Exercise may offset nicotine-induced injury in lung tissue: a preliminary histological study based on a rat model.

Nicotine appears to be the primary pharmacologic agent that causes smoking-related pulmonary diseases. An understanding of the effect of nicotine on lungs is essential to develop interventions that can be used to counter smoking-related diseases. Further, it is shown that physical exercise may partially reverse smoking-induced pathological changes in experimental animals. Hence, this study focuses on the pathological changes in rat lung following nicotine administration and the role of exercise in reversing the nicotine-induced lung injury. This is a randomized controlled trial with 3 groups of rats. Control (CG), nicotine-exposed (NG), and nicotine-exposed and exercise group (NEG). Control group received no intervention. Both NG and NEG were given 1.5 mg/kg nicotine base, daily, subcutaneously, but NEG were also subjected to an intensive daily swimming protocol. The rats were sacrificed and the lung tissue was processed for light and transmission electron microscopic and immunohistochemical studies. Compared with the control group, the nicotine group showed enlargement and destruction of the alveolar septum, cellular hyperplasia and interstitial fibrosis, and interstitial mononuclear cell infiltration with increased intraluminal macrophages. There was only modest morphological change between the nicotine administered and nicotine and exercise groups. Expression of superoxide dismutase (SOD) and catalase showed a mild increase in the NEG, whereas glutathione peroxidase (GPX) showed mild and moderate increase in the expression in the NG and NEG, respectively. This study shows that nicotine induces substantial pathological changes in the lung and prolonged exercise may have some beneficial effects in partially reversing the nicotine-induced lung injury by inducing the expression of antioxidants.

Low carbohydrate ketogenic diet prevents the induction of diabetes using streptozotocin in rats.

Diabetes continues to be an overwhelmingly prevalent endocrine disorder that leads to several micro- and macrocomplications. It has been widely accepted that changes in dietary habits could induce or prevent the onset of diabetes. It is shown that low carbohydrate ketogenic diet (LCKD) is effective in the amelioration of many of the deleterious consequences of diabetes. However, its role in preventing the onset of diabetes is not understood. Therefore, this study is focused on the effect of LCKD in preventing the induction of diabetes using streptozotocin (STZ) in rats by biochemical and histological methods. Forty-two Wistar rats weighing 150-250 g were used in this study. The animals were divided into three groups: normal diet (ND), low carbohydrate ketogenic diet (LCKD), and high carbohydrate diet (HCD). Specific diets ad libitum were given to each group of animals for a period of 8 weeks. Each group was further subdivided into normal control, sham control and diabetic groups. Animals in the diabetic group were given a single intraperitoneal injection of STZ (55 mg/kg). All the animals were sacrificed 4 weeks after the injection of STZ. Daily measurements of food and water intake as well as weekly measurement of body weight were taken during the whole 12 weeks of the experiment. After injecting with STZ, the blood glucose level of all the groups increased significantly except for the group fed on LCKD (p value<0.01). Also, food intake, water intake and urine output were significantly increased in all groups except for the LCKD group (p value<0.01). There was also a significant decrease in the weight gain of the animals that were fed on a LCKD as compared to other groups (p value<0.05). Although, substantial decrease in the number of ß cells was noticed in diabetic rats, there were no change in the number of ß cells in the LCKD treated diabetic animals as compared to LCKD control group. The results presented in this study, therefore, suggests that LCKD prevents the development of diabetes using streptozotocin in rats.

Protective effects of green tea on intestinal ischemia-reperfusion injury.

OBJECTIVE: The intestinal mucosa is known to be adversely affected by ischemia-reperfusion (I/R). Previously we showed that green tea protects the intestinal mucosa from fasting-induced damage. The aim of this study is to determine whether green tea has any protective role in I/R of the intestine. METHODS: Three groups of male rats were used in this study. Group I (I/R) underwent I/R of the intestine (30 min of ischemia followed by 1 h of reperfusion). Group II (green tea + I/R) was given green tea for 2 wk before inducing I/R. Group III (control) had sham I/R. After the experiments, the jejunum was removed and the tissues were processed for histopathologic examination and immunohistochemical analysis for cell proliferation markers and antioxidant enzymes. RESULTS: The intestinal mucosa in group II was preserved compared with that in group I. The expressions of cellular proliferation markers (proliferating cell nuclear antigen and Ki-67) and cellular antioxidants (superoxide dismutase and catalase) in group II were similar to those in group III and much less than in group I, reflecting the protective effects of green tea in group II animals. CONCLUSION: In this animal model, administration of green tea before inducing I/R protects the intestinal mucosa from injury.

