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Purpose@#In this study, the effect of the Vojta approach on neck stability and static balance in children with hypotonia was studied. @*Methods@#Seventeen children with hypotonia were randomly divided into the Vojta approach group (n=9) and the general physical therapy group (n=8). Each group was applied intervention for 30 minutes per session, 3 times a week, for a total of 4 weeks. Ultrasonography was used to measure deep neck flexor muscle thickness, craniovertebral angle (CVA) to measure neck alignment along the spine segment, and Balancia software program to measure static balance. @*Results@#In the Vojta approach group, the deep neck flexor muscle thickness was significantly increased (P<0.05), and the CVA was significantly improved (P<0.05). In addition, path area among static balance was significantly improved (P<0.05). @*Conclusions@#The Vojta approach can be suggested as an effective intervention method for improving neck stability and static balance in children with hypotonia.
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Purpose@#Poloxamer-407 (P-407) is used to induce hyperlipidemia. Exercise is effective in improving arteriosclerosis and cognitive impairment. In this research, the effect of treadmill running on short-term memory in the P-407-treated hyperlipidemia rats was studied focusing on neuroinflammation. @*Methods@#Rats were classified in normal group, normal and treadmill exercise group, P-407-treated group, and P-407-treated and treadmill exercise group. Hyperlipidemia rats were made by single intraperitoneal injection with P-407 (500 mg/kg). Treadmill exercise was conducted for 30 minutes once a day, 5 days per week during 28 days. Step-down avoidance task was done to measure short-term memory. Glial fibrillary acidic protein and ionized calcium binding adaptor molecule 1 were assessed by immunohistochemistry. Expression of adhesion molecules and proinflammatory cytokines was determined by western blot analysis. @*Results@#Treadmill exercise alleviated lipid profiles in the P-407-induced hyperlipidemia rats. Treadmill exercise improved short-term memory, inhibited reactive astrogliosis and microglia activation, and suppressed expression of adhesion molecules and proinflammatory cytokines in the hyperlipidemic rats. @*Conclusions@#Treadmill exercise exerts alleviating effect on memory deficits by inhibiting hippocampal neuroinflammation in the hyperlipidemia. The current results suggest that treadmill running serves as the treatment strategy for the cognitive dysfunction caused by hyperlipidemia.
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Purpose@#Thrombotic stroke is a type of ischemic stroke characterized by motor dysfunction and memory impairments. In the present study, the effect of treadmill exercise on motor function and short-term memory was evaluated in relation with synaptic plasticity in the mice with photothrombotic stroke. @*Methods@#Photothrombotic stroke was induced by cortical photothrombotic vascular occlusion. The mice in the treadmill exercise groups performed running on a motorized treadmill for 28 days. Motor function was determined using rota-rod test and foot fault test. Step-through avoidance task was conducted to evaluate short-term memory. Immunohistochemistry for 5-bromo-2′-deoxyuridine and doublecortin was conducted to detect new cell generation. Postsynaptic density protein 95, synaptophysin, brain-derived neurotrophic factor (BDNF), and tyrosine kinase B receptor (TrkB) were determined using western blot. The number of dendritic spines was determined using Golgi stain. @*Results@#Treadmill exercise improved motor function and short-term memory in mice with the photothrombotic stroke. The infarct size was reduced and the number of dendritic spines and expression of postsynaptic density protein 95 and synaptophysin in the peri-infarct cortex and hippocampus were increased by treadmill exercise in photothrombotic stroke mice. Treadmill exercise enhanced neurogenesis through increasing the expression of the hippocampal BDNF and TrkB in photothrombotic stroke mice. @*Conclusions@#Treadmill exercise improved motor function and short-term memory through increasing synaptic plasticity and neurogenesis in photothrombotic stroke mice. Treadmill exercise can be used as an effective treatment strategy to improve brain function related to stroke.
