MWM Test Research Articles

Influences Of Swimming On Learning And Memory And Expression Of Orexin And Ncam In Rat Hippocampus

PURPOSE: Through the different load intensity swimming exercise intervention in rats, we observed that the movement influenced on rats spatial learning and memory ability and detected the proteins expression of rat hippocampal. METHODS: 30 male SD rats were selected. After acclimatization to the laboratory for 1 week, the rats were randomly divided into 3 groups: Control Group(C), Medium load Group (M), over load Group (O).Group C were feed naturally; group M did swimming exercise intervention; group O did over load swimming exercise. The Morris Water Maze test (MWM) was performed to evaluate spatial learning and memory ability. Tissue samples were collected after the MWM test. 6 whole brain samples for immunofluorescence assay, while the bilateral hippocampus of the other 6 brains for western blot and real-time PCR analysis. RESULTS: (1) Blood testosterone detections: there was no significantly difference between group M and C (P>0.05), the blood testosterone of group O was significantly lower than group M and C (P<0.01); (2) MWM detection: during the navigation experiment, group M was easier to find the platform than group C (P<0.01). During the space exploration, rats in group M crossed where the platform was fixed more often than group C and O(p < 0.05),rats in group C crossed where the platform was fixed more often than group O(p < 0.05); (3) mRNA detection: the expression of NCAM mRNA and OXA mRNA of group M were significantly higher than group C (P<0.05), OX1R mRNA of group M was significantly lower than group C(P<0.05); (4) Protein detection: the expression of NCAM of group M was significantly higher than group C(P<0.05),the group O was significantly lower than group C(P<0.05). CONCLUSION:Medium load swimming exercise could improve the rats spatial learning and memory ability and significantly improve the expression of OXA, OX1R mRNA and OX1R, and significantly reduce the expression of OXA, OX1R mRNA, OX1R; Over load swimming exercise could damage the spatial learning and memory ability of rats, after over load swimming exercise, the expression of NCAM, OXA and OX1R was normal. Acknowledgments: Supported by the National Natural Science Foundation of China (No.31371202). Supported by the Sports Medicine key laboratory of State Administration of Sports/ Sichuan province Foundation.

The Effect of Long-Term Environmental Enrichment in Chronic Cerebral Hypoperfusion-Induced Memory Impairment in Rats.

Vascular dementia (VaD) is the second most common cause of dementia. It occurs when the cerebral blood supply is reduced by disarrangement of the circulatory system. Environmental enrichment (EE) has been associated with cognitive improvement, motor function recovery, and anxiety relief with respect to various neurodegenerative diseases and emotional stress models. The purpose of this study was to determine whether long-term EE influenced cognitive impairment in a rat model of chronic hypoperfusion induced by permanent occlusion of bilateral common carotid arteries (BCCAo). The Y-maze and Morris water maze tests were performed to evaluate the rats' cognitive functions. Also, the protein expression of brain-derived neurotrophic factor (BDNF), phosphorylated cAMP-calcium response element binding protein (pCREB), and vascular endothelial growth factor (VEGF) were confirmed by Western blot. The microvessels and angiogenesis-associated proteins in the hippocampal region were investigated using immunohistochemistry. The VaD + EE group showed significantly better cognitive functions than the VaD group in both the Y-maze and MWM tests. In addition, the VaD + EE group showed significantly increased expression of BDNF, pCREB, and VEGF in the hippocampus compared to the VaD group. Rats in the VaD + EE group also had increased length of microvessels and VEGF expression in the hippocampus. These results suggest that long-term EE exerts neuroprotective effects against cognitive impairment induced by chronic cerebral hypoperfusion through the enhancement of BDNF, pCREB, and VEGF expression and indicate that EE may be a good nursing intervention in vascular dementia patients.

