Investigation of Various Events Occurring in the Brain Tissue After Calvarial Defects in Rats (original) (raw)
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International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 1993
The astrocytic reaction in the rat after brain injury has been studied immunohistochemically for intermediate filaments (GFAP and vimentin), also with double staining procedures, and for markers of proliferation (BrdU and PCNA). GFAP-positive reactive astrocytes appeared around the lesion, where they were vimentin-positive and at a distance. BrdU and PCNA showed a high labelling index around the wound at day 2 and scattered positive nuclei were also found at a distance in the ipsilateral side. BrdU-positive astrocytes represented a minor fraction of GFAP- and vimentin-positive astrocytes. The expression of vimentin persisted at least 15 days after the lesion. Our results could suggest that distant reactive astrocytes originate through hypertrophy while those close to lesion arise by hyperplasia from mature or immature glial cells. The hypothesis is formulated that cells of the periventricular matrix contribute to the post-traumatic proliferative activity.
2019
684 Address for correspondence: Prof. E. Deveci, PhD, Dicle University, Faculty of Medicine, Department of Histology and Embryology, 21280, Diyarbakır, Turkey, tel: +90 412 2488001 ext. 4443 (faculty room), fax: +90 412 2488440, e-mail: devecie32@hotmail.com Expression of vascular endothelial growth factor and glial fibrillary acidic protein in a rat model of traumatic brain injury treated with honokiol: a biochemical and immunohistochemical study
Early release of glia maturation factor and acidic fibroblast growth factor after rat brain injury
Neuroscience Letters, 1988
A major component of the healing response of the brain to injury is the induction of growth and trophic factors. In the rat brain, glia maturation factor (GMF) and acidic fibroblast growth factor (aFGF) are not cxtracellular. However, within the first hour following brain injury, the amount of GMF and aFGF m the wound cavity increased by 7-and 13-fold. respectively, compared to the tissue adjacent to the wound. A cascade of cellular and biochemical events, leading to glial proliferation, the arrest of secondary neuronal death and axonal sprouting, may be initiated by the sudden increase in the extracellular concentration of these factors.
Brain Research, 1985
Injury to rat brain induces a 3-10-fold increase in the activity of factors capable of stimulating astrocyte DNA synthesis and cell division in vitro. Maximum mitogenic activity was reached 10-15 days post-lesion in both the tissue surrounding the wound and in the gelfoam filling the wound cavity. Factors capable of transforming the astrocyte morphology from polygonal-flat to fibrous-like (morphogens) could also be observed in brain tissue and showed increased activity beginning at l0 days postlesion. On the other hand, morphogenic activity was very low or absent in gelfoam extracts until 15 days postlesion. Both mitogenic and morphogenic factors were nondiffusible and were partly temperature and trypsin sensitive, i.e. they had the properties of protein-like substances, but seemed different from both epidermal and fibroblast growth factors. As judged by their filtration behavior on Amicon membranes, the molecular weight of mitogens and morphogens ranged from lower than 30,000 to greater than 100,000. Inhibitors of both mitogenic and morphogenic activities with molecular weight lower than 30,000 seemed to be also present in the brain extracts. The factors described here can account for the processes of astrocytosis and astrogliosis observed in vivo in response to CNS injury.
Traumatic brain injury models in rats
Journal of Cellular Neuroscience and Oxidative Stress, 2018
Speakers Speak No. 1. Pathophysiology of cation channels in pain: Focus on TRP Channels. Mustafa NAZIROĞLU…………….….………………….………………………………..………….776 Speak No. 2. Calcium imaging techniques in cell lines. Laszlo PECZE………….…………….………………….………….……………………..…………777 Speak No. 3. Western-blot, PCR and immunofluorescence analysis in mitochondrial biogenesis studies. Denis ROUSSEAU…………………….………………….………………………………..…………778 Speak No. 4. Intravenous NAD + effectively increased the NAD metabolome, reduced oxidative stress and inflammation, and increased expression of longevity genes safely in elderly humans.
Brain Research, 1989
Proliferative response of astrocytes to unilateral injury of the cerebral hemisphere was investigated in 30-day-old rats using a combination of [3H]thymidine autoradiography and immunocytochemical staining for glial fibritlary acidic protein. At different intervals following injury the animals were injected with [3H]thymidine and the distribution of double-labeled ceils was recorded 4 h (short-term experiment) or 40-days (long-term experiment) after each injection. Within the region of the lesion a strong reactive proliferation of astrocytes began as early as 2 h after injury, although, at that time all dividing neuroglial cells were located at a relatively long distance from the lesion margin. Forty days later, however, autoradiographically labeled astrocytes were observed in the center of the lesion. This was regarded as evidence for the ability of astrocytes to migrate towards the site of injury. Maximal reactive proliferation of astroglial cells was observed at day 2 after injury and then reached the postmitotic plateau at about day 8. The cells, while dividing, were mostly GFAP-negative. Therefore, the number of astrocytes produced at particular days after injury, and their contribution to post-traumatic scar formation could be assessed only in the long-term experiment, after the newly formed cells became GFAP-positive.
