Key Specifications Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|B, R||IHC, IH(P), WB||Rb||Serum||Polyclonal Antibody|
|Safety Information according to GHS|
|Material Size||500 µL|
References | 27 Available | See All References
|Reference overview||Pub Med ID|
|Immunohistochemical demonstration of specific antigens in the human brain fixed in zinc-ethanol-formaldehyde. |
Korzhevskii, DE; Sukhorukova, EG; Kirik, OV; Grigorev, IP
European journal of histochemistry : EJH 59 2530 2015
Tissue fixation is critical for immunohistochemistry. Recently, we developed a zinc-ethanol-formalin fixative (ZEF), and the present study was aimed to assess the applicability of the ZEF for the human brain histology and immunohistochemistry and to evaluate the detectability of different antigens in the human brain fixed with ZEF. In total, 11 antigens were tested, including NeuN, neuron-specific enolase, GFAP, Iba-1, calbindin, calretinin, choline acetyltransferase, glutamic acid decarboxylase (GAD65), tyrosine hydroxylase, synaptophysin, and α-tubulin. The obtained data show that: i) the ZEF has potential for use in general histological practice, where detailed characterization of human brain morphology is needed; ii) the antigens tested are well-preserved in the human brain specimens fixed in the ZEF.
|Co-Application of Corticosterone and Growth Hormone Upregulates NR2B Protein and Increases the NR2B:NR2A Ratio and Synaptic Transmission in the Hippocampus. |
Mahmoud, GS; Amer, AS
Sultan Qaboos University medical journal 14 e486-94 2014
This in vitro study aimed to investigate the possible mechanism underlying the protective effect of growth hormone (GH) on hippocampal function during periods of heightened glucocorticoid exposure.This study was conducted between January and June 2005 at the Joan C. Edwards School of Medicine, Marshall University, in Huntington, West Virginia, USA. The effects of the co-application of GH and corticosterone (CORT) were tested at different concentrations on the field excitatory postsynaptic potentials (fEPSPs) of the hippocampal slices of rats in two different age groups. Changes in the protein expression of N-methyl-D-aspartate receptor (NMDAR) subunits NR1, NR2B and NR2A were measured in hippocampal brain slices treated with either artificial cerebrospinal fluid (ACSF), low doses of CORT alone or both CORT and GH for three hours.The co-application of CORT and GH was found to have an additive effect on hippocampal synaptic transmission compared to either drug alone. Furthermore, the combined use of low concentrations of GH and CORT was found to have significantly higher effects on the enhancement of fEPSPs in older rats compared to young ones. Both GH and CORT enhanced the protein expression of the NR2A subunit. Simultaneous exposure to low concentrations of GH and CORT significantly enhanced NR2B expression and increased the NR2B:NR2A ratio. In contrast, perfusion with CORT alone caused significant suppression in the NR1 and NR2B protein expression and a decrease in the NR2B:NR2A ratio.These results suggest that NMDARs provide a potential target for mediating the GH potential protective effect against stress and age-related memory and cognitive impairment.
|NDRG2 as a marker protein for brain astrocytes. |
Flügge, G; Araya-Callis, C; Garea-Rodriguez, E; Stadelmann-Nessler, C; Fuchs, E
Cell and tissue research 357 31-41 2014
The protein NDRG2 (N-myc downregulated gene 2) is expressed in astrocytes. We show here that NDRG2 is located in the cytosol of protoplasmic and fibrous astrocytes throughout the mammalian brain, including Bergmann glia as observed in mouse, rat, tree shrew, marmoset and human. NDRG2 immunoreactivity is detectable in the astrocytic cell bodies and excrescencies including fine distal processes. Glutamatergic and GABAergic nerve terminals are associated with NDRG2 immunopositive astrocytic processes. Müller glia in the retina displays no NDRG2 immunoreactivity. NDRG2 positive astrocytes are more abundant and more evenly distributed in the brain than GFAP (glial fibrillary acidic protein) immunoreactive cells. Some regions with very little GFAP such as the caudate nucleus show pronounced NDRG2 immunoreactivity. In white matter areas, NDRG2 is less strong than GFAP labeling. Most NDRG2 positive somata are immunoreactive for S100ß but not all S100ß cells express NDRG2. NDRG2 positive astrocytes do not express nestin and NG2 (chondroitin sulfate proteoglycan 4). The localization of NDRG2 overlaps only partially with that of aquaporin 4, the membrane-bound water channel that is concentrated in the astrocytic endfeet. Reactive astrocytes at a cortical lesion display very little NDRG2, which indicates that expression of the protein is reduced in reactive astrocytes. In conclusion, our data show that NDRG2 is a specific marker for a large population of mature, non-reactive brain astrocytes. Visualization of NDRG2 immunoreactive structures may serve as a reliable tool for quantitative studies on numbers of astrocytes in distinct brain regions and for high-resolution microscopy studies on distal astrocytic processes.