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OBJECTIVE: Transient anterograde amnesia is occasionally observed in a number of conditions, including migraine, focal ischemia, venous flow abnormalities, and after general anesthesia. The inhalation anesthetic, isoflurane, is known to induce transient anterograde amnesia. We examined the involvement of brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) in the underlying mechanisms of the isoflurane-induced transient anterograde amnesia. METHODS: Adult male Sprague-Dawley rats were divided into three groups : the control group, the 10 minutes after recovery from isoflurane anesthesia group, and the 2 hours after recovery from isoflurane anesthesia group (n=8 in each group). The rats in the isoflurane-exposed groups were anesthetized with 1.2% isoflurane in 75% nitrous oxide and 25% oxygen for 2 hours in a Plexiglas anesthetizing chamber. Short-term memory was determined using the step-down avoidance task. BDNF and TrkB expressions in the hippocampus were evaluated by immunofluorescence staining and western blot analysis. RESULTS: Latency in the step-down avoidance task was decreased 10 minutes after recovery from isoflurane anesthesia, whereas it recovered to the control level 2 hours after isoflurane anesthesia. The expressions of BDNF and TrkB in the hippocampus were decreased immediately after isoflurane anesthesia but were increased 2 hours after isoflurane anesthesia. CONCLUSION: In this study, isoflurane anesthesia induced transient anterograde amnesia, and the expressions of BDNF and TrkB in the hippocampus might be involved in the underlying mechanisms of this transient anterograde amnesia.
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Adulto , Animales , Humanos , Masculino , Ratas , Amnesia Anterógrada , Anestesia , Anestesia General , Western Blotting , Factor Neurotrófico Derivado del Encéfalo , Técnica del Anticuerpo Fluorescente , Hipocampo , Inhalación , Isquemia , Isoflurano , Memoria a Corto Plazo , Trastornos Migrañosos , Óxido Nitroso , Oxígeno , Polimetil Metacrilato , Proteínas Tirosina Quinasas , Ratas Sprague-DawleyRESUMEN
PURPOSE: Prenatal environmental conditions affect the development of the fetus. In the present study, we investigated the effects of exposure to music and noise during pregnancy on neurogenesis and thickness in the motor and somatosensory cortex of rat pups. METHODS: The pregnant rats in the music-applied group were exposed to 65 dB of comfortable music for 1 hour, once per day, from the 15th day of pregnancy until delivery. The pregnant rats in the noise-applied group were exposed to 95 dB of sound from a supersonic sound machine for 1 hour, once per day, from the 15th day of pregnancy until delivery. After birth, the offspring were left undisturbed together with their mother. The rat pups were sacrificed at 21 days after birth. RESULTS: Exposure to music during pregnancy increased neurogenesis in the motor and somatosensory cortex of rat pups. In contrast, rat pups exposed to noise during pregnancy showed decreased neurogenesis and thickness in the motor and somatosensory cortex. CONCLUSIONS: Our study suggests that music and noise during the developmental period are important factors influencing brain development and urogenital disorders.
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Animales , Humanos , Embarazo , Ratas , Encéfalo , Feto , Madres , Corteza Motora , Música , Neurogénesis , Ruido , Parto , Corteza SomatosensorialRESUMEN
PURPOSE: Sleep deprivation may exert many negative effects on hippocampus-dependent cognitive function, such as learning and memory. The present study was conducted in order to investigate the effects of repetitive sleep deprivation on cognition, apoptotic neuronal cell death, and cell proliferation in the hippocampus, using mice. METHODS: To induce sleep deprivation, mice were placed in a water cage containing six platforms (3 cm in diameter), surrounded by water up to 1 cm beneath the surface of the platform for 24 h. Mice were randomly divided into four groups (n=20 in each group): control group, 24 h rest after 24 h sleep deprivation group, 48 h rest after 24 h sleep deprivation group, and 72 h rest after 24 h sleep deprivation group. This cycle was continued for 36 days. Novel objective recognition test and immunohistochemistry for 5-bromo-2'-deoxyuridine (BrdU), western blot for expression of Bax, Bcl-2, brain-derived neurotrophic factor (BDNF), and caspase-3 were performed. RESULTS: Results of the novel objective recognition test showed decreased cognition in the 24 h rest after 24 h sleep deprivation group, while a similar effect was observed in other groups, compared to the control group. Increased cell proliferation and enhanced expression of BDNF and Bax protein were observed in the 24 h rest after 24 h sleep deprivation group and the 48 h rest after 24 h sleep deprivation group, compared to the control group. Expression of Bcl-2 showed a decrease in the 24 h and 48 h rest groups, compared to the control group. Expression of caspase-3 in the dentate gyrus of the hippocampus showed a significant increase in the 24 h rest after 24 h sleep deprivation group and in the 48 h rest after 24 h sleep deprivation group, compared to the control group. CONCLUSION: Results of the present study indicate that insufficient rest after sleep deprivation may induce impairment of cognitive function. After sleep deprivation, at least 72 hr of rest time is needed for recovery.