Detection rate and clinical pattern of prostate cancer in Kuwait: a single-center experience.

OBJECTIVE: To determine the detection rate and clinical pattern of prostate cancer in Kuwait. SUBJECTS AND METHODS: One hundred and fifty-three males suspected of having prostate cancer based on elevation of prostate-specific antigen (PSA) of more than 4 ng/ml underwent transrectal-ultrasound (TRUS)-guided needle biopsy of the prostate between January 2003 and January 2008; these formed the study group. Analysis of prostate cancer was based on age, prostate volume, PSA level and on finding any abnormality based on a combination of the diagnostic tools. RESULTS: A diagnosis of prostate cancer was histologically confirmed in 42 (27.4%) patients. In those aged <55, 56-65, 66-75 and >76 years, the detection rates were 16.7, 17.6, 33.3 and 40.7%, respectively. In those with prostate volumes of >71, 51-70, 31-50 and <30 g, the detection rates were 18.2, 23.8, 30.8 and 42.9%, respectively. When the PSA levels were divided into groups of 4-10, 10-20, 20-100 and >100 ng/ml, the cancer detection rate was 11.8, 20.5, 47.1 and 83.3%, respectively. When 1, 2 and 3 of the 3 diagnostic tools (digital rectal examination, PSA, TRUS) were abnormal, the detection rate was 15.6, 27.9 and 80%, respectively. CONCLUSIONS: Our data showed that the prostate cancer rate differs according to the region and that the rate was low in our center. Higher PSA and higher number of diagnostic tools with abnormal findings were associated with a higher incidence of prostate cancer.

Fasting-induced intestinal damage is mediated by oxidative and inflammatory responses.

BACKGROUND: Green tea has been shown to repair fasting-induced mucosal damage in rat intestine. The aim of this study was to elucidate the underlying mechanism. METHODS: Five groups of rats were used. Group 1 had free access to chow diet and water, and those in group 2 were fasted for 3 days. Animals in group 3 were fasted for 3 days, then were allowed drinking water for a further 7 days. Groups 4 and 5 were fasted for 3 days, then given drinking water containing green tea or vitamin E respectively for 7 days. Blood was collected for estimation of total plasma antioxidants, and jejunal samples were used for immunohistochemical analysis of superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx), and for estimation of myeloperoxidase (MPO) activity. RESULTS: Use of green tea was associated with a significant increase in total plasma antioxidants (P < 0.001), and mucosal SOD (P < 0.001), catalase (P = 0.006) and GPx (P = 0.017), but a significant decrease in MPO activity (P < 0.001). Vitamin E produced similar changes, but the effects were smaller. CONCLUSION: Green tea reverses the fasting-induced damage to the intestinal mucosa by its antioxidant and anti-inflammatory effect.

Antagonistic interactions between the flavonoids hesperetin and naringenin and beta-lactam antibiotics against Staphylococcus aureus.

Flavonoids are a group of polyphenolic plant compounds with a range of biological activities. This study shows that the flavonoids hesperetin and naringenin have antibacterial activity against methicillin-sensitive and methicillin-resistant Staphylococcus aureus isolates. Minimum inhibitory concentrations for hesperetin were 250 and 500 microg/mL, respectively, and for naringenin were 125 and 250 microg/mL, respectively. This effect was reversed by the beta-lactam antibiotics methicillin, penicillin and oxacillin, but not by cefoxitin. For bacteria growing in the presence of these antibiotics, the flavonoids had no effect on the levels of beta-lactamase enzymes and PBP-2' compared to controls. Electron microscopy showed abnormal morphology in bacteria treated with subinhibitory concentrations of flavonoids. These results are interesting because previous studies have reported synergistic interactions between flavonoids and beta-lactam antibiotics. It is suggested that an interaction removes both inhibitors from the bacterial growth milieu.

Indications of the mechanisms involved in improved sperm parameters by zinc therapy.