A new model of diffuse brain injury in rats
Journal of Neurosurgery, 1994
✓ This report describes the development of an experimental head injury model capable of producing diffuse brain injury in the rodent. A total of 161 anesthetized adult rats were injured utilizing a simple weight-drop device consisting of a segmented brass weight free-falling through a Plexiglas guide tube. Skull fracture was prevented by cementing a small stainless-steel disc on the calvaria. Two groups of rats were tested: Group 1, consisting of 54 rats, to establish fracture threshold; and Group 2, consisting of 107 animals, to determine the primary cause of death at severe injury levels. Data from Group 1 animals showed that a 450-gm weight falling from a 2-m height (0.9 kg-m) resulted in a mortality rate of 44% with a low incidence (12.5%) of skull fracture. Impact was followed by apnea, convulsions, and moderate hypertension. The surviving rats developed decortication flexion deformity of the forelimbs, with behavioral depression and loss of muscle tone. Data from Group 2 anima...
Folia morphologica, 2018
Traumatic brain injury (TBI) is in part associated with the disruption of the blood-brain barrier. In this study, we analyzed the histopathological changes in E-cadherin and VEGF expression after traumatic brain injury in rats. The rats were divided into 2 groups as the control and the trauma groups. Sprague-Dawley rats were subjected to traumatic brain injury with a weight-drop device using 300 g⁻¹ m weight-height impact. After 5 days of traumatic brain injury, blood samples were taken under ketamine hydroxide anesthesia and biochemical analyzes were performed. The control and trauma groups were compared in terms of biochemical values. There was no change in glutathione (GSH) levels and blood brain barrier permeability. However, malondialdehyde (MDA) and myeloperoxidase activity (MPO) levels increased in the trauma group. In the histopathological examination, choroid plexus in the lateral ventricule, near the piamater membrane, was removed. In the traumatic group, some of epithelia...
Protective Effects of Glial Cell Line-Derived Neurotrophic Factor in Ischemic Brain Injury
Annals of the New York Academy of Sciences, 2002
RAUMATIC brain injury induces neuronal death from both primary and secondary injury mechanisms. The primary injury consists of the mechanical processes, which damage the tissue by stretching and tearing during the traumatic event. A few hours to weeks after the initial injury, several biochemical and molecular changes start in the tissue surrounding as well as distant from the site of the injury. 24 These secondary mechanisms constitute the potentially preventable component of the longterm neurological deficits a person with brain injury may experience. Following experimental TBI in rats, neurons in the hippocampal CA2 and CA3 regions undergo a secondary neuronal death. 2,3,6 A member of the TGF superfamily, GDNF is essential for differentiation of embryonic neurons and survival of mature neurons. 15 Also, GDNF has been shown to be neuroprotective in animal models of Parkinson disease and cerebral ischemia. 10,13,17,19,30 The neuroprotective efficacy of GDNF after TBI has not been evaluated, however, in previous studies. In the present study we evaluated the effect of intracerebroventricular infusion of GDNF on hippocam-pal neuronal death and astroglial reactivity following CCIinduced TBI in rats. Materials and Methods Controlled Cortical Impact-Induced TBI All surgical procedures were conducted and animals were cared for according to the animal welfare guidelines set forth in the Guide for the Care and Use of Laboratory Animals (Publication 85-23, United States Department of Health and Human Services, 1985). Sixteen adult male Sprague-Dawley rats weighing 250 to 300 g were anesthetized with halothane (induction dose 4%, maintenance dose 1.2%) in a 1:1 N 2 O/O 2 mixture. Each animal was placed in a stereotactic head frame and a 5-cm scalp and neck incision was made vertically. The scalp and temporalis muscles were reflected and a 6-mm craniectomy was performed between the coronal and lambdoid sutures 2 mm lateral to the midline. The dura was kept intact and care was taken to avoid injury to the vasculature. The TBI was induced at a velocity of 3 m/second, resulting in a 2-mm deformation, by using the CCI device as described earlier. 6 The exposed cortex was covered with Surgicel and the wound was closed with sutures. Sixteen sham-operated control rats were subjected to the same surgical procedure, including craniectomy, but received no cortical impact. Body and cranial temperatures were monitored with rectal and temporalis muscle probes, respectively, and maintained in a range of 37 to 38˚C (rectal) and 36 to 37˚C (cranial) with a heating blanket and lamp. The left femoral artery was cannulated for monitoring of arterial blood pressure and to obtain blood samples for measurement of pH, PaCO 2 , PaO 2 , and hemoglobin. After recov