|A ROCK Inhibitor Blocks the Inhibitory Effect of Chondroitin Sulfate Proteoglycan on Morphological Changes of Mesenchymal Stromal/Stem Cells into Neuron-Like Cells. |
Lim, HS; Joe, YA
Biomolecules & therapeutics 21 447-53 2013
Chondroitin sulfate proteoglycan (CSPG) inhibits neurite outgrowth of various neuronal cell types, and CSPG-associated inhibition of neurite outgrowth is mediated by the Rho/ROCK pathway. Mesenchymal stromal/stem cells (MSCs) have the potential to differentiate into neuron-like cells under specific conditions and have been shown to differentiate into neuron-like cells by co-treatment with the ROCK inhibitor Y27632 and the hypoxia condition mimicking agent CoCl2. In this study, we addressed the hypothesis that a ROCK inhibitor might be beneficial to regenerate neurons during stem cell therapy by preventing transplanted MSCs from inhibition by CSPG in damaged tissues. Indeed, dose-dependent inhibition by CSPG pretreatment was observed during morphological changes of Wharton's jelly-derived MSCs (WJ-MSCs) induced by Y27632 alone. The formation of neurite-like structures was significantly inhibited when WJ-MSCs were pre-treated with CSPG before induction under Y27632 plus CoCl2 conditions, and pretreatment with a protein kinase C inhibitor reversed such inhibition. However, CSPG treatment resulted in no significant inhibition of the WJ-MSC morphological changes into neuron-like cells after initiating induction by Y27632 plus CoCl2. No marked changes were detected in expression levels of neuronal markers induced by Y27632 plus CoCl2 upon CSPG treatment. CSPG also blocked the morphological changes of human bone marrow-derived MSCs into neuron-like cells under other neuronal induction condition without the ROCK inhibitor, and Y27632 pre-treatment blocked the inhibitory effect of CSPG. These results suggest that a ROCK inhibitor can be efficiently used in stem cell therapy for neuronal induction by avoiding hindrance from CSPG.
|Chronic psychosocial stress and citalopram modulate the expression of the glial proteins GFAP and NDRG2 in the hippocampus. |
Araya-Callís, C; Hiemke, C; Abumaria, N; Flugge, G
Psychopharmacology 224 209-22 2012
It has been suggested that there are causal relationships between alterations in brain glia and major depression.To investigate whether a depressive-like state induces changes in brain astrocytes, we used chronic social stress in male rats, an established preclinical model of depression. Expression of two astrocytic proteins, the intermediate filament component glial fibrillary acidic protein (GFAP) and the cytoplasmic protein N-myc downregulated gene 2 (NDRG2), was analyzed in the hippocampus. For comparison, expression of the neuronal protein syntaxin-1A was also determined.Adult male rats were subjected to daily social defeat for 5 weeks and were concomitantly treated with citalopram (30 mg/kg/day, via the drinking water) for 4 weeks.Western blot analysis showed that the chronic stress downregulated GFAP but upregulated NDRG2 protein. Citalopram did not prevent these stress effects, but the antidepressant per se downregulated GFAP and upregulated NDRG2 in nonstressed rats. In contrast, citalopram prevented the stress-induced upregulation of the neuronal protein syntaxin-1A.These data suggest that chronic stress and citalopram differentially affect expression of astrocytic genes while the antidepressant drug does not prevent the stress effects. The inverse regulation of the cytoskeletal protein GFAP and the cytoplasmic protein NDRG2 indicates that the cells undergo profound metabolic changes during stress and citalopram treatment. Furthermore, the present findings indicate that a 4-week treatment with citalopram does not restore normal glial function in the hippocampus, although the behavior of the animals was normalized within this treatment period, as reported previously.