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Animales , Ratones , Apoptosis , Proteína X Asociada a bcl-2 , Western Blotting , Factor Neurotrófico Derivado del Encéfalo , Bromodesoxiuridina , Caspasa 3 , Muerte Celular , Proliferación Celular , Cognición , Giro Dentado , Hipocampo , Inmunohistoquímica , Aprendizaje , Memoria , Memoria a Corto Plazo , Neuronas , Privación de Sueño , AguaRESUMEN
BACKGROUND: Spinal cord ischemia with resulting paraplegia remains one of the most common complications after repair of thoracoabdominal aortic aneurysms or dissection. Inducible nitric oxide synthase (iNOS) is known to have both neuroprotective and neurotoxic effects in the central nervous system. We investigated the possible relationship between the effect of pre-ischemic isoflurane exposure on mild spinal cord ischemia and the inducible nitric oxide synthase (iNOS) expression by using iNOS-specific antibody and pyrrolidinedithio carbamate (PDTC), NF-kappaB inhibitor, in the ventral horn of spinal cord in rats. METHODS: The animals were divided into five groups (n = 6 in each group): sham group, control group, PDTC-treated group, isoflurane-treated group, and PDTC/ isoflurane-treated group. In the PDTC-treated groups, 2% 100 mg/kg PDTC was administered intraperitoneally at 1 h before operation and at 24 h and 48 h after reperfusion. The rats in the isoflurane-treated groups received 30 min inhalation of 2.8% isoflurane at 24 h before spinal cord ischemia. Immunohistochemistry was performed to detect iNOS expression in the motor neuron of the ventral horn in spinal cord. RESULTS: Preconditioning with isoflurane increased the iNOS expression when compared to the control group (P < 0.05), whereas pre-treatment with both PDTC and isoflurane significantly decreased the iNOS expression compared to isoflurane-treated group (P < 0.05). CONCLUSIONS: Pre-ischemic isoflurane exposure was related with increase of the iNOS expression via a pathway modulated by NF-kappaB. iNOS may act as an important mediator of delayed preconditioning with isoflurane for the protective effect against spinal cord ischemia.
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Animales , Ratas , Aneurisma de la Aorta Torácica , Sistema Nervioso Central , Grupos Control , Cuernos , Inmunohistoquímica , Inhalación , Isoflurano , Neuronas Motoras , FN-kappa B , Óxido Nítrico , Óxido Nítrico Sintasa de Tipo II , Paraplejía , Prolina , Reperfusión , Salicilamidas , Médula Espinal , Isquemia de la Médula Espinal , TiocarbamatosRESUMEN
PURPOSE: Oxytocin is associated with the ability to form normal social attachments. c-Fos is an immediate early gene whose expression is used as a marker for stimulus-induced changes in neurons. The effect of phosphodiesterase-5 (PDE-5) inhibitors on oxytocin activation in the brain without sexual stimuli has not yet been reported. In the present study, we investigated the effects of vardenafil on oxytocin and c-Fos expression in the paraventricular nucleus (PVN) of conscious rats. METHODS: Male Sprague-Dawley rats weighing 300+/-10 g were divided into 6 groups (n=5 in each group): the control group, the 1-day-0.5 mg/kg, the 1-day-1 mg/kg, the 1-day-2 mg/kg, the 3-day-1 mg/kg, and the 7-day-1 mg/kg vardenafil administration group. The experiment was conducted without sexual stimulation. Vardenafil was orally administered. The animals in the control group received an equivalent amount of distilled water orally. The expression of oxytocin and c-Fos in the PVN was detected by immunohistochemistry. RESULTS: Oxytocin expression in the PVN was increased by 1 day administration of 2 mg/kg vardenafil, and this effect of vardenafil appeared in a duration-dependent manner. c-Fos in the oxytocin neurons of the PVN was increased by 1 day administration of 2 mg/kg vardenafil, and this effect of vardenafil also appeared in a duration-dependent manner. These results showed that vardenafil augments the expression of oxytocin with activation of oxytocin neurons in the PVN. CONCLUSIONS: In this study, we showed that the PDE-5 inhibitor, vardenafil directly enhances oxytocin expression and also activates oxytocin neurons in the PVN, which indicates that vardenafil may exert positive effects on affiliation behavior and social interaction.