OBJECTIVE: To determine possible indications of the mechanisms involved in improved sperm parameters by zinc therapy in asthenozoospermic men. SUBJECTS AND METHODS: Forty-five men with asthenozoospermia (>or=40% immotile sperm) were randomized into four therapy groups: zinc only: n = 11; zinc + vitamin E: n = 12 and zinc + vitamins E + C: n = 14 for 3 months, and non-therapy control group: n = 8. Semen analysis was done according to WHO guidelines. Malone dialdehyde, tumour necrosis factor-alpha (TNF-alpha), total antioxidant capacity, superoxide dismutase (SOD) and glutathione peroxidase were determined in the semen and serum. Antisperm antibodies IgG, IgM and IgA were evaluated by immunobeads. Sperm chromatin integrity was determined by acid denaturation by acridine orange and sperm apoptosis by light and electron microscopy. The effect of zinc on in vitro induced sperm oxidative stress by NADH was evaluated. RESULTS: Asthenozoospermia was significantly associated with oxidative stress with higher seminal malone dialdehyde (8.8 vs. 1.8 mmol/l, p < 0.001) and TNF-alpha (60 vs. 12 pg/l, p < 0.001), and low total antioxidant capacity (1.8 vs. 8.4, p < 0.01), SOD (0.8 vs. 3.1, p < 0.01) and glutathione peroxidase (1.6 vs. 4.2, p < 0.05), compared to normozoospermia. Zinc therapy alone, in combination with vitamin E or with vitamin E + C were associated with comparably improved sperm parameters with less oxidative stress, sperm apoptosis and sperm DNA fragmentation index (DFI). On the whole, there was no difference in the outcome measures between zinc only and zinc with vitamin E and combination of vitamins E + C. In the in vitro experiment zinc supplementation resulted in significantly lower DFI (14-29%, p < 0.05) compared to zinc deficiency. CONCLUSION: Zinc therapy reduces asthenozoospermia through several mechanisms such as prevention of oxidative stress, apoptosis and sperm DNA fragmentation.

Regional analysis of the ependyma of the third ventricle of rat by light and electron microscopy.

Ependymal lining of cerebral ventricles lies at the interface between the ventricular cavities and the brain parenchyma. Ependymal cells are involved in various functions within the brain and play a major role in the production of the chemical principals of the cerebrospinal fluid. Histological studies on the regional variation of the third ventricular ependyma and the subependyma of adult rats were carried out by light and electron microscopic methods. For light microscopic analysis, methacrylate sections were used. In addition to the routine haematoxylin and eosin (H and E) staining for histological studies, the sections were stained with toluidine blue, cresyl violet and periodic acid Schiff's reagent (PAS). A regional analysis of the ependyma of the third ventricle showed that in most regions the ependyma was monolayered. The sidewalls and floor of the ventral portion of the third ventricle showed a multilayered ependyma. For descriptive purposes at the light microscopic level, the ependymal cells were classified, based on the cell shape (flat, cuboidal or columnar), presence or absence of cilia and the number of cytoplasmic granules present in the cells. Studies of transmission electron microscope have shown that these granules represent the cell organelles of the ependyma. The subependyma also showed a regional morphological variation, and, in most instances, contained glial and neuronal elements. In regions of specific brain nuclei, neurons were the major cell type of the subependyma. PAS staining did not show any positive granules in the ependymal cytosol. Characteristic supraependymal elements were present at the ependymal surface of the third ventricle.

Effect of alpha-interferon and alpha-tocopherol in reversing hepatic cirrhosis in rats.

The aim of this study was to assess the effects of alpha-interferon and alpha-tocopherol (vitamin E), or a combination of both, in reversing hepatic fibrosis following the induction of cirrhosis using thioacetamide by histological and biochemical analysis. Fifty male Wistar rats were used in this study. The animals were divided equally into five groups. Animals in group I were used as controls. The remaining animals (groups II-V) were provided with 0.5 g/L of thioacetamide in order to induce liver cirrhosis. Group II animals were used as the cirrhotic control. Animals of groups III, IV and V were given alpha-interferon, alpha-tocopherol and interferon together with alpha-tocopherol, respectively, for 30 days. After 30 days the animals were killed and following gross morphological examination of the liver, the hepatic tissues were processed for histological analysis and the serum was used for liver function tests. Morphological analysis showed a decrease in the number of nodules on the surface of the liver in both interferon- as well as vitamin E-treated cirrhotic rats. Histopathological analysis showed that the abnormalities of the cirrhotic liver were partially reversed and liver function tests showed an overall improvement following treatment of animals of groups III, IV and V. Combination therapy using both interferon and alpha-tocopherol did not have any substantial effect on the rats compared with that when they were given separately. These findings suggest that alpha-interferon and alpha-tocopherol may have therapeutic value in reversing liver cirrhosis.

