Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neuronal specification”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

Neuron-specific enolase as a marker for intestinal neurons. An immunocytochemical study of the human intestinal tract.

Surgical specimens from various parts of the human intestinal tract as well as suction biopsy specimens, including mucosa and submucosa of the rectum, were fixed in formalin and embedded in paraffin by routine procedures. The distribution of immunoreactive areas indicating the presence of neuron-specific enolase (NSE) was then determined by using a sheep anti-human-NSE antiserum prepared in our laboratory. The immunocytochemical method revealed, in distinct contrast to other tissue components, the cell bodies of ganglion cells in the submucosa (Meissner's plexus) and in the muscle layers (Auerbach's plexus). The nerve bundles of the submucosa, of the muscle layers, and of the subserosal connective tissue were also stained, whereas the thin nerve processes of the mucosa were identified only rarely. The smooth muscle cells were stained weakly, but this reaction did not interfere with the identification of the neurons and their processes. Immunocytochemical demonstration of NSE is obviously a valuable additional method for visualization of the intrinsic intestinal innervation. It might well be that this technique will be of advantage in the diagnosis of pathologic processes, such as those occurring in Hirschsprung's disease and allied conditions.

Adolescent↗

Neuronal-specific gene expression--the interaction of both positive and negative transcriptional regulators.

Gene expression patterns in neurons are complex and are modulated in response to multiple extracellular stimuli. In addition, during development and as neurons differentiate into distinct neuronal phenotypes, there is a co-ordinated activation and repression of a variety of genes. It is becoming increasingly evident that negative regulatory elements are present in neuronal-specific promoters. These elements have been shown, in part, to restrict promoter activity to the correct physiological cell type, both in transient transfection and in transgenic mouse models. Repression can be effected by different mechanisms depending on location within the promoter of silencer complexes and their relationship to other bound transcription factors. This review will discuss the molecular mechanisms regulating promoter function, in particular: (1) the combinatorial interaction between transcription factors which generate regulated promoter function; and (2) the restriction of promoter function to the correct cell type by bound repressor molecules. Determination of the mechanism of regulated gene expression will allow advances in gene therapy and definition of novel targets for pharmaceutical intervention. At the more basic level, functional dissection of the promoters of specific neuronal expressed genes will provide information of importance in two key areas of neurobiology: (1) the mechanism by which extracellular factors, such as neurotrophins and cytokines, regulate gene expression; (2) the events which lead to the tissue-specific expression of genes in subpopulations of neurons, both in the adult and during development.

Animals↗

Neuron-specific and state-specific differences in calcium homeostasis regulate the generation and degeneration of neuronal architecture.

Many stimuli (e.g., neurotransmitters and electrical activity) regulate neuromorphogenesis by changing intracellular calcium. The ionophore A23187 was employed as a receptor-independent method to investigate neuronal calcium homeostasis. Distinctive neuron-specific (B5 versus B19) and state-specific (growing versus non-growing) differences in calcium homeostasis were observed in cultured identified Helisoma neurons. Fura-2 studies revealed that A23187 induced a transient rise in intracellular calcium in growing neurons B5 but a sustained rise in growing neurons B19. In stable-state (non-growing) cells A23187 evoked only a transient calcium rise. Both neuron-specific and state-specific differences in calcium homeostasis were dependent on extracellular sodium. Morphological studies also indicated that such differences in calcium-regulatory capacity can have profound consequences on the generation and degeneration of neuronal architecture.

Animals↗

Expression, purification and the 1.8 angstroms resolution crystal structure of human neuron specific enolase.

Human neuron-specific enolase (NSE) or isozyme gamma has been expressed with a C-terminal His-tag in Escherichia coli. The enzyme has been purified, crystallized and its crystal structure determined. In the crystals the enzyme forms the asymmetric complex NSE x Mg2 x SO4/NSE x Mg x Cl, where "/" separates the dimer subunits. The subunit that contains the sulfate (or phosphate) ion and two magnesium ions is in the closed conformation observed in enolase complexes with the substrate or its analogues; the other subunit is in the open conformation observed in enolase subunits without bound substrate or analogues. This indicates negative cooperativity for ligand binding between subunits. Electrostatic charge differences between isozymes alpha and gamma, -19 at physiological pH, are concentrated in the regions of the molecular surface that are negatively charged in alpha, i.e. surface areas negatively charged in alpha are more negatively charged in gamma, while areas that are neutral or positively charged tend to be charge-conserved.