Maternal separation exacerbates Alzheimer’s disease-like behavioral and pathological changes in adult APPswe/PS1dE9 mice

Alzheimer’s disease (AD), the most common neurodegenerative disorder that gradually destroys memory and cognitive abilities in the elderly, makes a huge emotional and economic burden on the patients and their families. The presence of senile plaques and the loss of cholinergic neurons in the brain are two neuropathological hallmarks of AD. Maternal separation (MS) is an animal paradigm designed to make early life stress. Studies on wild type rodents showed that MS could induce AD-like cognitive deficit and pathological changes. However, the effects of MS on AD susceptible population or AD animal models are still unclear. In the present study, male APPswe/PS1dE9 transgenic mice were separated from dam and pups 3h per day from postnatal day 2 to day 21. After weaning, all animals were housed under normal conditions (4 mice per cage). At 9-month age, MWM tests were performed to evaluate the learning and memory abilities. Then the pathological changes in the brain were measured by histology staining. The results showed MS mice had more severe deficit of learning and memory. Compared to the control, there were more senile plaques in cortex and hippocampus, fewer cholinergic neurons in nucleus basalis of Meynert in MS mice. These results indicate that MS exacerbates Alzheimer’s disease-like behavioral and pathological changes in APPswe/PS1dE9 mice.

Ameliorative effect of kolaviron, a biflavonoid complex from Garcinia kola seeds against scopolamine-induced memory impairment in rats: role of antioxidant defense system.

In Alzheimer's disease (AD) basal forebrain cholinergic neurons appear to be targeted primarily in early stages of the disease. Scopolamine (muscarinic receptor antagonist) has been used for decades to induce working and reference memory impairment in rodents. In this study, we evaluated the protective effect of kolaviron, a biflavonoid complex isolated from Garcinia kola seeds extract against scopolamine-induced memory impairment/oxidative stress. Rats were pretreated with kolaviron (25, 50 or 100mg/kg p.o.) for 3 consecutive days, scopolamine (3mg/kg, i.p.) was administered 1h post-treatment on day 3. Five minutes post-scopolamine injection, memory function was assessed using the Y-maze or Morris water maze tests (MWM) in rats. The rats were sacrificed and brains isolated on the 8th day after the MWM test for estimation of acetylcholinesterase activity and nitrosative/oxidative stress status. Scopolamine injection induced deficit (P<0.05) in percentage alternation behaviour in the Y-maze test indicating memory impairment which was ameliorated by kolaviron in a dose-dependent manner. Also, pre-training treatment with kolaviron significantly improved spatial learning evidenced in the session-dependent and more efficient localization of the hidden platform in the MWM test. Moreover, scopolamine injection induced significant increase in lipid peroxidation (prefrontal cortex), nitrite generation (striatum and hippocampus) and a decrease in glutathione (prefrontal cortex, striatum and hippocampus) and superoxide dismutase (striatum and hippocampus) level which was attenuated by kolaviron pre-treatment. These findings showed that kolaviron possesses cognition enhancing effect through enhancement of antioxidant defense and cholinergic systems.

Parthenolide, an NF-κB Inhibitor Ameliorates Diabetes-Induced Behavioural Deficit, Neurotransmitter Imbalance and Neuroinflammation in Type 2 Diabetes Rat Model

Diabetes is associated with behavioural and neurochemical alterations. In this manuscript, we are reporting the beneficial effects of parthenolide, an NF-κB inhibitor on behavioural and neurochemical deficits in type 2 diabetic rat model. Diabetes was induced by high-fat diet followed by low dose of streptozotocin (35mg/kg). Elevated plus maze, open-field, MWM and passive avoidance test paradigm were used to assess behavioural and cognitive deficits. Three-week treatment of parthenolide (0.25 and 0.50mg/kg; i.p.) attenuated diabetes-induced alteration in cognitive function in Morris water maze and passive avoidance test. Anxiety-like behaviour was also reduced by parthenolide treatment. Moreover, TNF-α and IL-6 levels were significantly decreased in cortex and hippocampus of parthenolide-treated rats. Three-week parthenolide treatment also toned down the alteration of GABA and glutamate homoeostasis. Results of this study corroborate the involvement of neuroinflammation in the development of behavioural and neurochemical deficits in diabetic animals and point towards the therapeutic potential of parthenolide in diabetes-induced alteration of learning, memory and anxiety behaviour.