|Chotosan (Diaoteng San)-induced improvement of cognitive deficits in senescence-accelerated mouse (SAMP8) involves the amelioration of angiogenic/neurotrophic factors and neuroplasticity systems in the brain. |
Qi Zhao,Takako Yokozawa,Koichi Tsuneyama,Ken Tanaka,Takeshi Miyata,Notoshi Shibahara,Kinzo Matsumoto
Chinese medicine 6 2011
ABSTRACT:Full Text Article
|Nitric oxide and interleukin-1beta mediate noradrenergic induced corticotrophin-releasing hormone release in organotypic cultures of rat paraventricular nucleus. |
CH Hsieh, HY Li, JC Chen
Neuroscience 165 1191-202 2010
Noradrenergic inputs from the brainstem are critical for the central stress response. It has been suggested that endogenous interleukin-1beta (IL-1beta) is involved in norepinephrine (NE)-induced release of corticotropin-releasing hormone (CRH) from the paraventricular nucleus of the hypothalamus (PVN). However, no IL-1 receptor on PVN CRH neurons has been identified. Therefore we hypothesized that the action of IL-1beta in the PVN requires downstream modulators that eventually lead to CRH release by PVN neurons. In the current study, we used organotypic cultures from neonatal rat PVN which display neuroendocrine characteristics suitable for in vitro studies. Pharmacological treatments with NE or IL-1beta elicited nitric oxide (NO) release from the PVN cultures, implying that local NO might be a candidate for modulating the action of IL-1beta. In addition, NE treatments significantly increased IL-1beta and CRH release. Treatment with IL-1beta or sodium nitroprusside also induced CRH release. Next, we also showed that either an IL-1 receptor antagonist or NOS inhibitor Nomega-nitro-L-arginine (L-NNA) attenuated the NE-induced CRH release. These results suggest that IL-1beta and NO are involved in NE-induced CRH release. Moreover, we found that application of L-NNA attenuated IL-1beta-induced CRH release, indicating that NO likely mediates this process. In summary, the current study demonstrates that IL-1beta plays a significant role in NE-induced CRH release, and that neuroendocrine response in the PVN may depend on local NO action.
|Localized donor cells in brain of a Hunter disease patient after cord blood stem cell transplantation. |
Ken Araya,Norio Sakai,Ikuko Mohri,Kuriko Kagitani-Shimono,Takeshi Okinaga,Yoshiko Hashii,Hideaki Ohta,Itsuko Nakamichi,Katsuyuki Aozasa,Masako Taniike,Keiichi Ozono
Molecular genetics and metabolism 98 2009
The efficacy of hematopoietic stem cell transplantation (HSCT) for Hunter disease (deficiency of iduronate-2-sulfatase, IDS) remains unclear. We treated a 6-year-old male suffering from a severe type of Hunter disease with cord blood stem cell transplantation (CBSCT); however, he died at 10 months post-therapy due to a laryngeal post-transplantation lymphoproliferative disorder. During the follow-up period after CBSCT, his hyperactivity, estimated mental age, and brain MR findings had not improved. We assessed the efficacy of CBSCT by biochemical and pathological analyses of the autopsied tissues. There were many distended cells with accumulated substrate in the brain, but not in the liver. IDS enzyme activity in the cerebrum remained very low, although that in the liver reached about 40% of the normal control level. However, a variable number of tandem repeats analyses demonstrated a weak donor-derived band not only in the liver but also in the cerebrum. Furthermore, IDS-immunoreactivity in the liver was recognized broadly not only in Kupffer cells but also in hepatocytes. On the other hand, IDS-immunoreactivity was recognized exclusively in CD68-positive microglia/monocytes in the patient's brain; whereas that in the normal brain was also detected in neurons and oligodendrocytes. These donor-derived IDS-positive cells were predominantly localized in perivascular spaces and some of them were evidently present in the brain parenchyma. The efficacy of CBSCT was judged to be insufficient for the brain at 10 months post-therapy. However, the pathological detection of donor-derived cells in the brain parenchyma suggests the potential of HSCT for treatment of neurological symptoms in Hunter disease. This is the first neuropathological report documenting the distribution of donor-derived cells in the brain after CBSCT into a Hunter disease patient.