Calorimetry, Differential Scanning↗

Neuron-specific enolase and neurofilament protein as markers of differentiation in medulloblastoma.

Immunocytochemical localization of neuron-specific enolase was performed attempting evaluation for neuronal cell differentiation in medulloblastoma. Twenty-seven cases of human medulloblastomas were stained with anti-neuron-specific enolase and antineurofilament protein serum using the peroxidase-antiperoxidase technique. All medulloblastomas showed neuron-specific enolase immunoreaction but only few had neurofilament protein-positive cells. These results suggest that a practically universal tendency towards neuronal cell differentiation occurs in medulloblastomas and that synthesis of neuron-specific enolase takes place before sufficient amounts of neurofilament protein are produced to become immunocytochemically detectable.

Cell Transformation, Neoplastic↗

Intrathecal sensory neuron-specific receptor agonists bovine adrenal medulla 8-22 and (Tyr6)-gamma2-MSH-6-12 inhibit formalin-evoked nociception and neuronal Fos-like immunoreactivity in the spinal cord of the rat.

The finding that sensory neuron-specific G-protein-coupled receptor mRNA is solely expressed in small primary sensory neurons suggests involvement of the receptor in nociceptive modulation. The present study was designed to assess effects of intrathecal administration of bovine adrenal medulla 8-22 and (Tyr6)-gamma2-MSH-6-12, selective sensory neuron-specific receptor agonists, on nocifensive behaviors and expression of spinal c-Fos-like immunoreactivity evoked by intraplantar injection of 2.5% formalin in rats. The agonists were administered 10 min before (pretreatment) and/or after (post-treatment) injection of formalin. Pretreatment with bovine adrenal medulla 8-22 dose-dependently (3, 10 and 30 nmol) decreased time lifting and licking the paw mainly in the second phase. Intrathecal bovine adrenal medulla 8-22 (30 nmol) remarkably suppressed nocifensive behaviors in the first and second phases and the expression of formalin-evoked c-Fos-like immunoreactivity in laminae I-II and V-VI of the spinal dorsal horn at L4-5. Moreover, naloxone (20 microg, intrathecal) failed to antagonize the inhibitory effects of bovine adrenal medulla 8-22. Post-treatment with bovine adrenal medulla 8-22 also exerted inhibition on the second phase behaviors in a dose-dependent manner with a similar efficacy observed in pretreatment groups. Furthermore, post-treatment with (Tyr6)-gamma2-MSH-6-12 (0.5, 1.5 and 5 nmol) also suppressed formalin-evoked nocifensive behaviors in the second phase and c-Fos-like immunoreactivity in the spinal dorsal horn similar with bovine adrenal medulla 8-22. Our results suggest that sensory neuron-specific receptor may play an important role in modulation of spinal nociceptive transmission. This is the first to demonstrate that activation of sensory neuron-specific receptor produces analgesia in the persistent pain model.

Animals↗

CSF and serum brain-specific creatine kinase isoenzyme (CK-BB), neuron-specific enolase (NSE) and neural cell adhesion molecule (NCAM) as prognostic markers for hypoxic brain injury after cardiac arrest in man.

Creatine kinase (CK) and its brain-specific isoenzyme (CK-BB), neuron-specific enolase (NSE), neural cell adhesion molecule (NCAM) and the ions sodium, potassium, chloride and calcium were measured both in CSF and serum and inorganic phosphate in CSF in order to assess their prognostic value in total brain ischemia due to cardiac arrest. The samples were collected at 4, 28 and 76 h after resuscitation. Twenty consecutive patients resuscitated from ventricular fibrillation or asystole were included in the study. Nine of the patients recovered consciousness (recovered) but eleven remained comatose (disabled). The follow-up period was 2 years after which only one patient was still alive. The earliest statistically significant differences between neurologically recovered and disabled patient groups were seen in CSF inorganic phosphate (P = 0.030) already at 4 h and CK-BB (P = 0.046) and NSE (P = 0.020) activity at 28 h. Later, at 76 h after the resuscitation CSF NSE differentiated the groups most clearly (P = 0.014). The values were higher in the disabled patients. A negative correlation between CSF parameters and Glasgow Coma scores was also seen at these timepoints. Statistically significant differences between the groups were seen in both CSF and blood pCO2, pO2, base excess (BE) and actual bicarbonate (HCO3-). CSF or serum NCAM has no prognostic value in anoxic-ischemic coma. The results suggest that in CSF CK-BB and NSE are useful prognostic indicators of hypoxic brain injury when measured 28-76 h after cardiac arrest whereas blood samples have no prognostic value.

