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Postnatal Rats (postnatal + rat)
Selected AbstractsSex Differences and the Roles of Sex Steroids in Apoptosis of Sexually Dimorphic Nuclei of the Preoptic Area in Postnatal RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2009S. Tsukahara The brain contains several sexually dimorphic nuclei that exhibit sex differences with respect to cell number. It is likely that the control of cell number by apoptotic cell death in the developing brain contributes to creating sex differences in cell number in sexually dimorphic nuclei, although the mechanisms responsible for this have not been determined completely. The milieu of sex steroids in the developing brain affects sexual differentiation in the brain. The preoptic region of rats has two sexually dimorphic nuclei. The sexually dimorphic nucleus of the preoptic area (SDN-POA) has more neurones in males, whereas the anteroventral periventricular nucleus (AVPV) has a higher cell density in females. Sex differences in apoptotic cell number arise in the SDN-POA and AVPV of rats in the early postnatal period, and an inverse correlation exists between sex differences in apoptotic cell number and the number of living cells in the mature period. The SDN-POA of postnatal male rats exhibits a higher expression of anti-apoptotic Bcl-2 and lower expression of pro-apoptotic Bax compared to that in females and, as a potential result, apoptotic cell death via caspase-3 activation more frequently occurs in the SDN-POA of females. The patterns of expression of Bcl-2 and Bax in the SDN-POA of postnatal female rats are changed to male-typical ones by treatment with oestrogen, which is normally synthesised from testicular androgen and affects the developing brain in males. In the AVPV of postnatal rats, apoptotic regulation also differs between the sexes, although Bcl-2 expression is increased and Bax expression and caspase-3 activity are decreased in females. The mechanisms of apoptosis possibly contributing to the creation of sex differences in cell number and the roles of sex steroids in apoptosis are discussed. [source] Distribution of progesterone receptor immunoreactivity in the midbrain and hindbrain of postnatal ratsDEVELOPMENTAL NEUROBIOLOGY, Issue 12 2008Princy S. Quadros Abstract Nuclear steroid hormone receptors are powerful transcription factors and therefore have the potential to influence and regulate fundamental processes of neural development. The expression of progesterone receptors (PR) has been described in the developing forebrain of rats and mice, and the mammalian brain may be exposed to significant amounts of progesterone, either from maternal sources and/or de novo synthesis of progesterone from cholesterol within the brain. The present study examined the distribution of PR immunoreactive (PRir) cells within the midbrain and hindbrain of postnatal rats. The results demonstrate that PR is transiently expressed within the first 2 weeks of life in specific motor, sensory and reticular core nuclei as well as within midbrain dopaminergic cell groups such as the substantia nigra and the ventral tegmental area. Additionally, robust PRir was observed in cells of the lower rhombic lip, a transient structure giving rise to precerebellar nuclei. These results suggest that progestins and progesterone receptors may play a fundamental role in the postnatal development of numerous midbrain and hindbrain nuclei, including some areas implicated in human disorders. Additionally, these findings contribute to the increasing evidence that steroid hormones and their receptors influence neural development in a wide range of brain areas, including many not typically associated with reproduction or neuroendocrine function. © 2008 Wiley Periodicals, Inc. Develop Neurobiol, 2008 [source] Sex differences in the level of Bcl-2 family proteins and caspase-3 activation in the sexually dimorphic nuclei of the preoptic area in postnatal ratsDEVELOPMENTAL NEUROBIOLOGY, Issue 13 2006Shinji Tsukahara Abstract In developing rats, sex differences in the number of apoptotic cells are found in the central division of the medial preoptic nucleus (MPNc), which is a significant component of the sexually dimorphic nucleus of the preoptic area, and in the anteroventral periventricular nucleus (AVPV). Specifically, male rats have more apoptotic cells in the developing AVPV, whereas females have more apoptotic cells in the developing