Changes in localization of synaptophysin following fluid percussion injury in the rat brain

Shojo, Hideki; Kibayashi, Kazuhiko

doi:10.1016/j.brainres.2006.01.063

Cited by 47 publications

(36 citation statements)

References 33 publications

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“…Further, the serum adrenaline concentration in the RSV infection group was significantly lesser than those in the control and anti-NGF antibody groups; this implied that the overexpression of NGF in RSV infection might induce the differentiation of the adrenal medullary cells of the endocrine phenotype, as mentioned above, and downregulate adrenaline expression, thereby promoting the progression of asthma. SYN, a marker protein for synaptic vesicle and an important component of the axon skeleton, is widely distributed in neuroendocrine tissue, including neural tissue, such as the brain, spinal cord, retina, and adrenal medulla (Shojo and Kibayashi, 2006;Kasprzak et al, 2007). Changes in its expression levels can indirectly reflect variations in the number of synapses and the gradual process of neuron development.…”

Section: Discussionmentioning

confidence: 99%

Neural-endocrine mechanisms of respiratory syncytial virus-associated asthma in a rat model

Li¹,

Wu²,

Li³

et al. 2012

Genet. Mol. Res.

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ABSTRACT. We examined the underlying neural-endocrine mechanisms of asthma associated with respiratory syncytial virus infection. Thirty Sprague-Dawley rats were randomly divided into control group, respiratory syncytial virus (RSV) group, and anti-nerve growth factor (NGF) IgG group. An RSV infection model was established by nasal drip once a week. In the anti-NGF antibody intervention group, each rat was given an intraperitoneal injection of anti-NGF IgG 3 h before RSV infection. Optical microscopy and transmission electron microscopy were used to observe the structural changes in adrenal medulla cells. Changes in adrenaline and norepinephrine in serum were detected by ELISA. NGF expression was assayed by immunohistochemistry. Expression differences in synaptophysin mRNA were detected by RT-PCR. Transmission electron microscopy displayed widened adrenal medulla intercellular spaces, reduced chromaffin particle concentration, and increased mitochondria in the RSV infection group. At the same time, NGF expression was increased in the RSV infection group significantly. In addition, the adrenaline concentration was significantly Mechanisms of respiratory syncytial virus-associated asthma decreased compared with the control and anti-NGF antibody groups. Synaptophysin mRNA expression was significantly increased in the RSV infection and anti-NGF antibody groups. However, compared with the RSV infection group, synaptophysin mRNA expression was significantly decreased in the anti-NGF antibody group. We conclude that RSV infection could induce adrenal medulla cell differentiation to nerve cells by over-expression of NGF, resulting in the decreased endocrine function found in asthma progression.

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Section: Discussionmentioning

confidence: 99%

Neural-endocrine mechanisms of respiratory syncytial virus-associated asthma in a rat model

Li¹,

Wu²,

Li³

et al. 2012

Genet. Mol. Res.

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“…Synaptophysin (SYP) plays a role in activity-dependent competitive synapse formation (7). Since loss of synapse correlates with the degree of brain dysfunction, the levels of SYP also serve as a functional marker of the brain (8). Therefore, in this study, we investigated the expression of SYP in the brains of rats subjected to NSC transplant following TBI.…”

Section: Transplantation Of Neural Stem Cells Enhances Expression Of mentioning

confidence: 99%

Transplantation of neural stem cells enhances expression of synaptic protein and promotes functional recovery in a rat model of traumatic brain injury

Shi

2011

Mol Med Report

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Abstract. Transplantion of neural stem cells (NSCs) hasshown promise for the treatment of traumatic brain injury (TBI). Although the functional mechanisms underlying transplant-mediated recovery following TBI have yet to be determined, previous studies demonstrated that transplanted NSCs may respond to the release of specific neurotransmitters, and/or the production of factors that promote neuronal growth. Therefore, we hypothesize that the direct transplantation of NSCs into the injured brain enhanced the expression of synaptic protein and regeneration-associated protein, which may be responsible for promoting functional recovery in a rat model of TBI. Our results showed that NSC transplant significantly improved neurological motor function in selected behavioral tests compared to saline control rats. Our data showed that the number of surviving cells engrafted into the rats was 4.1±0.9% of engrafted cells at 8 weeks post-transplantation, with 11.4±1.6% βⅢ-tubulin-immunopositive cells of these cells. RT-PCR and Western blot analysis demonstrated that the expression of synaptophysin (SYP) and regeneration-associated protein (GAP43) in the injured brain of NSC-transplanted rats was significantly increased compared to the saline control rats during the experimental period. These data suggest that NSCs transplanted directly into the injured brain are capable of surviving, differentiating into neurons and promoting functional recovery in a rat model of TBI. Engrafted NSCs increase the expression of SYP and GAP43 in the injured brain of NSC-transplanted rats, which is suggested as one of the mechanisms underlying the improved functional recovery on motor behavior due to the transplantation of NSCs following TBI.

