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PubMed2004

Detection of cancer-related gene expression profiles in severe cervical neoplasia.

The molecular signatures of 20 severe cervical intraepithelial neoplasia (CIN3) cases and 10 cervical squamous cell cancers were determined to define cancer-related gene expression profiles. RNAs extracted from microdissected tissues were amplified by SMART technology and used as probes for hybridization of commercially available cDNA array filters comprising 1,176 cancer-related genes. Ninety-two differentially expressed genes were identified by comparison of pooled cDNA from CIN3 vs. cervical cancer. Heterogeneity in expression of this subset of genes was then analyzed for each biopsy using an algorithm for self-organizing maps. For several gene clusters, the expression pattern for CIN3 differed significantly from that of cancer. Moreover, hierarchical clustering revealed significant differences in distribution of CIN and cancer. Several CIN cases were more strongly related to cancer, suggesting that gene expression profiling may be useful for subdividing pathologically indistinguishable precancers into different biologic entities. This approach also provides a basis for the identification of putative prognostic markers and for targeted molecular therapy.

Adult↗
PubMed2005

Involvement of the chaperone tapasin in HLA-B44 allelic losses in colorectal tumors.

Tumors can exhibit selective allelic losses of HLA class I antigens as part of altered HLA phenotypes. In colorectal tumors, the HLA class I allele most frequently lost is HLA-B44, although the precise mechanism responsible for this loss has not been described to date. From a total of 95 colorectal cryopreserved tumor samples, we selected (by immunohistochemical staining) 13 tumors with HLA-B44-negative expression. Loss of heterozygosity at 6p21.3 was demonstrated to be the cause of the negative expression in 4 cases. In the remaining 9 cases, structural analyses of microdissected tissue samples of the 3 subtypes of HLA-B44 loss in these tumors (B*4402, B*4403 and B*4405) did not reveal any mutations. However, all 3 subtypes of HLA-B44 presented in this study shared a common characteristic: the presence of an aspartic amino acid residue at position 114 in the HLA class I heavy chain. This residue has been described as determining tapasin dependence for the surface expression of these alleles and therefore for antigen presentation. We studied tapasin transcription by RT-PCR in these tumors and found tapasin downregulation in all 9 tumors samples with the HLA-B44-negative phenotype. In contrast, tapasin was normally transcribed in HLA-B44-positive colorectal tumors samples, as well as in 3 HLA-B44-negative laryngeal carcinomas and 1 bladder tumor. Defective tapasin transcription seems to be an alteration responsible for the absence of HLA-B44 expression in colorectal tumors, thus contributing to the generation of tumor immune escape phenotypes.

Antiporters↗
PubMed2002

Detection of prolactin receptor mRNA in the corpus striatum and substantia nigra of the rat.

The observation of prolactin modulation of the nigrostriatal dopaminergic system suggests the expression of prolactin receptor in the corpus striatum or substantia nigra. The present study investigated expression of prolactin receptor mRNA in tissues microdissected from the corpus striatum and substantia nigra of the rat. By using reverse transcription PCR combined with Southern hybridization, the long form of prolactin receptor mRNA was detected in the substantia nigra, caudate putamen, globus pallidus, and ventral pallidum in ovariectomized rats, whereas the short form was not detectable in any of these areas. Estrogen had no effect on expression of the long-form mRNA in the substantia nigra and corpus striatum. By using the RNase protection assay, the expression of both short and long forms of prolactin receptor mRNA was observed in the corpus striatum in ovariectomized rats. Again, levels of expression were not significantly altered by estrogen treatment. Both forms of prolactin receptor mRNA were clearly expressed in the choroid plexus and were up-regulated by estrogen treatment. The expression of both forms of prolactin receptor mRNA in nigrostriatal areas may help to support the hypothesis that prolactin has direct actions on these brain regions.

Animals↗
PubMed2002

Proteomic analysis of human prostate cancer.

Proteomics is a promising approach in the identification of proteins and biochemical pathways involved in tumorigenesis. In an effort to discover such proteins and pathways that are deregulated in prostate tumorigenesis, cellular proteomes of matched normal prostate epithelial cells and high-grade prostate cancer cells were analyzed by tissue microdissection, two-dimensional electrophoresis, and mass spectrometry. Forty protein alterations were detected in the tumors; however, the majority of these changes were not shared among the 12 neoplasms. In contrast, parallel cDNA microarray analysis identified a number of common gene expression changes. The marked heterogeneity of the observed protein alterations may have significance with regard to tumor biology and research strategies for molecular profiling analyses of human prostate cancer.