|Postnatal changes in the Rexed lamination and markers of nociceptive afferents in the superficial dorsal horn of the rat. |
Louis-Etienne Lorenzo,Michele Ramien,Manon St Louis,Yves De Koninck,Alfredo Ribeiro-da-Silva
The Journal of comparative neurology 508 2008
In this study, we investigated postnatal changes in Rexed's laminae and distribution of nociceptive afferents in the dorsal horn of the rat lumbar spinal cord at postnatal days 0, 5, 10, 15, 20, and 60. Transverse sections of the L4-L5 segments were processed for triple labeling with isolectin B4 (IB4)-binding as a marker of nonpeptidergic C-fibers, calcitonin gene-related peptide (CGRP) immunoreactivity to label peptidergic nociceptive afferents, and a fluorescent Nissl stain to visualize cells and lamination at different stages of postnatal development. The Nissl staining revealed that the thickness of lamina I (LI) and outer lamina II remained mostly unchanged from birth until adulthood. CGRP afferents terminated mostly in LI and the outer two-thirds of lamina II, whereas the termination area of fibers binding IB4 was centered on the middle one-third of lamina II at all ages studied. In absolute values, the overall width of the bands of intense CGRP and IB4 labeling increased with age but decreased as a percentage of the overall thickness of the dorsal horn with maturation. The overlap of CGRP termination area with that of IB4 afferents increased with age. The consequences of these findings are twofold. First, the size of the different laminae does not grow evenly across the dorsal horn. Second, CGRP and IB4 labeling cannot be considered per se to be reliable markers of lamination during development. These findings have implications for comparing data obtained in immature and mature tissues with respect to localization of structures in the dorsal horn.
|Short-term biological safety of a photoelectric dye used as a component of retinal prostheses. |
Kazuo Okamoto,Toshihiko Matsuo,Takayuki Tamaki,Akihito Uji,Hiroshi Ohtsuki
Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs 11 2008
We have designed a new type of retinal prosthesis with a photoelectric dye that transfers photon energy to generate electric potentials. The purpose of this study was to test the safety of a photoelectric dye, 2-[2-[4-(dibutylami no)phenyl]ethenyl]-3-carboxymethylbenzothiazolium bromide (NK-5962), used for retinal prostheses. The retinal cells, derived from chick neurosensory retinas at the 12-day embryonic stage, were a mixed population of retinal neurons and glial cells, and were cultured for 2 days either under protection from light or under continuous light exposure at 230 lux for 9 h daily in the presence of the photoelectric dye at varying concentrations (1.6 x 10(-5), 1.6 x 10(-6), and 1.6 x 10(-7) M) to assess cell viability by staining live cells and dead cells. Dispersed retinal pigment epithelial cells at the same embryonic stage were incubated with the photoelectric dye at varying concentrations (6.6 x 10(-5), 6.6 x 10(-6), and 6.6 x 10(-7) M) for 4 h under protection from light or under continuous light exposure at 320 lux to assess cytotoxicity by measuring the activity of lactate dehydrogenase leaking from cells. The majority of retinal cells were alive with only a small percentage of dead cells under the dark condition or the light condition in the presence or the absence of the photoelectric dye. The percentage of dead cells was significantly smaller at higher concentrations of the photoelectric dye (P = 0.0183, two-factor analysis of variance), while the percentage of dead cells was not significantly different between the dark condition and the light condition (P = 0.3102). Percent cytotoxicity values were negative, indicating protective effects in all groups of retinal pigment epithelial cells incubated with varying concentrations of the photoelectric dye. The photoelectric dye showed no cytotoxicity to chick retinal cells or retinal pigment epithelial cells on short-term exposure. In addition, this photoelectric dye might have protective effects on both types of cells.