Serum changes in trace elements during thyroid cancers.

The objective was to examine changes in trace elements due to thyroid cancer in humans. Serum levels and tissue contents of trace elements (Zn, Cu, Mn, Mg, Fe and Se) were measured in 43 patients with thyroid cancer before and 4 days after surgery were compared to normal values. The serum levels of zinc in cancer patients were lower than those of normal subjects. Surgical removal of the cancer resulted in the restoration of these levels. Although serum Cu levels in patients were not different from normal, but post-operatively these levels rose significantly (p < 0.001). Levels of Fe, Mg and Mn were significantly lower (p < 0.001) post-operatively. There was no significant change in Serum Se levels. The thyroid tissue contents of these trace elements did not show a difference between the normal (Juxta-tumor) thyroid tissue and the cancerous lesion. Out of the six trace elements examined, the decrease of serum levels of zinc in cancer patients may be linked to the disease condition. It is suggested that this change: (a) may be used to demonstrate successful cancer surgery and (b) may have implications for a long-term follow-up of thyroid cancer patients.

Expression of E-cadherin in human colorectal cancer.

AIM: To investigate the expression of E-cadherin, a calcium-dependent cell-cell adhesion molecule in colorectal carcinoma. Antibodies to E-Cadherin were used to establish the association of their expression with the clinicopathological characteristics of this disease using immunohistochemical methods. METHODS: Immunohistochemical analysis for E-cadherin was carried out in formalin-fixed, paraffin-embedded sections of neoplastic colorectal tissues and non-neoplastic ones adjacent to the lesion from 49 patients who underwent surgery, by the standard peroxidase-antiperoxidase method. Expression of this antigen in normal and malignant epithelium and stromal cells was compared. RESULTS: Both neoplastic and normal tissues showed expression of E-cadherin. There was, however, higher expression of E-cadherin in epithelial cells in both tumour and normal tissues than stromal cells. The percentage of expression in epithelial cells of well-differentiated tumours was significantly higher than moderately differentiated tumours. Loss of normal membranous expression and the presence of cytoplasmic and mixed staining were found frequently in tumour tissues (p = 0.004). This loss of membranous expression, however, did not correlate with Duke's staging, tumour grade, sex, size or site of the tumour. CONCLUSION: This study suggests that the lower expression of E-cadherin in less differentiated tumours may explain their aggressive nature, although loss of membranous expression was not significantly correlated to Duke's staging, tumour grade, sex, size and site of tumour.

Brain selenium accumulation in rat pups of selenium supplemented mothers.

Selenium is essential for normal mammalian development. Being a component of antioxidant enzyme, glutathione peroxidase, it plays a major role in protecting the cells from free radical damage. The level of glutathione peroxidase was directly related to the amount of selenium present in various tissues and organs. A decrease in selenium leads to various pathological changes in humans as well as in various laboratory animals. The aim of the present study was to understand whether there is an increase in the level of selenium in different brain regions of rat pups whose mothers were supplemented with selenium, either 2 or 4 mg/l of their drinking water throughout the period of their pregnancy. There was a significant increase in the level of selenium in the cerebellum, cortex and hypothalamic and hippocampal tissues of selenium supplemented mothers as compared with those of non-supplemented mothers. The brain stem of these animals did not show any significant difference in the level of selenium. Furthermore, the differences in the level of selenium between the rat pups of 2 mg/l selenium supplemented mothers and 4 mg/l selenium supplemented mothers were not statistically significant. These studies suggest that supplementation of selenium to mothers during the period of their pregnancy can selectively increase the level of this trace element in different brain regions. Further studies are necessary to understand the significance of selective accumulation of selenium in specific brain regions on brain development and function.

Level of superoxide dismutase, glutathione peroxidase and uric acid in thioacetamide-induced cirrhotic rats.

Levels of superoxide dismutase and glutathione peroxidase were determined in blood and hepatic tissues of thioacetamide-induced cirrhotic rats and compared to levels in age-matched control animals. The plasma level of uric acid was also determined in these animals. A general decrease was noticed in the level of all the antioxidants examined as compared to the control. This decrease was statistically significant in the level of all the antioxidants studied, except for the level of superoxide dismutase in blood. A decrease in the antioxidant level may indicate an increase in free radical level and thereby an increase in cellular damage in cirrhotic rats. The changes in the level of antioxidants showed a direct correlation with the changes in the level of trace elements observed in our previous studies. These studies suggest that antioxidants alone or in combination with trace elements may have beneficial effects in treating liver cirrhosis.

