• Refine Query
  • Source
  • Publication year
  • to
  • Language
  • 4
  • 2
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • Tagged with
  • 5
  • 5
  • 5
  • 2
  • 2
  • 2
  • 2
  • 2
  • 2
  • 2
  • 1
  • 1
  • 1
  • 1
  • 1
  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

The phencyclidine model of schizophrenia : dysregulation of brain dopamine systems induced by NMDA receptor antagonists : an experimental study /

Mathé, Jan M., January 1900 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 7 uppsatser.
2

Prenatal cocaine exposure: the effects on the rat brain dopaminergic system of the offspring.

January 1994 (has links)
by Choi, Heung Ling. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1994. / Includes bibliographical references (leaves 79-95). / Acknowledgement --- p.iv / Abstract --- p.vi / Chapter CHAPTER 1 --- INTRODUCTION / Chapter 1.1 --- Cocaine --- p.1 / Chapter 1.1.1 --- History --- p.1 / Chapter 1.1.2 --- Epidemiology --- p.2 / Chapter 1.1.3 --- Pharmacology --- p.3 / Chapter 1.2 --- Maternal Cocaine Abuse --- p.5 / Chapter 1.2.1 --- Human Studies --- p.5 / Chapter 1.2.1.1 --- Prevalence --- p.5 / Chapter 1.2.1.2 --- Effects of Cocaine on the Developing Fetus --- p.7 / Chapter 1.2.1.2.1 --- Fetal Mortality --- p.8 / Chapter 1.2.1.2.2 --- Placental Abruption --- p.9 / Chapter 1.2.1.2.3 --- Premature Birth --- p.9 / Chapter 1.2.1.2.4 --- Neonatal Effects --- p.10 / Chapter 1.2.1.3 --- Congenital Abnormalities --- p.11 / Chapter 1.2.1.3.1 --- Cardiovascular Abnormality --- p.11 / Chapter 1.2.1.3.2 --- Genitourinary Tract Malformation --- p.12 / Chapter 1.2.1.3.3 --- Gastrointestinal Abnormality --- p.12 / Chapter 1.2.1.3.4 --- Respiratory Disorders --- p.13 / Chapter 1.2.1.3.5 --- Visual and Hearing Disorders --- p.14 / Chapter 1.2.1.3.6 --- CNS and Behavioural Abnormalities --- p.15 / Chapter 1.2.2 --- Animal Studies --- p.17 / Chapter 1.2.2.1 --- "Routes of Administration, Dosage and Tissue Distribution " --- p.18 / Chapter 1.2.2.2 --- Maternal and Offspring Effects --- p.21 / Chapter 1.2.2.2.1 --- Fetal and Maternal Mortality --- p.22 / Chapter 1.2.2.2.2 --- Gestational Length --- p.22 / Chapter 1.2.2.2.3 --- Maternal Weight Gain and Fetal Weight --- p.23 / Chapter 1.2.2.2.4 --- Little Size --- p.24 / Chapter 1.2.2.3 --- Congenital Abnormalities --- p.24 / Chapter 1.2.2.4 --- Behavioral Changes --- p.26 / Chapter 1.2.2.5 --- Neurochemical Changes --- p.28 / Chapter 1.2.2.5.1 --- Glucose Metabolism --- p.28 / Chapter 1.2.2.5.2 --- Dopamine Transporter --- p.29 / Chapter 1.2.2.5.3 --- Dopamine D1 Receptor --- p.29 / Chapter 1.2.2.5.4 --- Dopamine D2 Receptor --- p.30 / Chapter 1.2.2.5.5 --- Tyrosine Hydroxylase --- p.30 / Chapter 1.2.2.5.6 --- Other Changes --- p.31 / Chapter 1.3 --- The Aim of the Study --- p.31 / Chapter CHAPTER II --- MATERIALS AND METHODS / Chapter 2.1 --- Administration of Cocaine --- p.34 / Chapter 2.2 --- Biochemical Studies --- p.35 / Chapter 2.2.1 --- Receptor Binding Assays --- p.36 / Chapter 2.2.1.1 --- Dopamine Transporter --- p.37 / Chapter 2.2.1.1.1 --- Specific Binding Assay and Scatchard Analysis --- p.37 / Chapter 2.2.1.2 --- Dopamine D1 Receptor --- p.38 / Chapter 2.2.1.2.1 --- Association Curve --- p.38 / Chapter 2.2.1.2.2 --- Competition Assay --- p.39 / Chapter 2.2.1.2.3 --- Specific Binding Assay and Scatchard Analysis --- p.39 / Chapter 2.2.1.3 --- Dopamine D2 Receptor --- p.39 / Chapter 2.2.1.3.1 --- Association Curve --- p.40 / Chapter 2.2.1.3.2 --- Competition Assay --- p.40 / Chapter 2.2.1.3.3 --- Specific Binding Assay and Scatchard Analysis --- p.40 / Chapter 2.2.1.4 --- Assay for Residual Cocaine in Maternal Brain --- p.41 / Chapter 2.3 --- Statistics --- p.42 / Chapter 2.4 --- Morphological Studies --- p.42 / Chapter 2.4.1 --- Tyrosine Hydroxylase (TH) Immunocytochemical Staining --- p.42 / Chapter 2.5 --- Molecular Genetic Studies --- p.44 / Chapter 2.5.1 --- Material for DNA Insert --- p.44 / Chapter 2.5.1.1 --- "Dopamine Transporter, D2 receptor and β-actin cDNA Probe " --- p.44 / Chapter 2.5.2 --- Preparation for DNA Insert --- p.45 / Chapter 2.5.2.1 --- Competent Cells and Transformation of Plasmid --- p.45 / Chapter 2.5.2.2 --- Growth Transformed Bacteria and Isolation of DNA --- p.46 / Chapter 2.5.2.3 --- Purification of cDNA by Geneclean® II Kit --- p.47 / Chapter 2.5.3 --- Isolation of Total mRNA From Tissue --- p.47 / Chapter 2.5.4 --- Northern Blot Analysis --- p.48 / Chapter 2.5.4.1 --- Analysis of Northern Blots --- p.50 / Chapter 2.5.5 --- In Situ Hybridization --- p.50 / Chapter 2.5.5.1 --- Tissue Preparation --- p.50 / Chapter 2.5.5.2 --- Preparation of Dopamine Transporter Ribroprobe …… --- p.50 / Chapter 2.5.5.3 --- In Situ Hybridization Histochemistry --- p.51 / Chapter CHAPTER III --- RESULTS / Chapter 3.1 --- "Litter Size, Birth Weight and Maternal Weight Gain " --- p.53 / Chapter 3.2 --- Biochemical Studies --- p.53 / Chapter 3.2.1 --- Specific Binding --- p.53 / Chapter 3.2.2 --- Dopamine Transporter - Scatchard Analysis --- p.54 / Chapter 3.2.3 --- Dopamine Receptor --- p.55 / Chapter 3.2.3.1 --- Association Curve --- p.56 / Chapter 3.2.3.2 --- Competitive Curve --- p.57 / Chapter 3.2.3.3 --- Scatchard Analysis --- p.57 / Chapter 3.2.4 --- Dopamine D2 Receptor --- p.59 / Chapter 3.2.4.1 --- Association Curve --- p.59 / Chapter 3.2.4.2 --- Competitive Curve --- p.59 / Chapter 3.2.4.3 --- Scatchard Analysis --- p.59 / Chapter 3.2.5 --- Residual Cocaine Assay in Maternal Brain --- p.61 / Chapter 3.2.5.1 --- Specific Binding --- p.61 / Chapter 3.2.5.1.1 --- Dopamine Transporter --- p.61 / Chapter 3.3.5.1.2 --- Dopamine D1 Receptor --- p.62 / Chapter 3.3.5.1.3 --- Dopamine D2 Receptor --- p.62 / Chapter 3.3 --- Morphological Studies --- p.62 / Chapter 3.3.1 --- Tyrosine Hydroxylase (TH) Immunocytochemical Staining --- p.62 / Chapter 3.4 --- Molecular Genetic Studies --- p.63 / Chapter 3.4.1 --- Northern Blot Analysis --- p.63 / Chapter 3.4.1.1 --- Dopamine Transporter --- p.63 / Chapter 3.4.1.2 --- Dopamine D2 Receptor --- p.64 / Chapter 3.4.2 --- In Situ Hybridization --- p.64 / Chapter CHAPTER IV --- DISCUSSION AND CONCLUSION / Chapter 4.1 --- Discussion --- p.65 / Chapter 4.2 --- Conclusion --- p.77 / References --- p.79 / Publications --- p.95
3