|A mouse model of tuberous sclerosis: neuronal loss of Tsc1 causes dysplastic and ectopic neurons, reduced myelination, seizure activity, and limited survival. |
Meikle, L; Talos, DM; Onda, H; Pollizzi, K; Rotenberg, A; Sahin, M; Jensen, FE; Kwiatkowski, DJ
The Journal of neuroscience : the official journal of the Society for Neuroscience 27 5546-58 2007
Tuberous sclerosis (TSC) is a hamartoma syndrome caused by mutations in TSC1 or TSC2 in which cerebral cortical tubers and seizures are major clinical issues. We have engineered mice in which most cortical neurons lose Tsc1 expression during embryonic development. These Tsc1 mutant mice display several neurological abnormalities beginning at postnatal day 5 with subsequent failure to thrive and median survival of 35 d. The mice also display clinical and electrographic seizures both spontaneously and with physical stimulation, and some seizures end in a fatal tonic phase. Many cortical and hippocampal neurons are enlarged and/or dysplastic in the Tsc1 mutant mice, strongly express phospho-S6, and are ectopic in multiple sites in the cortex and hippocampus. There is a striking delay in myelination in the mutant mice, which appears to be caused by an inductive neuronal defect. This new TSC brain model replicates several features of human TSC brain lesions and implicates an important function of Tsc1/Tsc2 in neuronal development.
|hsp72, a host determinant of measles virus neurovirulence. |
Carsillo, T; Traylor, Z; Choi, C; Niewiesk, S; Oglesbee, M
Journal of virology 80 11031-9 2006
Transient hyperthermia such as that experienced during febrile episodes increases expression of the major inducible 70-kDa heat shock protein (hsp72). Despite the relevance of febrile episodes to viral pathogenesis and the multiple in vitro roles of heat shock proteins in viral replication and gene expression, the in vivo significance of virus-heat shock protein interactions is unknown. The present work determined the in vivo relationship between hsp72 levels and neurovirulence of an hsp72-responsive virus using the mouse model of measles virus (MV) encephalitis. Transgenic C57BL/6 mice were created to constitutively overexpress hsp72 in neurons, and these mice were inoculated intracranially with Edmonston MV (Ed MV) at 42 h of age. The mean viral RNA burden in brain was approximately 2 orders of magnitude higher in transgenic animals than in nontransgenic animals 2 to 4 weeks postinfection, and this increased burden was associated with a fivefold increase in mortality. Mice were also challenged with an Ed MV variant exhibiting an attenuated in vitro response to hsp72-dependent stimulation of viral transcription (Ed N-522D). This virus exhibited an attenuated neuropathogenicity in transgenic mice, where mortality and viral RNA burdens were not significantly different from nontransgenic mice infected with either Ed N-522D or parent Ed MV. Collectively, these results indicate that hsp72 levels can serve as a host determinant of viral neurovirulence in C57BL/6 mice, reflecting the direct influence of hsp72 on viral gene expression.Full Text Article
|Localization of orexin-1 receptors to vagal afferent neurons in the rat and humans. |
Galina Burdyga, Simon Lal, David Spiller, Wen Jiang, David Thompson, Stephen Attwood, Shakeel Saeed, David Grundy, Andrea Varro, Rod Dimaline, Graham J Dockray
Gastroenterology 124 129-39 2003
BACKGROUND AIMS: Orexin-A and -B are brain-gut peptides that stimulate food intake via orexin-R1 and -R2 receptors. Cholecystokinin (CCK) inhibits food intake via CCK(A) receptors expressed on vagal afferent neurons. The purpose of the study was to determine whether vagal afferent neurons express OX-R1 and OX-R2 and whether orexin-A inhibits responses to CCK. METHODS: OX-R1 and -R2 expression by rat and human nodose ganglia was examined by reverse-transcriptase polymerase chain reaction (RT-PCR). Receptor localization was determined by immunohistochemistry. Responses of rat jejunal afferent fibers were examined by electrophysiology. RESULTS: Both rat and human nodose ganglia expressed OX-R1 as detected by RT-PCR, and humans also expressed OX-R2. The identity of the products was confirmed by sequencing. Immunohistochemistry indicated expression of OX-R1 in both species in neurons that also expressed CCK(A) and leptin receptors. In human ganglia there was also expression in glial cells that was absent in rats. Orexin-A had no effect on the resting discharge of afferent nerve fibers but inhibited responses to CCK. CONCLUSIONS: OX-R1 and CCK(A) receptors are expressed by human and rat vagal afferent neurons. Orexin inhibits responses to CCK suggesting a role in modulation of gut to brain signaling.