Adult↗

Neuron-specific enolase as a marker of in vitro neuronal damage. Part II: Investigation of the astrocyte protective effect against kainate-induced neurotoxicity.

The protective effect of astrocytes on hippocampal neurons against kainate-induced toxicity was investigated using neuron-specific enolase as an indicator of neuronal death. Astrocyte-rich and astrocyte-poor mixed rat hippocampal cultures were submitted to various concentrations of kainate. At each kainate concentration, the amount of NSE released by neurons was significantly greater in astrocyte-poor than in astrocyte-rich cultures (p < 0.05). This protective effect was not observed when neuronal survival was tested on astrocyte-poor cultures in astrocyte-conditioned culture medium with or without 10(-4) M kainate. In conclusion, astrocytes significantly attenuate kainate toxicity on hippocampal neurons, and this effect is not mediated by a diffusible factor.

Animals↗

[The value of neuron specific enolase (NSE) in patients with brain tumors].

gamma gamma-Enolase is considered a specific protein of neuron, which is called neuron specific enolase (NSE). Recent reports clarified that NSE exists not only in neurons but also in neuroendocrine cells, thrombocytes and lymphocytes. Besides normal neuronal tissues, high serum levels of NSE were noticed in the patients with neuroblastomas, small cell carcinomas of the lung, and malignant gliomas, etc. In order to clarify the usefulness of NSE as a marker for intracranial neoplasms or an indicator for prognosis of the patients with intra-cranial tumors, we studied serum, CSF and intratumoral fluid levels of NSE in 62 patients with intra-cranial tumors by radioimmunoassay. Serum level of NSE in healthy adults ranged from 4.1 to 8.9 ng/ml (5.6 +/- 1.38 ng/ml, n = 15) and that of CSF ranged from 4.9 to 7.3 ng/ml (means 6.1 ng/ml, n = 3). Serum samples from patients with malignant gliomas and primitive neuroectodermal tumors contained abnormally high level of NSE, of which mean value were 22.3 ng/ml and 16.1 ng/ml, respectively. However, serum samples from patients with low grade gliomas and other intracranial tumors arising from non-neuroectodermal tissues were within normal range. In 9 patients, not only serum levels but CSF levels and/or intratumoral cyst levels of NSE were examined at the same time. Except one meningioma case, CSF levels of NSE were higher (4.9-55.3 ng/ml, mean: 19.3 ng/ml) than that of serum levels (2.3-17.3 ng/ml, mean: 12.7 ng/ml). Mean NSE concentrations of intratumoral fluids in both malignant and benign tumors were 181.7 ng/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Cytokeratin 19 fragment CYFRA 21-1 compared with carcinoembryonic antigen, squamous cell carcinoma antigen and neuron-specific enolase in lung cancer. Results of an international multicentre study.