Electrophoresis, Gel, Two-Dimensional↗
PubMed1992

Role of mutations at codon 61 of the c-Ha-ras gene during diethylnitrosamine-induced hepatocarcinogenesis in C3H/He mice.

Liver tumors of certain strains of mice frequently contain mutations at codon 61 of the c-Ha-ras gene. In our study, we investigated the significance of these mutations in the carcinogenic process. Male C3H/He mice received a single injection of diethylnitrosamine (DEN) on day 15 after birth, and groups of animals were killed at various time intervals between 11 and 52 wk after treatment. At the earlier time points (11-29 wk), we analyzed microdissected tissue from precancerous glucose-6-phosphatase-deficient liver lesions larger than approximately 200 microns in diameter, for the presence and pattern of c-Ha-ras codon 61 mutations. In parallel, the growth characteristics of these liver lesions were studied by pulse labeling with [3H]thymidine and by determining the size distribution of the lesions. At the later time points (42-52 wk after DEN treatment), liver tumors were dissected and also analyzed for the presence of c-Ha-ras mutations. We found mutations to be already present in some of the enzyme-altered liver lesions at weeks 11-29, suggesting that the mutations occurred early in the carcinogenic process. Whereas about 10% of the precancerous focal liver lesions showed mutations in the c-Ha-ras gene, the mutation frequency was increased to about 50% in the later-appearing hepatocellular adenomas and carcinomas, suggesting that c-Ha-ras codon 61 mutations may provide a selective advantage to the mutated cell clones.

Animals↗
PubMed1994

Absence of p53 mutations and various frequencies of Ki-ras exon 1 mutations in rat hepatic tumors induced by different carcinogens.

Mutations of p53 and Ki-ras exon 1 were investigated in rat hepatic lesions induced by four kinds of hepatocarcinogenic protocols: continuous feeding of 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB), daily intraperitoneal injection of aflatoxin B1 (AFB1), and the Solt and Farber regimen (Nature 236:701-703, 1976), in which diethylnitrosamine (DEN) or nitrosomethylurea (NMU) was used as initiating agents. DNA from microdissected tissue sections was amplified by the polymerase chain reaction (PCR) directly using primers for p53 exons 5-8 and Ki-ras exon 1 and analyzed for mutations by denaturing gradient gel electrophoresis (DGGE) or constant denaturant gel electrophoresis (CDGE). One or both of the p53 PCR primers were located within introns to prevent amplifying the p53 processed pseudogenes. In a total of 59 hepatocellular carcinomas (HCCs), no p53 aberrations were detected, indicating that p53 mutations are not very important in rat hepatic carcinogenesis. On the other hand, Ki-ras codon 12 mutations were found at low frequency in HCCs, hyperplastic foci, and cholangiofibroses induced by 3'-Me-DAB and by AFB1 but not in the lesions induced by the Solt and Farber regimen. Although Ki-ras codon 12 mutations are generally infrequent in rat hepatic tumors, their incidence thus appears to vary depending on the carcinogen used for their induction.

Animals↗
PubMed2004

Loss of heterozygosity at chromosome 9p21 is a frequent finding in enteropathy-type T-cell lymphoma.

Enteropathy-type T-cell lymphoma (ETL) and ulcerative jejunitis (UJ) are rare disorders often occurring in patients with coeliac disease. The genetic events associated with the accumulation of intraepithelial lymphocytes in coeliac disease and tumour development are largely unknown. Deletions at chromosome 9p21, which harbours the tumour suppressor genes p14/ARF, p15/INK4b, and p16/INK4a, and 17p13, where p53 is located, are associated with the development and progression of lymphomas. To examine whether deletions at 9p21 and 17p13 play a role in ETL, 22 cases of ETL and seven cases of UJ were screened for loss of heterozygosity (LOH) by tissue microdissection and polymerase chain reaction (PCR) analysis for microsatellite markers. Furthermore, p53 and p16 protein expression was examined by immunohistochemistry. In addition, polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP) analysis for detection of mutations in exons 5-8 of the p53 gene was performed in five cases of ETL and three cases of UJ. LOH was found in at least one microsatellite marker at the 9p21 locus in 8 of 22 (36%) ETLs, but not in UJ. Five of nine (56%) tumours composed of large cells showed LOH at 9p21, as opposed to two of eight (25%) tumours with small- or medium-sized cell morphology. The region spanning the p14/p15/p16 gene locus was most frequently affected (five cases); LOH at these markers coincided with loss of p16 protein expression in all of these cases. p53 overexpression was demonstrated in all ETLs examined and in four of seven cases of UJ. However, no alterations of the p53 gene were detected by LOH or PCR-SSCP analysis. The results of this study show that LOH at chromosome 9p21 is frequent in ETL, especially in tumours with large cell morphology; this finding suggests that gene loss at this locus may play a role in the development of ETL.