|A 72 kDa heat shock protein is protective against the selective vulnerability of CA1 neurons and is essential for the tolerance exhibited by CA3 neurons in the hippocampus. |
K Sato, N Matsuki
Neuroscience 109 745-56 2002
The correlation between the expression of a 72 kDa heat shock protein and vulnerability of hippocampal CA1, CA3, and dentate gyrus regions to glutamate toxicity was investigated using a highly specific antisense oligonucleotide technique. Glutamate (1 mM, 15 min) caused region-dependent neuronal damage in cultured hippocampal slices 24 h after exposure and the most severe damage was observed in CA1. When slices were heat-shocked (43.5 degrees C, 30 min) before exposure to glutamate, neuronal damage in CA1 was attenuated. The strongest protection was observed when the interval between the heat shock and the exposure to glutamate was 3 days, which coincided with the maximal induction of a 72 kDa heat shock protein in neurons. When the expression of a 72 kDa heat shock protein was suppressed by the antisense oligonucleotide, the protective effect of the heat shock was completely inhibited. Glutamate itself also induced a 72 kDa heat shock protein in neurons, region-dependently, 24 h after the exposure. The signal of a 72 kDa heat shock protein in CA3 and dentate gyrus was significantly stronger than that in CA1. When the antisense oligonucleotide was applied, the damage in CA3 and dentate gyrus was exaggerated dose-dependently, and this effect was more remarkable in CA3 than in the dentate gyrus. Based on these data, we concluded that: (i) a 72 kDa heat shock protein has a protective effect against the selective vulnerability of CA1 neurons, (ii) a 72 kDa heat shock protein is an essential factor for the tolerance exhibited by CA3 neurons, and (iii) dentate gyrus tolerance is based on mechanisms other than those mediated through a 72 kDa heat shock protein.
|CGRP receptors in the gerbil spiral modiolar artery mediate a sustained vasodilation via a transient cAMP-mediated Ca2+-decrease. |
M Herzog, E Q Scherer, B Albrecht, B Rorabaugh, M A Scofield, P Wangemann
The Journal of membrane biology 189 225-36 2002
Alteration of cochlear blood flow may be involved in the etiology of inner ear disorders like sudden hearing loss, fluctuating hearing loss and tinnitus. The aim of the present study was to localize the vasodilator calcitonin gene-related peptide (CGRP) and to identify CGRP receptors and their signaling pathways in the gerbil spiral modiolar artery (SMA) that provides the main blood supply of the cochlea. CGRP was localized in perivascular nerves by immunocytochemistry. The vascular diameter and cytosolic Ca2+ concentration [Ca2+]i in the smooth muscle cells were measured simultaneously with videomicroscopy and fluo-4-microfluorometry. Calcitonin receptor-like receptor (CRLR) mRNA was identified by RT-PCR as a specific 288 bp fragment in total RNA isolated from the vascular wall. The SMA was preconstricted by a 2-min application of 1 nM endothelin-1 (ET1). CGRP, forskolin, and dibutyryl-cAMP caused a vasodilation (EC50 = 0.1 nM, 0.3 mM, and 20 mM). CGRP and forskolin caused an increase in cAMP production and a transient decrease in the [Ca2+]i. The CGRP-induced vasodilation was antagonized by CGRP8-37 (KDB = 2 mM). The K+-channel blockers iberiotoxin and glibenclamide partially prevented the CGRP- or forskolin-induced vasodilations but failed to reverse these vasodilations. These results demonstrate that CGRP is present in perivascular nerves and causes a vasodilation of the ET1-preconstricted SMA. The data suggest that this vasodilation is mediated by an increase in the cytosolic cAMP concentration, a transient activation of iberiotoxin-sensitive BK and glibenclamide-sensitive KATP K+ channels, a transient decrease in the [Ca2+]i and a long-lasting Ca2+ desensitization.
|Quantitative immunochemistry on neuronal loss, reactive gliosis and BBB damage in cortex/striatum and hippocampus/amygdala after systemic kainic acid administration. |
Ding, M, et al.
