Malaviya, 2000; Fox, Jewel, and Whitacre, 1994). In addition, mast cells synthesize, store, and secrete a wide variety of bioactive molecules, including neuropeptides, neurotransmitters, prostaglandins, chemotactic factors, and (Galli, 2000;Metcalfe, Baram, and Mekori, 1997;Silver, Silverman, Vitkovic, and Lederhendler, 1996;Johnson and Krenger, 1992).Mast cells are normally present in the mammalian brain, both in the leptomeninges and within the parenchyma along the blood vessels of several dorsal thalamic nuclei (Dropp, 1972(Dropp, , 1976Theoharides, 1990;Goldschmidt, Hough, Glick, and Padawer, 1984). The number of brain mast cells is modulated by physiological and behavioral state. Our demonstration that mature mast cells can migrate from the vasculature into the adult rat brain parenchyma provides a possible mechani...

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Distribution and local differentiation of mast cells in the parenchyma of the forebrain

Cited by 47 publications

References 71 publications

Deleterious Effects of IL-9–Activated Mast Cells and Neuroprotection by Antihistamine Drugs in the Developing Mouse Brain

Deleterious Effects of IL-9–Activated Mast Cells and Neuroprotection by Antihistamine Drugs in the Developing Mouse Brain

Knockout of the mu opioid receptor enhances the survival of adult-generated hippocampal granule cell neurons

Stimuli from Conspecifics Influence Brain Mast Cell Population in Male Rats

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