A transient phase of cell death in the developing medial forebrain of the perinatal ferret

Johnson, Jessica; Berman, Nancy E.J.

doi:10.1016/s0165-3806(96)80007-1

Cited by 5 publications

(5 citation statements)

References 26 publications

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“…(A) ISEL/ cells (arrows point to three of them) are shown in an area immediately rostral to the corpus callosum (CC) in a horizontal section from a P1 male ferret. This result replicates a previous study in the ferret(Johnson and Berman, 1996). (B) DNAase I treatment induced DNA fragmentation in a section containing normal cells from a P2 male ferret POA/ AH.…”

supporting

confidence: 90%

“…always available. All experiments were performed in accordance with protocols (IACUC: A3522-01) approved First, we replicated the previous observation by Johnson and Berman (1996), who reported the presence of con-by the Laboratory Animal Care Committee of Boston University. Estrous females were left with a breeding siderable numbers of ISEL/ cells in a cortical area rostral to the corpus callosum (CC) of P1 ferret brains.…”

Section: Control Experimentssupporting

confidence: 73%

“…A recent study enough to replicate previous reports of large numbers of ISEL/ cells in several different tissues and using fetal mice (Blaschke et al, 1996) suggested that significantly more cell death may occur as cells situations. Johnson and Berman (1996), using P1 ferrets, found a high concentration of dying cells in proliferate than was previously believed, although the magnitude of this effect is disputed (Thomaidou a cortical region rostral to the CC [the medial forebrain apoptotic zone (MFAZ)] using the TUNEL et al, 1997). In the current study, numerous dying cells were seen adjacent to the third ventricle in method.…”

Section: Distribution Of Dying Cellsmentioning

confidence: 98%

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Cell death in the sexually dimorphic dorsal preoptic area/anterior hypothalamus of perinatal male and female ferrets

1998

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A sexually dimorphic male nucleus (MN) is present in Nissl‐stained sections through the dorsal (d) preoptic area/anterior hypothalamus (POA/AH) of male ferrets. The MN‐POA/AH is composed of a cluster of large cells which is organized in males by the action of estradiol, formed via the neural aromatization of circulating testosterone (T), during the last quarter of a 41‐day gestation. Several recent studies using rodent species have raised the possibility that the hormone‐induced masculinization of POA/AH morphology is mediated at least in part by a perinatal modulation of cell death. We asked whether a perinatal reduction in cell death contributes to the differentiation of the MN‐POA/AH in the male ferret, which is a carnivore species. The appearance of internucleosomal DNA fragmentation, detected by in situ end labeling (ISEL) using the ApopTag™ kit (Oncor Corp.) and of pyknotic cell nuclei in Nissl‐stained sections were used to estimate the occurrence of cell death. Male and female ferret kits were killed at four different ages spanning the perinatal period during which the MN‐POA/AH is organized and assumes an adult phenotype. A peak density of dying cells was present in both sexes at postnatal day (P) 2, which is nearly 1 week after the age, embryonic day (E) 37, when the MN‐POA/AH is first visible in male ferrets using Nissl stains. The density of cells in the sexually dimorphic dPOA/AH which were either ISEL‐positive or pyknotic was similar in males and females on E34, as well as on P2, 10, and 20. In the nondimorphic ventral POA/AH, the highest density of dying cells was present in both sexes at E34, and there were significantly more ISEL‐positive cells present in males than females at this particular age. In contrast to previous studies using rodents, our results suggest that in fetal male ferrets a modulation of the incidence of cell death contributes little to estradiol's organizational action in the dPOA/AH. © 1998 John Wiley & Sons, Inc. J Neurobiol 34: 242–252, 1998

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supporting

confidence: 90%

Section: Control Experimentssupporting

confidence: 73%

Section: Distribution Of Dying Cellsmentioning

confidence: 98%

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Cell death in the sexually dimorphic dorsal preoptic area/anterior hypothalamus of perinatal male and female ferrets

1998

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“…Formalin-fixed paraffin-embedded (FFPE) sections containing systemic organs or brain were stained using rabbit antiserum against influenza A virus or antibodies against specific markers of cell lineage, including glial fibrillary acidic protein (Dako, Carpinteria, CA), cytokeratin (AE1/AE3; Dako), and microtubule-associated protein-2 (SMI52; Covance, Princeton, NJ). For lectin histochemistry to detect ferret macrophages (38), sections were incubated with biotin-conjugated Griffonia (Bandeiraea) simplicifolia isolectin B 4 (Vector Laboratories, Burlingame, CA) instead of antibodies.…”