MPNc. To determine the mechanisms for the sex differences in apoptosis in these nuclei, we compared the expression of the Bcl-2 family members and active caspase-3 in postnatal female and male rats. Western blot analyses for the Bcl-2 family proteins were performed using preoptic tissues isolated from the brain on postnatal day (PD) 1 (day of birth) or on PD8. In the AVPV-containing tissues of PD1 rats, there were significant sex differences in the level of Bcl-2 (female > male) and Bax (female < male) proteins, but not of Bcl-xL or Bad proteins. In the MPNc-containing tissues of PD8 rats, there were significant sex differences in the protein levels for Bcl-2 (female < male), Bax (female > male), and Bad (female < male), but not for Bcl-xL. Immunohistochemical analyses showed significant sex differences in the number of active caspase-3-immunoreactive cells in the AVPV on PD1 (female < male) and in the MPNc on PD8 (female > male). We further found that active caspase-3-immunoreactive cells of the AVPV and MPNc were immunoreactive for NeuN, a neuronal marker. These results suggest that there are sex differences in the induction of apoptosis via the mitochondrial pathway during development of the AVPV and MPNc. © 2006 Wiley Periodicals, Inc. J Neurobiol, 2006 [source] MyD88 expression in the rat dental follicle: implications for osteoclastogenesis and tooth eruptionEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 4 2010Dawen Liu Liu D, Yao S, Wise GE. MyD88 expression in the rat dental follicle: implications for osteoclastogenesis and tooth eruption. Eur J Oral Sci 2010; 118: 333,341. © 2010 The Authors. Journal compilation © 2010 Eur J Oral Sci Myeloid differentiation factor 88 (MyD88) is a key adaptor molecule in the interleukin (IL)-1 and IL-18 toll-like receptor signaling pathways. Because MyD88 is present in dental follicle (DF) cells in vitro, the purpose of this study was to determine its chronological expression in vivo, as well as its possible role in osteoclastogenesis and tooth eruption. An oligo DNA microarray was used to determine expression of the Myd88 gene in vivo in the DFs from the first mandibular molars of postnatal rats from days 1 to 11. The results showed that MyD88 was expressed maximally on day 3. Using small interfering RNA (siRNA) to knock down MyD88 expression in the DF cells also reduced the expression of the nuclear factor-kappa B-1 (NFKB1) and monocyte chemoattractant protein 1 (MCP-1) genes. Interleukin-1, up-regulated the expression of NFKB1, MCP-1, and receptor activator of nuclear factor kappa B ligand (RANKL), but knockdown of MyD88 nullified this IL-1, effect. Conditioned medium from DF cells with MyD88 knocked down had reduced chemotactic activity for mononuclear cells and reduced osteoclastogenesis, as opposed to controls. In conclusion, the maximal expression of MyD88 in the DF of postnatal day 3 rats may contribute to the major burst of osteoclastogenesis needed for eruption by up-regulating MCP-1 and RANKL expression. [source] Monocyte chemoattractant protein-1 (MCP-1) produced via NF-,B signaling pathway mediates migration of amoeboid microglia in the periventricular white matter in hypoxic neonatal ratsGLIA, Issue 6 2009Y. Y. Deng Abstract Monocyte chemoattractant protein-1 (MCP-1), a member of ,-chemokine subfamily, regulates the migration of microglia, monocytes, and lymphocytes to the inflammatory site in the central nervous system. We sought to determine if amoeboid microglial cells (AMC) produce MCP-1 that may be linked to migration of AMC in the corpus callosum periventricular white matter in hypoxic neonatal rats. A striking feature in 1-day-old rats subjected to hypoxia was a marked increase in cell numbers of AMC and immunoexpression of MCP-1 and its receptor (CCR2). By BrdU immunostaining, there was no significant change in the proliferation rate of AMC after hypoxic exposure when compared with the corresponding control rats. When injected intracerebrally into the corpus callosum of 7-day-old postnatal rats, MCP-1 induced the chemotactic migration of AMC to the injection site. In primary microglial cell culture subjected to hypoxia, there was a significant increase in MCP-1 release involving NF-,B signaling pathway. In in vitro chemotaxis assay, the medium derived from hypoxia-treated microglial cultures attracted more migratory microglial cells than that from the control microglial culture. The present results suggest that following a hypoxic