Adult↗
PubMed2005

Increased CD59 protein expression predicts a PSA relapse in patients after radical prostatectomy.

BACKGROUND: Human protectin (CD59) is a regulator of complement activation that inhibits complement-mediated cell lysis, and thus might confer immune resistance to tumor cells. CD59 expression has been described in a variety of human malignancies, including breast cancer. Since a comprehensive investigation of CD59 expression in prostate cancer has not been conducted yet, we aimed to determine the significance of CD59 expression in prostate cancer. METHODS: Eighty-six primary adenocarcinomas of the prostate were immunostained using a monoclonal CD59 antibody (clone MEM-43) and a standard detection system. The immunoreactivity of the tumor was evaluated as low versus high for statistical analysis. Additionally, CD59 mRNA levels were determined by real-time PCR in matched (tumor/normal) microdissected tissues from 26 cases. RESULTS: Cytoplasmic CD59 immunoreactivity was found in epithelia of prostate cancer, prostatic intraepithelial neoplasia, benign hyperplasia, atrophic, and normal glands. High rates of CD59 expression were noted in 36% of prostate cancer cases and were significantly associated with tumor pT stage (P = 0.043), Gleason grade (P = 0.013) and earlier biochemical (PSA) relapse in Kaplan-Meier analysis (P = 0.0013). On RNA level, we found an upregulation in 19.2% (five cases), although the general rate of CD59 transcript was significantly lower in tumor tissue (P = 0.03). CONCLUSION: CD59 protein is strongly expressed in 36% of adenocarcinomas of the prostate and and is associated with disease progression and adverse patient prognosis.

Adenocarcinoma↗
PubMed2001

An 800-kb region of deletion at 13q14 in human prostate and other carcinomas.

Deletions of regions at 13q14 have been detected by various genetic approaches in human cancers including prostate cancer. Several studies have defined one region of loss of heterozygosity (LOH) at 13q14 that seems to reside in a DNA segment of 7.1 cM between genetic markers D13S263 and D13S153. To define the smallest region of overlap (SRO) for deletion at 13q14, we first applied tissue microdissection and multiplex PCR to detect homozygous deletion and/or hemizygous deletion at 13q14 in 134 prostate cancer specimens from 114 patients. We detected deletions at markers D13S1227, D13S1272, and A005O48 in 13 (10%) of these tumor specimens. Of the 13 tumors with deletions, 12 were either poorly differentiated primary tumors or metastases of prostate cancer. To fine-map the deletion region, we then constructed a high-resolution YAC/BAC/STS/EST physical map based on experimental and database analyses. Several markers encompassing the deletion region were analyzed for homozygous deletion and/or hemizygous deletion in 61 cell lines/xenografts derived from human cancers of the prostate, breast, ovary, endometrium, cervix, and bladder, and a region of deletion was defined by duplex PCR assay between markers A005X38 and WI-7773. We also analyzed LOH at 13q14 in the 61 cell lines/xenografts using the homozygosity mapping of deletion approach and 26 microsatellite markers. We found 24 (39%) of the cell lines/xenografts to show LOH at 13q14 and defined a region of LOH by markers M1 and M5. Combination of homozygous or hemizygous deletion and LOH results defined the SRO for deletion to be an 800-kb DNA interval between A005X38 and M5. There are six known genes located in or close to the SRO for deletion. This region of deletion is at least 2 Mb centromeric to the RB1 tumor-suppressor gene and the leukemia-associated genes 1 and 2, each of which is located at 13q14. These data suggest that the 800-kb DNA segment with deletion contains a gene whose deletion may be important for the development of prostate and other cancers. This study also provides a framework for the fine-mapping, cloning, and identification of a novel tumor-suppressor gene at 13q14.

Adult↗
PubMed1986

Gluconeogenic-glycolytic capacities and metabolic zonation in liver of rats with streptozotocin, non-ketotic as compared to alloxan, ketotic diabetes.