The diagnostic value of the water-soluble cytokeratin 19 fragment CYFRA 21-1 in lung cancer was assessed in comparison with carcinoembryonic antigen, squamous cell carcinoma antigen, and neuron-specific enolase. The cut-off value, defined as 95% specificity versus a group of 526 patients suffering from benign chest diseases, was set at 3.3 micrograms/l for cytokeratin 19 fragment CYFRA 21-1 (carcinoembryonic antigen: 7.8 micrograms/l, squamous cell carcinoma antigen: 1.9 micrograms/l, neuron-specific enolase: 13.7 micrograms/l). Elevated pretreatment cytokeratin 19 fragment CYFRA 21-1 concentrations were recorded: in 112 of 244 (46%) patients with all histological types of lung cancer (carcinoembryonic antigen: 32%, squamous cell carcinoma antigen: 25%, neuron-specific enolase: 28%), in 89 of 177 (50%) patients with non-small cell lung cancer (carcinoembryonic antigen: 33%, squamous cell carcinoma antigen: 24%, neuron-specific enolase: 12%), in 47 of 81 (58%) patients with squamous cell carcinoma (carcinoembryonic antigen: 23%, squamous cell carcinoma antigen: 32%, neuron-specific enolase: 14%), in 27 of 63 (42%) patients with adenocarcinoma (carcinoembryonic antigen: 44%, squamous cell carcinoma antigen: 14%, neuron-specific enolase: 9%), in 15 of 33 (45%) patients with other non-small cell lung cancer (carcinoembryonic antigen: 36%, squamous cell carcinoma antigen: 24%, neuron-specific enolase: 14%), and in 20 of 55 (36%) patients with small cell lung cancer (carcinoembryonic antigen: 32%, neuron-specific enolase: 77%). Three of 12 patients with undefined histological type showed cytokeratin 19 fragment CYFRA 21-1 elevations. The best performance in terms of sensitivity and diagnostic accuracy was attained with the cytokeratin 19 fragment CYFRA 21-1 test in squamous cell carcinoma. In small cell lung cancer neuron-specific enolase was confirmed to be superior to the other markers. Cytokeratin 19 fragment CYFRA 21-1 concentrations increased with the extent of the malignant disease in non-small cell lung cancer. The positivity rate of cytokeratin 19 fragment CYFRA 21-1 in tumour stage TNM I was only 23% (carcinoembryonic antigen: 23%, squamous cell carcinoma antigen: 14%), i.e. the markers under study cannot be used for the diagnosis of early stage disease. Cytokeratin 19 fragment CYFRA 21-1 differentiated significantly between squamous cell carcinoma and the other histological types (p < 0.01). In addition, cytokeratin 19 fragment CYFRA 21-1 distinguished significantly the operable group TNM I-IIIa from inoperable TNM IIIb-IV (p < 0.05), but not TNM IIIa from IIIb. Out of 177 patients with non-small cell lung cancer, 90 individuals were monitored after surgery.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenocarcinoma↗

Neurons switch from non-neuronal enolase to neuron-specific enolase during differentiation.

The enolase (EC 4.2.1.11) isoenzymes, neuron-specific enolase (NSE, gamma gamma) and non-neuronal enolase (NNE, alpha alpha), are markers for neurons and glia, respectively, in adult mammalian brain. In developing fetal and early postnatal brain, levels of non-neuronal enolase (NNE) are high. Neuron-specific enolase (NSE) appears only after neurogenesis begins in a given region and only slowly attains adult levels. Immunocytochemistry in developing rat and rhesus monkey brain reveals that proliferative zones that give rise to neurons are NNE(+). Thus, nerve cells must undergo a switch from NNE to NSE. In addition, study of neurons in cerebellum and neocortex reveals that they are NNE(+) during migration and only become NSE(+) in their final location, presumably after making full synaptic connections. Such migrating cells may contain hybrid enolase (alpha gamma) and some (e.g. cerebellar stellate/basket cells) may not completely switch over to NSE even in the adult. Neuron-specific enolase is not only a specific molecular marker for mature nerve cells, but is closely correlated to the differentiated state.

Animals↗

Characterization of the BM88 promoter and identification of an 88 bp fragment sufficient to drive neurone-specific expression.

BM88 is a neurone-specific protein implicated in cell cycle exit and differentiation of neuronal precursors. It is widely expressed in terminally differentiated neurones but also in neuronal progenitors, albeit in lower levels. Thus BM88 expression shows a tight correlation with the progression of progenitor cells towards neuronal differentiation. Here we report the genomic organization and proximal promoter characterization of the human and mouse BM88 genes. Both promoters lie in a CpG island, are TATA-less and have multiple transcription start sites. Deletion analysis performed on the human BM88 gene revealed an 88 bp minimal promoter fragment that is preferentially active in neural cells. Importantly, this minimal promoter is sufficient to confer specific transcriptional activity in primary neurones, but not in glial cells. Within the promoter region there are four functional Sp1-binding sites. Simultaneous mutations to all four Sp1 sites results in complete loss of promoter activity. Transactivation experiments revealed that Sp1 directly activates the BM88 promoter while activation also occurs in the presence of neurogenin-1. Characterization of the promoter elements that control neurone-specific and developmental expression of BM88 should contribute to the elucidation of the transcriptional networks that regulate the transition from a proliferative neural progenitor to a post-mitotic neurone.

Animals↗

Neuron specific enolase in retinal detachment.