Temporary inactivation reveals that the CA1 region of the mouse dorsal hippocampus plays an equivalent role in the retrieval of long-term object memory and spatial memory

Recognition of a previously experienced item or object depends upon the successful retrieval of memory for the object. The neural mechanisms that support object recognition memory in the mammalian brain are not well understood. The rodent hippocampus plays a well-established role in spatial memory, and we previously demonstrated that temporary inactivation of the mouse hippocampus impairs object memory, as assessed with a novel object preference (NOP) test. The present studies were designed to test some remaining issues regarding the contribution of the CA1 sub-region of the mouse dorsal hippocampus to long-term object memory. Specifically, we examined whether the retrieval of spatial memory (as assessed by the Morris water maze; MWM) and object recognition memory are differentially sensitive to inactivation of the CA1 region. The current study used pre-test local microinfusion of muscimol directly into the CA1 region of dorsal hippocampus to temporarily interrupt its function during the respective retrieval phases of both behavioral tasks, in order to compare the contribution of the CA1 to object memory and spatial memory. Histological analyses revealed that local intra-CA1 injection of muscimol diffused within, and not beyond, the CA1 region of dorsal hippocampus. The degree of memory retrieval impairment induced by muscimol was comparable in the two tasks, supporting the view that object memory and spatial memory depend similarly on the CA1 region of rodent hippocampus. Further, we confirmed that the muscimol-induced impairment of CA1 function is temporary. First, mice that exhibited impaired object memory retrieval immediately after intra-CA1 muscimol, subsequently exhibited unimpaired retrieval of object memory when tested 24h later. Secondly, a cohort of mice that exhibited impaired object memory retrieval after intra-CA1 muscimol later acquired spatial memory in the MWM comparable to that of control mice. Together, these results offer further support for the involvement of the CA1 region of mouse hippocampus in object recognition memory, and provide evidence to suggest that the NOP task is as much a test of hippocampal function as the classic MWM test.

Comparative Analysis of Intrahippocampal Amyloid Beta (1-42) and Intracerbroventricular Streptozotocin Models of Alzheimer's Disease: Possible Behavioral, Biochemical, Mitochondrial, Cellu lar and Histopathological Evidences

Background: Alzheimer’s disease (AD), one of the most common progressive neurodegenerative disorders that leads to dementia in aged humans. Amyloid beta [Aβ (1-42)] model has an ability to mimic many pathological aspects of human AD. Intracerebroventricular streptozotocin (icv-STZ) is an another relevant model for sporadic dementia of Alzheimer’s type. However, both the models are frequently used to AD in experimental animals. Objective: Aim of the present study was to compare these two animal models of AD in order to comment on the best and reliable model of AD as well as screening of the neuroprotectants. Materials and Methods: Animals received a single bilateral intrahippocampal (ih) injection of Aβ (1-42) (1 μg/μl; 4 μl/site) and single bilateral icv injection of STZ (3 mg/kg; 4 μl/site). Galantamine (2 mg/kg) was used as a standard drug and administered for a period of 21 days. Various neurobehavioral parameters were evaluated, followed by biochemical (oxidative stress parameters), molecular (TNF-α level), mitochondrial respiratory enzyme complexes (Complex I, II, III, IV) and histopathological (H&E staining) parameters. Results: In the present study, ih-Aβ (1-42) administration significantly impaired cognitive performance on MWM test, increased oxidative stress markers (raised lipid peroxidation, nitrite concentration, reduced glutathione, catalase activity), increased AChE level and neuroinflammation (increased TNF-α levels), reduced mitochondrial respiratory enzyme complexes (complex I,II,III,IV) and histopathological alterations as compared to single bilateral icv-STZ administration. The effect of galantamine (2 mg/kg) was significantly produced its protective effect in reversing these neurobehavioral, biochemical, cellular and histopathological parameters as compared to their respective controls [ih-Aβ (1-42) and icv-STZ] Conclusions: Result of the present study suggests that the single bilateral ih-Aβ (1-42) model is the most effective and reliable model of AD as compared to single bilateral icv-STZ.