Expression of CD44s in human colorectal cancer.

CD44s is a cell adhesion molecule, which belongs to the family of hyaluronan binding proteins. Anti-body to CD44s is used to establish the association of its expression with the clinicopathological characteristics of colorectal cancer using immunohistochemical methods. The aim of this study is to investigate the expression of the standard form of CD44 (CD44s) in colorectal cancer tissues as compared to adjacent normal colonic tissues. Furthermore, the level of expression of CD44s in colorectal cancer tissues was correlated with the degree of histological differentiation, Duke s classification, sex, size and site of the tumor. Immunohistochemical analysis for CD44s was carried out in 49 paraffin-fixed sections of neoplastic colorectal tissues and non-neoplastic ones adjacent to the lesion, by the standard peroxidase-antiperoxidase method. Expression of these antigens were compared in normal and malignant epithelium and stromal cells. The results show that the level of CD44s in the epithelial and stromal cells was significantly higher in the colorectal cancer tissues than the normal ones. However, there was no association between the percentages of expressions of CD44s and the degree of histological differentiation, Duke s classification, sex or size of the tumor. There was however, a significantly higher expression of CD44s in the epithelium of rectal cancer than that of colonic cancer. This study indicates that the expression of CD44s is significantly higher in colorectal cancer tissues. However, further studies are required to understand its role in tumor progression and metastasis of this disease.

Pre- and postnatal tissue selenium of the rat in the growing state.

The aim of this study is to quantify the selenium (Se) content (in microg/g) during different gestational periods in rat fetal tissues, and to follow up the changes in the Se content of the placenta, fetal head, liver and lung during gestation and postpartum periods. Locally reared virgin female Wistar rats were mated. Pregnant rats were sacrificed on days 15, 18 and 21 of pregnancy. Newborn pups at the age of 3 days and rats at the age of 1 month were also investigated. There was a gradual increase in placental and whole head Se content as gestation proceeded compared to day 15; however, the differences between the groups were not statistically significant. The liver Se content at day 18 of gestation was significantly higher than at day 21 of gestation and in rats at 3 days of age, but lower than the Se content of the liver of rats at the age of 1 month and the differences were statistically significant. The lung Se content was higher at day 18 of gestation than at day 21 and in the 3-day-old rats, and all differences between all groups were statistically significant except when the lung Se content at day 18 is compared to that of 1-month-old animals. The continuous increase in the Se content of the placental tissues and the whole head, although not significant statistically, may indicate that the fetus relies heavily on its supply of Se from the maternal blood and in part on the supply of thyroid hormones which are important for brain development, as evidence exists that T(4) and T(3) are present in the fetal brain in early fetal life before the onset of fetal thyroid function. The higher content of Se on day 18 and its decline on day 21 of gestation in the liver may imply that it is stored and being utilized partly in other tissues for other functions and particularly for thyroid hormone synthesis, metabolism and functions.

Levels of IL-8 and myeloperoxidase in the lungs of pneumonia patients.

Interleukin-8 (IL-8) is considered as the major polymorphonuclear neutrophils (PMNs) chemoattractant cytokine in lung diseases such as asthma and adult respiratory distress syndrome (ARDS). However, controversial results were obtained regarding the involvement of IL-8 in the pathogenesis of pneumonia. This study examines the role of IL-8 in the recruitment and activation of PMNs in the lung of pneumonia patients. The interesting aspect of this study is that it is a site- specific analysis of the infected and uninfected lungs of the same patient. The level of IL-8 mRNA, protein and myeloperoxidase present in the cells of the bronchioalveolar lavages (BALs) taken from the areas of known pneumonic consolidations on chest X-ray (infected lung) are compared with the BALs obtained from areas of no obvious infiltrate (non-infected lung). The results obtained from the infected and non-infected lungs of pneumonic patients were further compared with that of a control group of non-smoking patients. The level of IL-8 mRNA and protein were determined by RT-PCR and ELISA respectively. There was a significant increase in the level of IL-8 mRNA in the infected lung as compared to its level in the non-infected lung (p < 0.001). In correlation with the increase in mRNA, IL-8 protein concentrations in BAL fluids from the infected lung were 6 fold higher than those taken from the non-infected lung (p < 0.0001). This pattern was also consistent with MPO activity in the BALs (4.5 fold more MPO activity in the infected lung as compared to that of the non-infected lung), indicating that IL-8 is directly implicated in neutrophil accumulation that follows acute respiratory infection. The results of the present study, therefore, indicate the involvement of IL-8 in the pathogenesis of pneumonia.