Activities (mumol X min-1 X g liver) and zonal distributions of key enzymes of carbohydrate metabolism were studied in livers of streptozotocin-diabetic rats and compared to the values in alloxan-diabetes. Streptozotocin led to a non-ketotic diabetes with blood glucose being increased by more than fivefold but ketone bodies being in the normal range, while alloxan produced a ketotic diabetes with blood glucose, acetoacetate and beta-hydroxybutyrate being elevated by more than fivefold. Portal insulin was decreased to about 20% in streptozotocin- and more drastically to about 7% in alloxan-diabetes. Conversely, portal glucagon was increased in the two states to about 250% and 180%, respectively. The glucogenic key enzyme phosphoenolpyruvate carboxykinase (PEPCK) was enhanced in streptozotocin- and alloxan-diabetes to over 300%, while the glycolytic pyruvate kinase L (PKL) was lowered to 65% and 80%, respectively. The normal periportal to perivenous gradient of PEPCK of about 3:1, as measured in microdissected tissue samples, was maintained with elevated activities in the two zones. The normal periportal to perivenous gradient of PKL of 1:1.7 was diminished with lowered activities in the two zones. The glucogenic glucose-6-phosphatase (G6Pase) was increased in streptozotocin- and alloxan-diabetes to 130% and 140%, respectively, while the glucose utilizing glucokinase (GK) was decreased to 60% and 50%, respectively. The normal periportal to perivenous gradient of G6Pase, demonstrated histochemically, remained unaffected. Carnitine palmitoyltransferase (CPT) was increased to over 190% and acetyl-CoA carboxylase (ACC) was decreased to 60% in streptozotocin, non-ketotic diabetes, while the two enzymes were altered more drastically to 400% and 50%, respectively, in alloxan, ketotic diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Alloxan↗
PubMed1984

Cytokeratins in normal lung and lung carcinomas. I. Adenocarcinomas, squamous cell carcinomas and cultured cell lines.

The various epithelial cells of the lower respiratory tract and the carcinomas derived from them differ markedly in their differentiation characteristics. Using immunofluorescence microscopy and two-dimensional gel electrophoresis of cytoskeletal proteins from microdissected tissues we have considered whether cytokeratin polypeptides can serve as markers of cell differentiation in epithelia from various parts of the human and bovine lower respiratory tract. In addition , we have compared these protein patterns with those found in the two commonest types of human lung carcinoma and in several cultured lung carcinoma cell lines. By immunofluorescence microscopy, broad spectrum antibodies to cytokeratins stain all epithelial cells of the respiratory tract, including basal, ciliated, goblet, and alveolar cells as well as all tumor cells of adenocarcinomas and squamous cell carcinomas. However, in contrast, selective cytokeratin antibodies reveal cell type-related differences. Basal cells of the bronchial epithelium react with antibodies raised against a specific epidermal keratin polypeptide but not with antibodies derived from cytokeratins characteristic of simple epithelia. When examined by two-dimensional gel electrophoresis, the alveolar cells of human lung show cytokeratin polypeptides typical of simple epithelia (nos. 7, 8, 18 and 19) whereas the bronchial epithelium expresses, in addition, basic cytokeratins (no. 5, small amounts of no. 6) as well as the acidic polypeptides nos. 15 and 17. Bovine alveolar cells also differ from cells of the tracheal epithelium by the absence of a basic cytokeratin polypeptide. All adenocarcinomas of the lung reveal a "simple-epithelium-type" cytokeratin pattern (nos. 7, 8, 18 and 19). In contrast, squamous cell carcinomas of the lung contain an unusual complexity of cytokeratins. We have consistently found polypeptides nos. 5, 6, 8, 13, 17, 18 and 19 and, in some cases, variable amounts of cytokeratins nos. 4, 14 and 15. Several established cell lines derived from human lung carcinomas (SK-LU-1, Calu -1, SK-MES-1 and A-549) show a uniform pattern of cytokeratin polypeptides (nos. 7, 8, 18 and 19), similar to that found in adenocarcinomas. In addition, vimentin filaments are produced in all the cell lines examined, except for SK-LU-1.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenocarcinoma↗
PubMed2002

Beta-catenin expression and allelic loss at APC in sporadic colorectal carcinogenesis.