PURPOSE: Neuron Specific Enolase (NSE) is released following central nervous system (CNS) distress. As retina is part of the CNS, NSE levels were measured in the subretinal fluid (SRF), aqueous, and serum of patients with primary rhegmatogenous retinal detachment (RD). METHODS: Radioimmunoassay was used to determine NSE levels in the SRF, aqueous, and serum of 13 patients (28-92 years old, mean = 71 years) with RD. As controls, NSE was measured in the aqueous of 6 patients undergoing cataract surgery and in serum of 18 patients without ophthalmological or neurological diseases. RESULTS: SRF levels of NSE ranged from 50-200 microg/l (mean +/- s.d. = 150 +/- 57). NSE levels in aqueous from patients with RD were 2-140 microg/l (mean +/- s.d. = 39 +/- 42), significantly higher than in controls (0-6 microg/l; mean +/- s.d. = 1.58 +/- 2.24; p = 0.04). Serum NSE levels in RD patients ranged from 6.5-80 microg/l (mean +/- s.d. = 26 +/- 21) and was significantly higher than in controls (5.3 +/- 1.66 microg/l; p = 0.005). CONCLUSIONS: Retinal neuron injury in retinal detachment (RD) releases sufficient Neuron Specific Enolase (NSE) to be detected in subretinal fluid, aqueous, and even in serum. Thus, NSE could index disease severity in RD and provide a means by which to assess the response to neuroprotection in RD.

Adult↗

A bi-functional activator/repressor element required for transcriptional activity of the human UCH-L1 gene assembles a neuron-specific protein: single-strand DNA complex.

The ubiquitin C-terminal hydrolase (UCH)-L1 gene is expressed in a tissue- and cell-specific manner with expression restricted to neurons and neuroendocrine cells. Regulatory DNA sequences from the 5' untranscribed region of the human UCH-L1 gene will promote neuron specific transcription providing that a 59 bp sequence located between nucleotides -182 and -123 is present in reporter gene constructs. We show that this 59 bp sequence is a bi-functional regulator of transcription, acting as an activator in human neuroblastoma cells (SH-SY5Y) and a strong repressor in HeLa cells. The sense strand of the UCH-L1 activator/repressor element can interact with nuclear proteins that recognize single stranded DNA in a sequence specific manner. Nuclear extracts from neuroblastoma cells generate a protein:ssDNA interaction called complex 1B could be converted into a lower mobility complex (1A) by increasing the protein:DNA ratio. This conversion was not observed when using nuclear extracts from HeLa cells. Formation of neuron specific complex 1A could be prevented by incubation of protein:ssDNA complexes at 2 degrees C or in the presence of mM concentrations of MgCl2. In conclusion, we have identified a novel bi-functional regulatory DNA element in the promoter of the human UCH-L1 gene that contributes to neuron-restricted transcription and which can assemble a neuron specific protein:ssDNA complex on its sense strand.

DNA, Single-Stranded↗

Variable subcellular localization of a neuron-specific protein during NTera 2 differentiation into post-mitotic human neurons.

The current report describes the molecular characterization of the human (the D4S234 locus) and mouse (the m234) homologs of a gene that was isolated during our genomic analysis of the Huntington disease gene region. Sequence comparisons of full-length cDNA clones revealed that the mouse and human homologs encoded evolutionarily conserved 21-kDa proteins with greater than 90% amino acid sequence identity. Extensive sequence identity between the D4S234 gene and the rat p1A75 gene (a previously identified rat neuron-specific gene) showed that these genes are interspecies homologs. Furthermore, the D4S234 protein exhibited significant amino acid similarity to a 19-kDa mouse protein that localizes to the Golgi apparatus of embryonic neurons. However, nonconservative sequence differences suggested that these genes are independent members of a multigene family. Northern analyses revealed that rodent D4S234 expression occurred predominantly in the brain and included all brain regions. Neuron-specific expression was demonstrated using Northern analysis of cultured glial cells and quinolinic acid-treated rat brain samples. Minimal amounts of the rodent D4S234 mRNA were detected prenatally; however, elevated adult levels were detected within 1 month of birth. Sequence analyses of the human and mouse D4S234 proteins identified an evolutionarily conserved hydrophobic sequence and a consensus nuclear localization signal in both genes. Immunofluorescence microscopy, using an antipeptide antibody, established that the human D4S234 protein preferentially localized to the nucleus of mitotic cultured cells. Since the rat p1A75 protein was previously mapped to the neuronal cytoplasm by in situ hybridization, the subcellular localization of the D4S234 protein was subsequently examined during differentiation of the NTera 2 (NT2) cell line. Following differentiation into postmitotic NT2-N neurons, the D4S234 protein demonstrated cytoplasmic staining and reduced or undetectable nuclear staining in many cells. The variation in the intracellular localization of the D4S234 protein in mitotic and nonmitotic cells suggests that the subcellular localization of this protein is developmentally regulated and provides clues about the biochemical function of this protein.