Cholangiocarcinoma and liver cirrhosis in relation to changes due to thioacetamide.

Different doses of thioacetamide (0.05%, 0.1% and 0.15%) were used to induce liver cirrhosis in Wistar rats. Thioacetamide at 0.5% caused cirrhosis by the twelfth week of treatment. A severe bile duct proliferation and cholangiocarcinoma was seen at longer intervals. Animals treated with higher doses (0.1% and 0.15%) of thioacetamide developed more severe intense degenerative changes in the liver and died in the twelfth and eighth week respectively. The serum and tissue contents of Zn and Cu changed in a characteristic fashion that was consistent with the severity of the liver damage. Serum Zn and Cu concentrations were at their lowest in the animals that developed severe degenerative liver and died at higher dose (0.15%) of thioacetamide. This study indicates that treatment of rats with 0.05% thiocetamide is more effective and appropriate for the induction of liver cirrhosis. Continued administration of the drug at this dosage led to the development of further changes in the liver. This model may be suitable for studying these long term changes that occur in the liver and lead to cirrhosis. Events that precede the development of severe bile duct proliferation and cholangiocarcinoma may also be studied.

Thioacetamide toxicity and the spleen: histological and biochemical analysis.

Exposure to thioacetamide is associated with the development of liver cirrhosis in experimental animals. In addition to liver, thioacetamide toxicity has been observed in other organs. In this study, the toxic effect of thioacetamide on the spleen was investigated at 0, 4, 8 and 12 weeks post-treatment durations. The level of tissue copper and selenium increased until the eighth week when a significant drop was observed. The zinc level was also increased but returned back to normal by week 8, thereafter it showed further increase. Calculation of the copper/zinc ratio showed an increase, but, recovered and returned to normal value by week 12. The level of manganese fluctuated until the eighth week. It then increased rapidly. Histological studies of the spleen tissue showed a significant increase in extramedullary haematopoiesis in the red pulp region and marked hyperplasia in the marginal zone and follicles. The results of this study, demonstrate an intimate association between trace element levels and spleen pathology, as observed in studies of other organs.

Association between supraependymal nerve fibres and the ependymal cilia of the mammalian brain.

The ciliated ependymal cells that line the floor of the fourth ventricle in adult Wistar rats are overlaid by an immense network of supraependymal nerve fibres. This study presents morphological evidence of a characteristic association of supraependymal nerve fibres with the cilia of the ependymocytes of the ventricular surface. It is found that the supraependymal nerve fibres accumulate and/or terminate at the base of the clusters of ependymal cilia. These fibres are varicose in nature and consist of large-diameter fibres with numerous prominent varicosities and small-diameter fibres with less frequent and less prominent varicosities. The characteristic association of the supraependymal nerve fibres with the ciliated ependymocytes suggests that these nerve fibres may be involved in producing co-ordinated ciliary movements in the mammalian brain.

Regeneration of supraependymal nerve fibers in rat.

Factors intrinsic and extrinsic to the neurons regulate the regeneration of axons following axotomy. Elucidation of these mechanisms will provide fundamental information on the regulation of growth in mammalian neurons. To understand the role of environmental factors in nerve regeneration, this study focuses on the axotomy-induced regeneration of supraependymal nerve fibers that inhabit an environment different from other central nervous system neurons and the neurons of the peripheral nervous system. These fibers are ideally located to receive various neuroactive substances that are streaming in the cerebrospinal fluid. Transmission electron microscopic studies reveal the presence of three types of fibers on the ventricular surface. They are fibers with clear synaptic vesicles, those containing small dense core vesicles together with clear synaptic vesicles and fibers containing large dense core granules. To study the regenerative potential of supraependymal nerve fibers, they were axotomized by inflicting mechanical injury to the floor of the third ventricle. Following axotomy, the regenerative ability of the supraependymal nerve fibers was monitored between five and thirty days, by scanning electron microscopy. By the fifth day, there was a noticeable increase in the neuronal network that gradually increased throughout the experimental period. The regenerative ability of supraependymal neurons, as compared with other neurons in the central nervous system, could be due to the differences in their environment. These studies suggest that mammalian cerebral ventricles may be an adequate site for neural transplantation.