beta-catenin is involved in E-cadherin-mediated cell adhesion, intracellular signal transduction, and also interacts with adenomatous polyposis coli (APC) protein. We previously found that 31% of colorectal adenomas and 84% of carcinomas showed reduced membranous staining of beta-catenin, while 46% of adenomas and 79% of carcinomas displayed beta-catenin nuclear expression. Importantly, a reciprocal relationship between reduced membranous and increased nuclear beta-catenin expression was demonstrated in the development from adenoma to carcinoma. To clarify whether this relates to an abnormality of the APC gene ( APC), we have now studied allele loss in microdissected tissues from 74 adenomas and 21 carcinomas (sporadic cases, previously immunostained for beta-catenin) by analysis of the microsatellites D5S346, D5S82 and D5S299. Fifty-five tumors (57.8%) showed allele loss at APC (no difference between adenomas and carcinomas). Thirty-one of these 55 (31/55, 56.4%) displayed both increased nuclear localization and reduced membranous staining of beta-catenin, and thirteen tumors (13/55, 23.6%) manifested either nuclear expression without changes in membranous expression or reduced membranous staining without nuclear expression (9 and 4 cases, respectively), while 11 (11/55, 20.0%) preserved normal membranous expression. Adenomas and carcinomas showing both nuclear and reduced membranous expression of beta-catenin, compared with those with normal membranous expression, tended to show allele loss ( P<0.01). In addition, 24 (24/95, 25.6%) tumors showed a change in the pattern of beta-catenin expression, but did not exhibit allele loss. These results suggest that although there may be a number of mechanisms responsible for changes in beta-catenin expression in colorectal tumors, dysfunction of APC may be the major cause of this phenomenon.

Adenoma↗
PubMed2005

Intratumoral heterogeneous expression of p53 correlates with p53 mutation, Ki-67, and cyclin A expression in endometrioid-type endometrial adenocarcinomas.

To further elucidate the significance of p53 mutation in endometrial carcinoma, we investigated it in endometrioid-type endometrial carcinomas showing intratumoral heterogeneous p53 expression. In addition, we also examined the correlation of p53 mutation and cyclin A expression, because we previously reported a topological correlation between the expression of p53 and cyclin A. The p53 mutation in exons 5-8 in 54 cases of endometrial carcinoma showing immunohistochemical expression of p53 was examined using microdissected tissue DNAs. Of the 54 p53-positive endometrial carcinomas, 23 (43%) had p53 mutation with a tendency in histologically higher grade tumors. Ten of the 54 showed a heterogeneous p53 expression, and in 9 of the 10 cases, p53 mutation was present only in p53-positive sites, which were often found in histologically less differentiated areas with elevated Ki-67 in the same tumor. Cyclin A expression was topologically observed in p53-positive areas; however, it was noted in both tumors with (12/23, 52%) and without (18/31, 58%) p53 mutation. These results suggest that p53 mutation is a late event and plays an important role in the acquisition of malignant potentials in endometrioid-type endometrial adenocarcinomas. Unexpectedly, accumulation of the p53 protein itself may be important in cyclin A overexpression.

Adult↗
PubMed1991

Intraacinar profiles of alcohol dehydrogenase and aldehyde dehydrogenase activities in human liver.

The intraacinar activity profiles of alcohol dehydrogenase and the aldehyde dehydrogenases (I, I plus II, and total) were determined, using liver biopsy samples from eight male and eight female patients. Microchemical assays were performed in microdissected tissue samples from the whole length of the sinusoid. Alcohol dehydrogenase activity in men less than 53 years of age showed a maximum in the intermediate zone, whereas in women less than 50 years of age an increase in the gradient toward the perivenous zone was observed. Furthermore, alcohol dehydrogenase activity in the livers of women was significantly higher than in men. After the age of 53 in men and 50 in women, the sex specificity of the distribution profiles was no longer apparent. The intraacinar profiles of aldehyde dehydrogenase isoenzymes showed only minor variations in the different groups; they were not statistically significant. This is also true for low-Michaelis constant (Km) aldehyde dehydrogenase, which is most important for acetaldehyde oxidation in vivo. Thus, of the variations in zonal heterogeneity of ethanol-degrading enzymes, it is mainly the activity of alcohol dehydrogenase that may contribute to the sex- and age-related susceptibility of liver parenchyma.

Adolescent↗
PubMed1983

Application of high-performance liquid chromatography with electrochemical detection to the determination of catecholamines in microdissected regions of the rat brain.

High-pressure liquid chromatography (HPLC) with electrochemical detection was applied for measurement of catecholamines in microdissected tissues from discrete brain regions. Brain areas were dissected, extracted and processed for HPLC assay without further purification. The advantage of this method is its simplicity and relatively low cost and may therefore be applied to the measurement of amines in brain micropunches.