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Animales , Humanos , Masculino , Ratas , Encéfalo , Fosfodiesterasas de Nucleótidos Cíclicos Tipo 5 , Imidazoles , Relaciones Interpersonales , Neuronas , Oxitocina , Núcleo Hipotalámico Paraventricular , Piperazinas , Ratas Sprague-Dawley , Sulfonas , Triazinas , Agua , Diclorhidrato de VardenafilRESUMEN
PURPOSE: Cyclosporine A (CsA) is a potent immunosuppressive agent, and it has been used to prevent rejection of transplanted organs and to treat autoimmune diseases. Many side effects of CsA, including various types of endothelial dysfunction, have been reported. Pentoxifylline (PTX) is a non-selective phosphodiesterase inhibitor that is used for the treatment of peripheral vascular diseases. METHODS: We investigated the effect of CsA on collagen synthesis and clarified whether PTX has protective effects against CsA-induced arterial vasculopathy using calf pulmonary artery endothelial cells. This study was carried out using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, reverse transcription- polymerase chain reaction (RT-PCR), Western blot analysis, nitric oxide (NO) detection, and cyclic guanosine monophosphate (cGMP) enzyme immunoassay. RESULTS: CsA treatment significantly increased the expression of collagen type I mRNA and protein and decreased the production of NO and cGMP. However, pre-treatment with PTX exerted anticollagen effect by suppressing the CsA-induced formation of collagen, but this effect of PTX was not modulated by NO and cGMP. CONCLUSION: Based on the present results, it is expected that PTX may have a protective effect against CsA-induced arterial vasculopathy, although the mechanism of PTX needs to be clarified in future studies.
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Enfermedades Autoinmunes , Western Blotting , Colágeno , Colágeno Tipo I , GMP Cíclico , Ciclosporina , Células Endoteliales , Guanosina Monofosfato , Técnicas para Inmunoenzimas , Óxido Nítrico , Pentoxifilina , Enfermedades Vasculares Periféricas , Reacción en Cadena de la Polimerasa , Arteria Pulmonar , Rechazo en Psicología , ARN Mensajero , Sales de Tetrazolio , Tiazoles , TrasplantesRESUMEN
Fucoidan, a sulfated polyanionic polymer of L-fucose, is obtained from brown marine macroalgae. In the present study, neuroprotective effect of fucoidan against N-methyl- D-aspartate (NMDA)-induced excitotoxicity in the hippocampus was investigated. The patch clamp study revealed that fucoidan significantly inhibited NMDA receptor-activated ion current in the acutely dissociated hippocampal CA1 neurons. In an organotypic hippocampal slice culture, fucoidan inhibited NMDA-induced neuronal cell death in a dose-dependent manner. The present study showed that fucoidan possesses a neuroprotective effect against NMDA-induced excitotoxicity, and that the suppressive effect of fucoidan on the NMDA-induced ion current can be suggested as being the underlying neuroprotective mechanism of fucoidan.
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Animales , Ratas , Muerte Celular , Ácido D-Aspártico , Hipocampo , N-Metilaspartato , Neuronas , Fármacos Neuroprotectores , Polímeros , Polisacáridos , Algas MarinasRESUMEN
This study was conducted to evaluate the effects of vardenafil (Levitra), a phosphodiesterase-5 (PDE-5) inhibitor, on cell proliferation in the hippocampal dentate gyrus and on 5-hyroxytryptamine (5-HT, serotonin) synthesis and tryptophan hydroxylase (TPH) expression in the rat dorsal raphe nucleus. Male Sprague-Dawley rats were divided into 6 groups (n=5 in each group): a control group, a 0.5 mg/kg-1 day vardenafil-treated group, a 1 mg/kg-1 day vardenafil-treated group, a 2 mg/kg-1 day vardenafil-treated group, a 1 mg/kg-3 day vardenafil-treated group, and a 1 mg/kg-7 day vardenafil-treated group. 5-bromo-2'-deoxyuridine (BrdU) immunohistochemistry was then performed to evaluate cell proliferation in the dentate gyrus. In addition, 5-HT and TPH immunohistochemistry was conducted to evaluate serotonin expression in the dorsal raphe. The results revealed that treatment with vardenafil increased cell proliferation in the dentate gyrus and enhanced 5-HT synthesis and TPH expression in the dorsal raphe in a dose- and duration-dependent manner. The findings demonstrate that the increasing effect of vardenafil on cell proliferation is closely associated with the enhancing effect of vardenafil on serotonin expression under normal conditions.