insult, AMC in the neonatal rats increase MCP-1 production via NF-,B signaling pathway. This induces the migration and accumulation of AMC from the neighboring areas to the periventricular white matter (PWM). It is concluded that the preponderance and active migration of AMC, as well as them being the main cellular source of MCP-1, may offer an explanation for the PWM being susceptible to hypoxic damage in neonatal brain. © 2008 Wiley-Liss, Inc. [source] Sex Differences and the Roles of Sex Steroids in Apoptosis of Sexually Dimorphic Nuclei of the Preoptic Area in Postnatal RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2009S. Tsukahara The brain contains several sexually dimorphic nuclei that exhibit sex differences with respect to cell number. It is likely that the control of cell number by apoptotic cell death in the developing brain contributes to creating sex differences in cell number in sexually dimorphic nuclei, although the mechanisms responsible for this have not been determined completely. The milieu of sex steroids in the developing brain affects sexual differentiation in the brain. The preoptic region of rats has two sexually dimorphic nuclei. The sexually dimorphic nucleus of the preoptic area (SDN-POA) has more neurones in males, whereas the anteroventral periventricular nucleus (AVPV) has a higher cell density in females. Sex differences in apoptotic cell number arise in the SDN-POA and AVPV of rats in the early postnatal period, and an inverse correlation exists between sex differences in apoptotic cell number and the number of living cells in the mature period. The SDN-POA of postnatal male rats exhibits a higher expression of anti-apoptotic Bcl-2 and lower expression of pro-apoptotic Bax compared to that in females and, as a potential result, apoptotic cell death via caspase-3 activation more frequently occurs in the SDN-POA of females. The patterns of expression of Bcl-2 and Bax in the SDN-POA of postnatal female rats are changed to male-typical ones by treatment with oestrogen, which is normally synthesised from testicular androgen and affects the developing brain in males. In the AVPV of postnatal rats, apoptotic regulation also differs between the sexes, although Bcl-2 expression is increased and Bax expression and caspase-3 activity are decreased in females. The mechanisms of apoptosis possibly contributing to the creation of sex differences in cell number and the roles of sex steroids in apoptosis are discussed. [source] Involvement of brain-derived neurotrophic factor (BDNF) in the functional elimination of synaptic contacts at polyinnervated neuromuscular synapses during developmentJOURNAL OF NEUROSCIENCE RESEARCH, Issue 7 2010N. Garcia Abstract We use immunohistochemistry to describe the localization of brain-derived neurotrophic factor (BDNF) and its receptors trkB and p75NTR in the neuromuscular synapses of postnatal rats (P6,P7) during the synapse elimination period. The receptor protein p75NTR is present in the nerve terminal, muscle cell and glial Schwann cell whereas BDNF and trkB proteins can be detected mainly in the pre- and postsynaptic elements. Exogenously applied BDNF (10 nM for 3 hr or 50 nM for 1 hr) increases ACh release from singly and dually innervated synapses. This effect may be specific for BDNF because the neurotrophin NT-4 (2,8 nM) does not modulate release at P6,P7. Blocking the receptors trkB and p75NTR (with K-252a and anti-p75-192-IgG, respectively) completely abolishes the potentiating effect of exogenous BDNF. In addition, exogenous BDNF transiently recruits functionally depressed silent terminals, and this effect seems to be mediated by trkB. Calcium ions, the L-type voltage-dependent calcium channels and protein kinase C are involved in BDNF-mediated nerve ending recruitment. Blocking experiments suggest that endogenous BDNF could operate through p75NTR receptors coupled to potentiate ACh release in all nerve terminals because the anti-p75-192-IgG reduces release. However, blocking the trkB receptor (K-252a) or neutralizing endogenous BDNF with the trkB-IgG fusion protein reveals a trkB-mediated release inhibition on almost mature strong endings in dual junctions. Taken together these results suggest that a BDNF-induced p75NTR -mediated ACh release potentiating mechanism and a BDNF-induced trkB-mediated release inhibitory mechanism may contribute to developmental synapse disconnection. © 2009 Wiley-Liss, Inc. [source] | |||||||||||||