Animals↗
PubMed1986

Further evidence for excitatory amino acid transmission in the lateral habenular projection to the rostral raphe nuclei: lesion-induced decrease of high affinity glutamate uptake.

In previous autoradiographic studies we reported selective retrograde D-[3H]aspartate labelling of lateral habenular afferents to the nuclei raphe dorsalis (NRD) and centralis superior (RCS). This study reports biochemical support, lesion-induced decrease of high affinity glutamate uptake, for excitatory amino acid transmission in the habenulo-raphe connection. Rats received bilateral electrolytic lesions in the lateral habenular nuclei and survived 9-10 days. Brainstems were sectioned on a Vibratome, and NRD and RCS tissue microdissected. Glutamate uptake in sham-operated rats was in the NRD 23.6 +/- 2.3 nmol/g prot. (mean +/- S.E.M.) ([3H]glutamate 10(-7) M, 3 min, 25 degrees C) and in the RCS 14.6 +/- 1.0 nmol/g. Habenular lesions reduced glutamate uptake in the NRD by 20.7 +/- 2.0% (P less than 0.001) and in the RCS by 10.7 +/- 4.3% (P less than 0.05).

Amino Acids↗
PubMed1986

Thalamic control of dopaminergic functions in the caudate-putamen of the rat--II. Studies using ibotenic acid injection of the parafascicular-intralaminar nuclei.

We have investigated the role of the parafascicular-intralaminar thalamus in the regulation of dopaminergic function in the caudate-putamen by making unilateral injections of the excitotoxin, ibotenic acid, into the thalamus of the halothane-anaesthetized rat. Dopamine utilization was measured at 4 h, 18 h, and 7 days after operation in microdissected tissue from caudate-putamen, substantia nigra, and nucleus accumbens. High performance liquid chromatography with electrochemical detection was used to simultaneously determine dopamine, 3,4-dihydroxyphenylacetic acid and homovanillic acid. Dopamine utilization was recorded as a ratio of metabolite to its parent amine. At 4 h following injection large bilateral increases in dopamine utilization were recorded in both medial and lateral sectors of caudate-putamen. The percentage increases found for homovanillic acid-based ratios were larger than those found for 3,4-dihydroxyphenylacetic acid-based ratios. These results probably reflect increased dopamine release resulting from the acute effects of ibotenic acid. These changes were independent of dopamine utilization ratios recorded in the substantia nigra, which showed no change either ipsilateral or contralateral to the injection. In contrast to these findings, at 7 days following injection, dopamine utilization ratios were reduced both ipsilateral and contralateral to the injection, although only the ipsilateral reductions were significant. Again, no change was found for this survival time in the substantia nigra. At 18 h survival an intermediate pattern between the 4 h and 7 day result was found. In the nucleus accumbens, ibotenic acid injection produced similar results to those found in caudate-putamen, i.e. a bilateral increase in dopamine utilization at early time intervals and a unilateral ipsilateral decrease at long intervals following injection. These results show that dopamine release in the caudate-putamen is sensitive to experimentally induced changes in neural activity and lesions of its thalamic input. Since the effect of presumed stimulation is markedly greater than lesion, it would appear that, under the conditions employed in these experiments, the thalamus is relatively silent; a suggestion consistent with other evidence. Furthermore, since the changes found occurred in the absence of changes in utilization ratios in the substantia nigra, the mechanisms whereby thalamus regulates dopamine release may be exerted via a local circuit and/or a presynaptic mechanism in the region of dopamine terminals. The anatomical routes responsible for these effects are discussed.(ABSTRACT TRUNCATED AT 400 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed2006

BDNF regulation in the rat dorsal vagal complex during stress-induced anorexia.

The dorsal vagal complex (DVC) is the satiety reflex-integrating center of adult mammals. Immobilization stress (IS) is known to elicit anorexia and to up-regulate BDNF expression in adult rat forebrain; intra-DVC delivery of BDNF was shown to elicit anorexia. Therefore, we addressed here whether IS would increase BDNF signaling in rat DVC by using PCR and western-blot on microdissected tissue extracts. Significant variations of BDNF expression in DVC after IS include exon V mRNA increase at 3 h, decreases of both protein and exon III mRNA at 24 h, and exon I mRNA decrease at 72 h. At the receptor level, IS elicited a highly significant induction of both full-length and truncated-1 TrkB mRNAs at 24 h after IS. In vivo recruitment of BDNF signaling in DVC during stress thus differs from hypothalamus, the relevance of which to anorexia is discussed.

Analysis of Variance↗