The effects of prenatal heroin exposure on postnatal brain development and behavior in rats. / CUHK electronic theses & dissertations collection

January 2000 (has links)
Zhu Jian-hui. / "July 2000." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (p. 174-215). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.
4

Effect of estrogen therapy and sex on brain structures in aging : importance of lifelong endogenous and exogenous estrogen exposure

Lord, Catherine, 1978- January 2007 (has links)
No description available.
5

Effect of DHA deficiency on spatial learning behavior and antioxidant status in rat brain. / CUHK electronic theses & dissertations collection

January 2006 (has links)
DHA depletion in brain was associated with impairment on spatial learning and memory in rat. The Morris water maze test found that the n-3 deficient rats spent more time and swam a longer distance to find the hidden platform compared with the n-3 adequate group, indicating that n-3 Def rats had a poorer spatial learning ability and memory. The results suggest that learning and memory are partially related to the brain DHA status in rat. / Docosahexaenoic acid (DHA, 22-6n-3) and arachidonic acid (AA, 22:4n-6) are long-chain polyunsaturated fatty acids (LCPUFA), which are important for the structural development of mammalian central nervous system and are accumulated in large amounts in the developing brain, retina and sperm. Deficiency in DHA and AA syndromes can occur if these fatty acids and their precursors (linoleic and linolenic acid) are insufficient in diet. It had been reported that DHA deficiency in animal brain led to a poor performance in learning ability and other abnormal behavior in rodents. In addition, DHA and AA are the unique fatty acids in human milk. Many studies reported that children who were breast-fed got higher intelligent scores than those who were formula-fed. Thus, a large number of studies suggested that DHA and AA should be added into infant formula to mimic the composition of human milk. / In summary, DHA distribution, depletion and recovery were region-specific in rat brain. DHA deficiency could lead to impairment on spatial learning in rat. The underlying mechanism of learning deficit might not be attributed to changes in antioxidant enzymes in rat brain. Although impairment on spatial learning was observed in DHA-deficient rat, a meta-analysis of published data demonstrated that DHA and AA supplement in infant formula had no effect on cognitive development in children. / No significant relationship between DHA level and brain antioxidant enzyme activities was observed, including catalase (CAT), Cu-Zn superocide dismutase (Cu-Zn SOD), Mn superocide dismutase (Mn SOD) and glutathione peroxidase (GPx). These enzyme activities varied with regions of brain. A lower activity of CAT, Mn SOD and GPx in hippocampus and cortex would make them particularly susceptible to oxidation damage compared with other regions. The present results did not support the view that the spatial learning and memory impairment in DHA depletion was associated with antioxidant status in brain. / The meta-analysis indicated that breast-feeding was positively associated with a higher cognitive development than formula-feeding. However, no benefit was found for infants who received formula supplemented with DHA alone or DHA plus AA compared with those fed traditional formula based on available data. The results suggest that the beneficial effect of breast-feeding over formula-feeding can not be solely attributed to DHA and AA present in breast milk. / The objectives of present study were to (1) examine the distribution, depletion and recovery of DHA in rat brain; (2) investigate the effect DHA deficiency in rat brain on spatial learning behavior; (3) study the effect of DHA deficiency on antioxidant enzymes in rat brain; and (4) analyze whether DHA and AA supplementation has any beneficial effect on cognitive development and quantify their effect size in children by conducting a meta-analysis of the published data, and adult rats, the region with the highest DHA percentage was cortex, whereas in aged rats, both cortex and cerebellum were the regions with the highest DHA percentage. DHA concentration in rat brain increased with age. DHA was not proportionally depleted and recovered in different regions of rat brain when the rats were maintained on an n-3 fatty acid deficient diet for two generations. The present results demonstrated that the distribution of DHA and AA was region-specific. / Xiao Ying. / "August 2006." / Adviser: Zhen Yu Chen. / Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1566. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (p. 140-156). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.

Page generated in 0.0567 seconds