Amino Acid Sequence↗

Neuron-specific enolase in gerbil brain and serum after transient cerebral ischemia.

BACKGROUND AND PURPOSE: The sensitivity and validity of serum neuron-specific enolase as a marker of brain injury were tested after global cerebral ischemia. METHODS: Sixty-nine Mongolian gerbils were perfusion fixed after variable reperfusion after 5-minute (group 1) or 15-minute (group 2) bilateral carotid occlusion. Neuron-specific enolase was analyzed by an enzyme immunoassay in serum of control, sham-operated, and ischemic animals before euthanasia and in nonischemic gerbil brains. Brains were processed for histology, immunohistochemistry, and morphometric evaluation of ischemic neuronal damage. RESULTS: After cerebral ischemia, loss of neuronal immunoreactivity was closely associated with increased neuron-specific enolase serum levels, which were significantly elevated by 24 hours (group 1) or by 4 hours (group 2) of reperfusion (P < .001). Response of serum levels depended on the duration of preceding ischemia, and maximum concentrations were approximately 3-fold (group 1) or 20-fold (group 2) those of nonischemic control. Morphological damage became apparent 48 hours (group 1) or 12 hours (group 2) after ischemia, as indicated by histological and morphometric data. CONCLUSIONS: Significantly elevated neuron-specific enolase serum levels could be demonstrated as a consequence of ischemia-induced cytoplasmic loss of neuron-specific enolase in central nervous system neurons, corresponded quantitatively to the severity of cerebral ischemia, and were detectable before irreversible neuronal injury. Therefore, analysis of serum neuron-specific enolase is suggested to be both a valuable diagnostic tool in clinical management of the initial stages of global cerebral ischemia and a prognostic parameter during the postischemic course.

Animals↗

Neuron-specific Bcl-2 homology 3 domain-only splice variant of Bak is anti-apoptotic in neurons, but pro-apoptotic in non-neuronal cells.

We have identified and characterized N-Bak, a neuron-specific isoform of the pro-apoptotic Bcl-2 family member Bak. N-Bak is generated by neuron-specific splicing of a novel 20-base pair exon, which changes the previously described Bak, containing Bcl-2 homology (BH) domains BH1, BH2, and BH3, into a shorter BH3-only protein. As demonstrated by reverse transcription-polymerase chain reaction and RNase protection assay, N-Bak transcripts are expressed only in central and peripheral neurons, but not in other cells, whereas the previously described Bak is expressed ubiquitously, but not in neurons. Neonatal sympathetic neurons microinjected with N-Bak resisted apoptotic death caused by nerve growth factor (NGF) removal, whereas microinjected Bak accelerated NGF deprivation-induced death. Overexpressed Bak killed sympathetic neurons in the presence of NGF, whereas N-Bak did not. N-Bak was, however, still death-promoting when overexpressed in non-neuronal cells. Thus, N-Bak is an anti-apoptotic BH3-only protein, but only in the appropriate cellular environment. This is the first example of a neuron-specific Bcl-2 family member.

Alternative Splicing↗

Transgenic mice expressing beta-galactosidase in mature neurons under neuron-specific enolase promoter control.

To gain insights into transcription factors defining neuronal identity, we generated transgenic mice carrying a 1.8 kb rat neuron-specific enolase (NSE) promoter fragment fused to an E. coli lacZ gene. Four of seven transgenic families expressed transgene RNA in the nervous system but not in most other tissues. Histochemical analysis of adult brain from the two lines with highest lacZ mRNA levels showed neuron-specific, pan-neuronal beta-galactosidase activity. Developmental RNA and histochemical analyses showed parallel onset of transgene and endogenous NSE gene expression in various neuronal cell types, although the magnitude of NSE mRNA accumulation later in development was not matched by the transgene. These results suggest that cis-acting regulatory elements, subject to neuron-specific control, are located within 1.8 kb upstream from the NSE gene.

Animals↗