Section: Animals and Infectionsmentioning

confidence: 99%

H1N1, but Not H3N2, Influenza A Virus Infection Protects Ferrets from H5N1 Encephalitis

Bissel

Wang

Carter

et al. 2014

J Virol

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Seasonal influenza causes substantial morbidity and mortality because of efficient human-to-human spread. Rarely, zoonotic strains of influenza virus spread to humans, where they have the potential to mediate new pandemics with high mortality. We studied systemic viral spread after intranasal infection with highly pathogenic avian influenza virus ( IMPORTANCESeasonal influenza is efficiently transmitted from human to human, causing substantial morbidity and mortality. Rarely, zoonotic strains of influenza virus spread to humans, where they have the potential to mediate new pandemics with high mortality. Infection of naive ferrets with H5N1 avian influenza virus causes a rapid and lethal systemic disease. We studied systemic H5N1 viral spread after infection of ferrets with or without prior exposure to either of two seasonal influenza virus strains, H1N1 and H3N2. Ferrets previously infected with H1N1 survive H5N1 challenge while those previously infected with H3N2 die of encephalitis. However ferrets protected from lethal H5N1 infection develop persistent low-level infection of the small intestine, liver, or spleen, providing a nidus for future viral strain recombination. The mechanism by which prior infection with specific strains of seasonal influenza virus protect from lethal H5N1 challenge needs to be elucidated in order to design effective immunization and treatments.

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“…Factors released during cell death may in¯uence microglial migration, as several authors have reported that microglial precursors are attracted towards regions of the nervous parenchyma where intense cell death occurs (Hume et al, 1983;Ashwell, 1991;Perry and Gordon, 1991;Pearson et al, 1993), and accumulations of macrophages/microglial cells appear in regions of the developing CNS where intense cell death occurs (Ashwell, 1990(Ashwell, , 1991Milligan et al, 1991a;Johnson and Berman, 1996) or where transitory axonal projections are being eliminated (Innocenti et al, 1983). In addition, microglial cells increase in number and/or move in response to cell death pro- cesses (Thanos, 1992;Thanos and Richter, 1993;Ferrer et al, 1995;Nitatori et al, 1995;Finsen et al, 1996;LaÂ zaÂ r and PaÂ l, 1996;Roque et al, 1996).…”

Section: Factors That Control Migration Of Microglial Cellsmentioning

confidence: 99%

The origin and differentiation of microglial cells during development

Cuadros

Navascués

1998

Progress in Neurobiology

269

177

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AbstractÐSome authors claim that microglia originate from the neuroepithelium, although most now believe that microglial cells are of mesodermal origin, and probably belong to the monocyte/macrophage cell line. These cells must enter the developing central nervous system (CNS) from the blood stream, the ventricular space or the meninges. Afterward microglial cells are distributed more or less homogeneously through the entire nervous parenchyma. Stereotyped patterns of migration have been recognized during development, in which long-distance tangential migration precedes radial migration of individual cells. Microglial cells moving through the nervous parenchyma are ameboid microglia, which apparently di erentiate into rami®ed microglia after reaching their de®nitive location. This is supported by the presence of cells showing intermediate features between those of ameboid and rami®ed microglia. The factors that control the invasion of the nervous parenchyma, migration within the developing CNS and di erentiation of microglial cells are not well known. These phenomena apparently depend on environmental factors such as soluble or cell-surface bound molecules and components of the extracellular matrix. Microglial cells within the developing CNS are involved in clearing cell debris and withdrawing misdirected or transitory axons, and presumably support cell survival and neurite growth. #

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A transient phase of cell death in the developing medial forebrain of the perinatal ferret

Cited by 5 publications

References 26 publications

Cell death in the sexually dimorphic dorsal preoptic area/anterior hypothalamus of perinatal male and female ferrets

Cell death in the sexually dimorphic dorsal preoptic area/anterior hypothalamus of perinatal male and female ferrets

H1N1, but Not H3N2, Influenza A Virus Infection Protects Ferrets from H5N1 Encephalitis

The origin and differentiation of microglial cells during development

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