Neurochem. Int., 36: 313-8 (2000) 2000
Cell specific markers were quantified in the hippocampus, the amygdala/pyriform cortex, the frontal cerebral cortex and the striatum of the rat brain after systemic administration of kainic acid. Neuron specific enolase (NSE) reflects loss of neurons, glial fibrillary acidic protein (GFAP) reflects reactive gliosis, and brain levels of serum proteins measures blood-brain-barrier permeability. While the concentration of NSE remained unaffected in the frontal cerebral cortex and the striatum, their GFAP content increased during the first three days. In the hippocampus and amygdala, NSE levels decreased significantly. GFAP levels in the hippocampus were unaffected after one day and decreased in the amygdala/pyriform cortex. After that, GFAP increased strikingly until day 9 or, in the case of amygdala/pyriform cortex, even longer. This biphasic time course for GFAP was accompanied by a decrease of S-100 during days 1-9 followed by a significant increase at day 27 above the initial level. The regional differences in GFAP and S-100 could result from the degree of neuronal degeneration, the astrocytic receptor set-up and/or effects on the blood-brain barrier.
|Ephrin-dependent growth and pruning of hippocampal axons |
Gao, P P, et al
Proc Natl Acad Sci USA, 96:4073-7 (1999) 1999
|Identification of the dopamine D3 receptor in oligodendrocyte precursors: potential role in regulating differentiation and myelin formation. |
Bongarzone, E R, et al.
J. Neurosci., 18: 5344-53 (1998) 1998
Expression of the dopamine D3 receptor (D3r) was found in primary mixed glial cultures from newborn brain and in the corpus callosum in vivo during the peak of myelination. Expression of the D3r mRNA, but not D2r mRNA, was detected as early as 5 d in vitro (DIV) by RT-PCR. Immunoblot studies revealed D3r protein was also expressed in the cultures. Double immunofluorescence analysis for the D3r and for surface markers of specific stages of oligodendrocyte development indicated that D3r expression occurred in precursors and in immature oligodendrocytes but not in mature oligodendrocytes (i.e. , A2B5(+) 007(-) 01(-) and A2B5(+) 007(+) 01(-) cells but not A2B5(-) 007(+) 01(+) cells). Confocal microscopic analysis indicated that D3r was associated with cell bodies and cell membranes but not with the processes emanating from cell somas. Immunohistochemistry of brain sections revealed the presence of D3r in some oligodendrocytes located mainly within the genu and radiato of the corpus callosum during the active period of myelination. Treatment of cultures with 20 microM quinpirole led to decreased numbers of O1(+) oligodendrocytes possessing myelin-like membranes as well as an increase in the number of precursors in 14 DIV cultures. This effect was prevented by the dopamine antagonist haloperidol. These results show that the D3r expression is not restricted to neurons but it is also expressed in differentiating oligodendrocytes before terminal maturation. It also suggests that dopamine or some other D3r ligand may play a role in oligodendrocyte differentiation and/or the formation of myelin by mature oligodendrocytes.
|Neuronal and glial marker proteins in encephalopathy associated with acute liver failure and acute hyperammonemia in the rabbit |
Groeneweg, M, et al
Metabolic brain disease, 8:95-106 (1993) 1993
|Distinction of two different classes of small-cell lung cancer cell lines by enzymatically inactive neuron-specific enolase |
Splinter, T A, et al
Br J Cancer, 66:1065-9 (1992) 1992
|The effect of an N-methyl-D-aspartate lesion in the hippocampus on glial and neuronal marker proteins |
Wang, S, et al
Brain Res, 541:334-41 (1991) 1991
|A simple quantitative dot-immunobinding assay for glial and neuronal marker proteins in SDS-solubilized brain tissue extracts |
Wang, S, et al
J Neurosci Methods, 33:219-27 (1990) 1990
|Immunoradiometric assay for alpha gamma- and gamma gamma-enolase (neuron-specific enolase), with use of monoclonal antibodies and magnetizable polymer particles |
Paus, E and Nustad, K
Clin Chem, 35:2034-8 (1989) 1989
|Presence of nerve growth factor-like immunoreactivity in carcinoid tumour cells and induction of a neuronal phenotype in long-term culture. |
Ahlman, H, et al.
Int. J. Cancer, 43: 949-55 (1989) 1989
|Differentiation markers (S-100, GFAP, NSE and D2) in fetal rat brain cells during malignant transformation in cell culture |
Laerum, O D, et al
J Neurooncol, 3:137-46 (1985) 1985
|Neurone-specific enolase is a molecular marker for peripheral and central neuroendocrine cells. |
Schmechel, D, et al.
Nature, 276: 834-6 (1978) 1978
|Localization of 14-3-2 protein in the rat brain by immunoelectron microscopy. |
Grasso, A, et al.
Brain Res., 122: 582-5 (1977) 1977
|RABBIT ANTI-NEURON SPECIFIC ENOLASE (NSE)|