The effects of fibroblast growth factor-2 and pluripotent astrocytic stem cells on cognitive function in a rat model of neonatal hypoxic-ischemic brain injury

Objective: This study aimed to determine the effect of pluripotent astrocytic stem cells (PASCs) and fibroblast growth factor-2 (FGF-2) on cognitive function in neonatal rats with hypoxic-ischemic brain injury (HIBI).Methods: The study was performed on 7-d-old rats that were randomly divided into four groups. All rats, except those in the sham group, were kept in a hypoxic chamber containing 8% oxygen for 2 h after the ligation of the right carotid artery. Next, 5 d after HIBI was induced, PASCs were administered to the motor cortex, and FGF-2 was administered intraperitoneally to group AF; PASCs were administered to the motor cortex, and salt solution buffered with phosphate was administered intraperitoneally to group A; and fresh cell culture solution (medium) was administered to group M. Immunofluorescence was used to localize the administered PASCs in the brains of rats from groups A and AF. The Morris water maze tank (MWM) test was performed to assess the rats’ cognitive functions at week 12. The rats that were administered PASCs were observed for the development of neoplasms and autopsies were performed after 30 months.Results: PASCs migrated to damaged brain regions surrounding the hippocampus in groups A and AF. The mean platform finding time (PFT) significantly decreased over time in each group on day 1–4 of MWM testing (p < 0.001). On day 2–4, the mean PFT was shortest in group S followed by group AF. In group A, the PFT was significantly longer than in group S on day 3–4 (p = 0.01 and 0.007, respectively). On day 5 of the MWM test, the time spent in the eastern quadrant (which previously contained the platform) was longest in group S followed by groups AF, A, and M; however, the differences between groups were not significant (p = 0.51). After 30 months, none of the rats in groups A or AF had benign or malignant neoplasms.Conclusions: Following the administration of PASCs in rats with experimentally induced HIBI, PASCs migrated to the injured brain regions; however, treatment with PASCs did not have a positive effect on cognitive function. The administration of FGF-2 together with PASCs resulted in positive cognitive results, although not at the level of significance.

Inflammation During Gestation Induced Spatial Memory and Learning Deficits: Attenuated by Physical Exercise in Juvenile Rats.

Gestational infections induced inflammation (GIII) is a cause of various postnatal neurological deficits in developing countries. Such intra uterine insults could result in persistent learning-memory disabilities. There are no studies elucidating the efficacy of adolescence exercise on spatial learning- memory abilities of young adult rats pre-exposed to inflammatory insult during fetal life. The present study addresses the efficacy of physical (running) exercise during adolescent period in attenuating spatial memory deficits induced by exposure to GIII in rats. Pregnant Wistar dams were randomly divided into control and lipopolysaccharide (LPS) groups, injected intra peritoneally (i.p) with saline (0.5ml) or lipopolysaccharide (LPS) (0.5mg/kg) on alternate days from gestation day 14 (GD 14) till delivery. After parturition, pups were divided into 3 groups (n=6/group) a) Sham control and LPS group divided into 2 subgroups- b) LPS and c) LPS exercise group. Running exercise was given only to LPS exercise group during postnatal days (PNDs) 30 to 60 (15min/day). Spatial learning and memory performance was assessed by Morris water maze test (MWM), on postnatal day 61 to 67 in all groups. Young rats pre-exposed to GIII and subjected to running exercise through juvenile period displayed significant decrease in latency to reach escape platform and spent significant duration in target quadrant in MWM test, compared to age matched LPS group. Results of the current study demonstrated that exercise through juvenile/adolescent period effectively mitigates gestational inflammation-induced cognitive deficits in young adult rats. Inflammation during gestation impairs offspring's spatial memory and learning abilities. Whereas, early postnatal physical exercise attenuates, to higher extent, cognitive impairment resulted from exposure to LPS induced inflammation during intrauterine growth period.

Pecan Oil Influences Learning and Memory and NF-κB Levels in the Hippocampus of Rats after MWM Test

We assessed the effectiveness and mechanism of action of Pecan oil on learning and memory and NF-κB levels in the hippocampus of rats after Morris water maze (MWM test). Pecan oil (200,400 or 800 mg/kg/d) were administered by intragavage once daily for 14 consecutive days. The Morris water maze test was used to evaluate the ability of Pecan oil to increase learning and memory impairment. The levels of NF-κB in hippocampus of rats were detected by Westernblot after MWM test. Compared to untreated controls (P&lt;0.01), MWM could be prolonged after Pecan oil treatment (P&lt;0.05 for low and intermediate dose groups). Westernblot analysis showed that the protein expression of NF-κB was decreased in different concentration Pecan oil(P&lt;0.05 and P&lt;0.01, respectively). The results suggest that Pecan oil is effective in improving the learning and memory in rats, the mechanism of which may be related NF-κB expression decreasing.

Soybean Isoflavones Influences Learning and Memory and Caspase-3 Levels in the Hippocampus of Rats after MWM Test

We assessed the effectiveness and mechanism of action of Soybean Isoflavones on learning and memory and Caspase-3 levels in the hippocampus of rats after Morris water maze (MWM test). Soybean Isoflavones (200,400 or 800 mg/kg/d) were administered by intragavage once daily for 14 consecutive days. The Morris water maze test was used to evaluate the ability of Soybean Isoflavones to increase learning and memory impairment. The levels of Caspase-3 in hippocampus of rats were detected by Westernblot after MWM test. Compared to untreated controls (P&lt;0.01), MWM could be prolonged after Soybean Isoflavones treatment (P&lt;0.05 for="" low="" and="" intermediate="" dose="" groups="" westernblot="" analysis="" showed="" that="" the="" protein="" expression="" of="" caspase-3="" was="" decreased="" in="" different="" concentration="" soybean="" isoflavones="" i=""&gt;P&lt;0.05 and="" i=""&gt;P&lt;0.01, respectively). The results suggest that Soybean Isoflavones is effective in improving the learning and memory in rats , the mechanism of which may be related Caspase ways.

The Effects of Tianeptine, Olanzapine and Fluoxetine on the Cognitive Behaviors of Unpredictable Chronic Mild Stress-exposed Mice

Strong evidence indicates that impaired cognition is a core element of depression, and antidepressant treatment may ameliorate cognitive impairments experienced by depressive patients. Present study was performed to investigate effects of chronic tianeptine (5 mg/kg) or olanzapine (2.5 mg/kg) administration on cognitive behaviors of unpredictable chronic mild stress (UCMS)-exposed mice and to compare these effects to those induced by widely used SSRI antidepressant fluoxetine (15 mg/kg) in mice. To investigate effects of these drugs, the Morris water maze test (MWM), elevated plus maze test (EPM) and radial arm maze test (RAM) were used. The effects of stress and drugs on gene expression in the hippocampus was determined by quantitative Real Time-PCR. In MWM test, fluoxetine significantly increased escape latency of non-stressed mice in acquisition sessions and decreased time spent in escape platform quadrant in probe trial; tianeptine and olanzapine decreased enhancement in escape latency, and only olanzapine significantly enhanced attenuation in time spent in the escape platform quadrant in UCMS-exposed mice. In EPM test, all drugs significantly decreased enhancement in transfer latency in UCMS-exposed mice. In RAM test, fluoxetine significantly increased number of errors made by both non-stressed and UCMS-exposed mice. Quantitative real-time PCR revealed that CREB and BDNF gene expression levels were significantly decreased in UCMS-exposed group, and this effect was significantly reversed by each of drugs tested. Our results seem to be test dependent and should be further investigated using different learning and memory tasks.

Ucf-101 protects against cerebral oxidative injury and cognitive impairment in septic rat

Omi/HtrA2 is a proapoptotic mitochondrial serine protease involved in caspase-dependent and caspase-independent cell apoptosis. It has been verified that Omi/HtrA2 is related to apoptosis due to oxidative stress, which may play an important role in the integrity of mitochondria. Ucf-101 is a specific inhibitor of Omi/HtrA2 and it has been demonstrated that Ucf-101 has organ protective effects in a variety of in vitro and in vivo studies. The aim of our study was to examine the neuroprotective effects of Ucf-101 on cerebral oxidative injury and cognitive impairment in septic rats. Male Sprague Dawley rats are subjected to cecal ligation and puncture (CLP) or sham-operated laparotomy. Rats were divided into 4 groups: (1) a sham group plus normal saline (10 mL/kg); (2) a sham group plus Ucf-101 (10 umol/kg); (3) CLP plus normal saline (10 mL/kg); and (4) CLP plus Ucf-101 (10 umol/kg). Brain tumor necrosis factor (TNF)-α level, caspase-3 and caspase-9 activities, malondialdehyde (MDA) content and catalase (CAT) activities were examined. TUNEL staining was utilized to evaluate the amount of apoptosis and the cognitive function was evaluated by the MWM test. The study also assessed the clinical scores of animals and the survival time for the 7-day period. CLP resulted in a poor survival rate, evidence of hippocampal oxidative injury, cell apoptosis and cognitive dysfunction as well as elevated TNF-α level and caspases activities, increased weight loss and clinical scores. Ucf-101 pre-treatment could significantly inhibit caspases activities and cell apoptosis, reduce TNF-α and MDA levels, slightly reverse CAT activities in the brain and attenuate this CLP effect on cognitive dysfunction. In addition, the survival rate and survival time was significantly improved by pre-treatment with Ucf-101. The present results demonstrated that ucf-101 has the neuroprotective effects on cerebral oxidative injury and cognitive impairment in septic rats.

Glycogen Synthase Kinase 3β; Inhibiton Improves Diabetes‐induced Cognitive Deficits in Type‐2 Diabetic Rats

Challenges to neural homeostasis in diabetes may produce different responses and damage in CNS and alteration in many measures of cognition in diabetes. This study was carried out to investigate the effect of GSk3β inhibitor (SB216763; SB) on diabetes‐induced cognitive deficit and its mechanism of neuroprotection in type 2 diabetic (T2D) rats. High fat diet with STZ was used to develop T2D in rats. Rats were tested for place navigation, fear &amp; spatial memory using behavioral paradigms on 9, 12, 15 &amp; 18 week after induction of T2D. Brain regions were tested for biochemical and neurotransmitter level. Treatment with SB was given from 15 week to 18 week at 3 doses 0.3, 0.6 &amp; 1.2 mg/kg. T2D rats showed cognitive deficits after 15 week duration of diabetes and continue on 18th week compared to control. Further, elevated brain GABA level was observed after 15th week in T2D rats. Reduced glutamate level was also observed in T2D rats. Treatment with SB (0.6 mg/kg) for 3 weeks improved the diabetes‐induced cognitive deficits in passive avoidance, Y‐maze and MWM test. Improvement in memory also supported with decrease in GABA level and increased glutamate level. Administration of SB in diabetic rats also showed reduction in neuroinflammation in hippocampus and cortex. Improvement in cognitive deficits in diabetic rats by GSK3β inhibitor was attributed to reversal of neurotransmitters changes and reduction of neuroinflammation.

Spatial learning and memory impairment in an acute experimental autoimmune encephalomyelitis

Event Abstract Back to Event Spatial learning and memory impairment in an acute experimental autoimmune encephalomyelitis Dejana Kosanovic1*, Aleksandra Stojkovic1, Natasa Vukov1 and Katica Jovanova-Nesic1 1 Biomedical Center of the Institute Torlak, Neuroimmunology, Serbia Experimental autoimmune encephalomyelitis (EAE) could be associated with cognitive disturbances, so the aim of the study was investigation of spatial learning in mice with EAE. EAE was induced in eight-week-old C57BL/6 female mice by subcutaneous immunization (MOG35-55 in complete Freund’s adjuvant) and pertussis vaccine intraperitoneally. Animals were scored daily for clinical signs of EAE. Morris water maze test (MWM), consisting of a circular tank filled with water and a submerged platform in a fixed spot was performed before and after EAE induction. The path, time, and motor function during MWM test were observed. Hematoxylin-eosin staining of brain tissue was used for histological examination. After two trials mice mostly swam in the quadrant with the platform and after 8 training days all the mice swam directly to the platform. 50 % of mice with EAE showed partial loss of tail tonicity approximately 13 days post immunization. In all mice with EAE hind limb weakness after swimming was observed 18 days post immunization. Significant difference (p<0.05) in the time for finding the platform was found between mice with mild clinical signs of EAE in comparison with other mice (EAE without symptoms and non-treated). Interindividual behavioral difference within mice with EAE signs were observed, in 40 % there were no changes while in 60 % signs of disorientation and anxiety-like behavior was noted. Histopathological examination showed lesions in the brain parenchyma, especially in the hippocampal region of EAE mice. Hippocampal tissue destruction in EAE mice indicates the cognitive learning and memory impairment detected. Keywords: EAE, Morris water maze, Spatial learning, memory loss, Animal Models Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Immune-mediated disease pathogenesis Citation: Kosanovic D, Stojkovic A, Vukov N and Jovanova-Nesic K (2013). Spatial learning and memory impairment in an acute experimental autoimmune encephalomyelitis. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00169 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 11 Mar 2013; Published Online: 22 Aug 2013. * Correspondence: Miss. Dejana Kosanovic, Biomedical Center of the Institute Torlak, Neuroimmunology, Belgrade, 11000, Serbia, dr.dejana@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Dejana Kosanovic Aleksandra Stojkovic Natasa Vukov Katica Jovanova-Nesic Google Dejana Kosanovic Aleksandra Stojkovic Natasa Vukov Katica Jovanova-Nesic Google Scholar Dejana Kosanovic Aleksandra Stojkovic Natasa Vukov Katica Jovanova-Nesic PubMed Dejana Kosanovic Aleksandra Stojkovic Natasa Vukov Katica Jovanova-Nesic Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Treatment of TBI with Collagen Scaffolds and Human Marrow Stromal Cells Increases the Expression of Tissue Plasminogen Activator

This study examines the effects of combination therapy of collagen scaffolds and human marrow stromal cells (hMSCs) on the expression of tissue plasminogen activator (tPA) after traumatic brain injury (TBI) in rats. Adult male Wistar rats (n=48) were injured with controlled cortical impact and treated either with scaffolds suffused with hMSCs (3×10(6)) or hMSCs (3×10(6)) alone transplanted into the lesion cavity 1 week after TBI. A control group was treated with saline. Neurological function was assessed using the Morris Water Maze test (MWM) and modified Neurological Severity Scores (mNSS). The rats were sacrificed 14 days after TBI and brain samples were processed for immunohistochemical analysis and quantitative Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) studies. Enhanced functional improvement was observed on both the mNSS and MWM tests in the scaffold+hMSC-treated group compared to the other two groups. Immunostaining with anti-human mitochondrial antibody (E5204) showed more hMSCs in the injury zone of the scaffold+hMSC group compared to the hMSC-alone group. Triple staining showed that more neurons were tPA-positive in the scaffold+hMSC group compared to the other two groups (p<0.05). Western blot analysis and qRT-PCR showed that scaffold+hMSC and hMSC-alone treatment enhanced the expression of tPA compared to controls (p<0.05), but tPA expression was significantly greater in the scaffold+hMSC group. The induction of tPA by hMSCs after TBI may be one of the mechanisms involved in promoting functional improvement after TBI.

P.4.011 Analogues of cyclo-L-prolylglycine and their anxiolytic, nootropic and antihypoxic activity

Type 1 diabetes (T1DM) is a common chronic disease in childhood. Increasing insulin resistance in puberty gives rise to higher doses of insulin usage in treatment. Of this reason new approaches in treatment are needed. Noopept researches suggest it to have anti-diabetic properties. We tried to determine the effects of noopept on pubertal diabetes.The research was made with 60 prepubertal, 28 day-old, male, Sprague Dawley rats. The rats were divided into randomised 6 groups (n = 10/group). i) Control, ii) Diabetes Control, iii) Noopept Control, iv) Diabetes + Noopept, v) Diabetes + Insulin, vi) Diabetes + Insulin + Noopept. T1DM model was induced by streptozotocin on postnatal 28th day. 0.5 mg/kg noopept and 1 IU insulin were administered intraperitoneally for 14 days. Blood glucose and body weight measurements, puberty follow-up and MWM tests were performed. Hippocampus, hypothalamus and testis were evaluated histologically. Hypothalamic GnRH and kisspeptin were studied immunohistochemically. Serum LH, FSH and insulin, hippocampal homogenate NGF and BDNF levels were determined by ELISA.Delayed puberty was normalized by noopept (p < 0.05). Blood glucose levels were lower in noopept-administered diabetic groups (p < 0.05). Noopept decreased HOMA-IR in insulin administered diabetic group (p < 0.05). Number of degenerated cells in hippocampus and testis were higher in diabetes control group when compared with other groups (p < 0.05). GnRH immunoreactivity in Diabetes + Noopept group was increased when compared to insulin + noopept group (p = 0.018). There was no difference in kisspeptin, serum LH, FSH, hippocampal NGF-BDNF levels and spatial learning assessment among groups (p > 0.05).Noopept may have positive effect in treatment of pubertal diabetes.

The impact of age on emotional and cognitive behaviours triggered by experimental neuropathy in rats

Chronic pain syndromes encompass several clinical entities that frequently affect the individuals’ emotional and cognitive behaviours which, in turn, can also alter pain perception. Additionally, both pain perception and motivational-affective behaviours change with increasing age. In order to evaluate the influence of age upon the interaction between chronic pain and affective/cognitive behaviours, 3-, 10- and 22-month-old rats with 1month neuropathy (spared nerve injury, SNI model) were compared with age-matched sham-operated controls in the open field (OF; locomotor and exploratory behaviours), elevated plus-maze (EPM; anxiety-like behaviour), forced swimming (FST; depressive-like behaviour), working memory water maze (WM; spatial short-term memory), Morris water maze (MWM; spatial reference memory) and spatial reversal (behavioural flexibility) tests. Locomotor and exploratory activities decreased steadily with age and were further reduced by SNI. Aging was associated with increased anxiety-like behaviour, which was potentiated by SNI in both 3- and 22-month-old rats. The performance in the FST was affected by SNI but only in mid-aged animals. Cognitive performances in the MWM and spatial reversal tests deteriorated with age; however, the SNI lesion was only detrimental in the reversal task to mid-aged animals. Our data demonstrate that the influence of neuropathic pain on affective and cognitive behaviours is age dependent and varies with the behavioural domain that is tested. Importantly, mid-aged animals seem to be more susceptible to depression and cognitive deterioration associated to chronic pain than young and old groups.

Age-related spatial cognitive impairment is correlated with a decrease in ChAT in the cerebral cortex, hippocampus and forebrain of SAMP8 mice

At present, the mechanisms underlying cognitive disorders remain unclear. The senescence-accelerated mice (SAM) prone/8 (P8) has been proposed as a useful model for the study of aging, and SAM resistant/1 (R1) is its control as a normal aging strain. The purpose of this study was to investigate choline acetyltransferase (ChAT) expression in SAM brain. The age-related decline of learning and memory ability in P8 mice (4, 8 and 12 months old, n = 10 for each group) was proved in Morris water maze test (MWM). After the behavioral test, protein and mRNA levels of ChAT were determined in the cerebral cortex, hippocampus and forebrain by means of immunostaining, Western blotting, and real time quantitative PCR (QPCR). Comparing with 4-month-old P8 and R1, 8- and 12-month-old P8 showed age-related cognitive impairment in MWM test. The latencies of the 4-month-old P8 in a hidden platform trial were significantly shorter, and the retention time was significantly longer than that of the older P8 groups. In addition, significantly low level of ChAT protein was observed in older P8 groups. Comparing with the 4-month-old P8, ChAT mRNA in the 12-month-old P8 declined significantly in all three regions of P8 brain. Pearson correlation test showed that the latencies in the MWM were positively correlated with the level of ChAT in P8. Such phenomenon could not be detected in normal aging R1 mice. These findings suggest that the decrease of ChAT in P8 mice was responsible for the age-related learning and memory impairments in some sense.

Light stress effects on Subicular and CA1 place cells and its implications in a MWM test in young wistar rats

Light stress effects on Subicular and CA1 place cells and its implications in a MWM test in young wistar rats