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“…When used at very high doses it produces profound euphoria, increased heart rate, respiration, agitation and dopamine mediated neurotoxicity Krasnova and Cadet, 2009). However, when administered at low doses, methamphetamine produces a more controlled release of catecholamines, capable of activating multiple neuroprotective pathways in the brain (Feeney and Hovda, 1983;Feeney et al, 1981Feeney et al, , 1982 [31][32][33][34][35][36][37][38][39][40] observed with the highest therapeutic dose (0.500 mg/kg/h) tested in rats. However, recently published data indicates that a single i.v.…”

Section: Discussionmentioning

confidence: 99%

“…Dosing rats with 0.500 mg/kg/h or 0.250 mg/kg/h beginning 8 h after injury significantly reduced the time required to locate the A B [31][32][33][34][35][36][37][38][39][40] escape platform (Fig. 2A).…”

Section: Methamphetamine Improves Cognitive Outcomes When Administratmentioning

confidence: 99%

“…Brains were isolated, post-fixed in 4% paraformaldehyde for 2 days at room temperature, and then processed for paraffin sectioning. Using light microscopy and a laser scanning confocal microscope (Zeiss LSM 510), we measured a composite index of independent measurements from multiple immunohistochemical stainings for axons (Bielschowsky's silver and Luxol fast blue, BLFB [30]; monoclonal antibody to nonphosphorylated neurofilaments, SMI-32 [31]), dendrites (microtubule-associated protein 2, MAP-2 [32]) and synapses (synaptophysin, SYP [33]). Data were expressed as density, or percentage of area of immunoreactive proteins, to the area of the FOV.…”

Section: Mri Of Neuronal Recovery After Low-dose Methamphetamine Treamentioning

confidence: 99%

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Preclinical and Clinical Development of Low Dose Methamphetamine for the Treatment of Traumatic Brain Injury

Poulsen¹

2014

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATEApril PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) AND ADDRESS(ES) PERFORMING ORGANIZATION REPORT NUMBERUniversity of Montana 32 Campus Dr. Missoula, MT 59812 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel CommandFort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTThis proposal addresses additional preclinical characterization of low dose methamphetamine as a neuroprotective agent for TBI. We have previously demonstrated that treatment with methamphetamine within 12 hours after TBI significantly improved cognition and functional behavior in 2-3 month old male Wistar rats. These studies were intended to examine the therapeutic effects of methamphetamine in female and aged male rats. We also repeated a MRI time course study with the intent of determining if there was a dose response effect associated with methamphetamine induced white matter track remodeling. We have determined that female rats represent a poor model for TBI. Unlike humans, female rats have a 3-day estrous cycle. This means they are endogenously exposed to the neuroprotective effects of estrogen and progesterone before, during and after injury. This allows them to recover to near normal levels within a few weeks of after injury. In this context, it is not possible to observe any kind of drug effect on cognitive or behavioral outcomes. We have determined that methamphetamine does not exhibit a therapeutic effect in aged rats. A number of changes exist in aged rats that could account for this observation. First, they have reduced dopamine receptors. We have shown that methamphetamine-mediated neuroprotection is dependent, in part, on the activation of dopamine receptors. This reduction of dopamine receptors also contributes to a condition of chronic inflammation. We have shown that methamphetamine reduces neuroinlammatory signaling. Thus, the reduction of dopamine receptor mediated signaling could explain the loss of protectiv...

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Changes in localization of synaptophysin following fluid percussion injury in the rat brain

Cited by 47 publications

References 33 publications

Neural-endocrine mechanisms of respiratory syncytial virus-associated asthma in a rat model

Neural-endocrine mechanisms of respiratory syncytial virus-associated asthma in a rat model

Transplantation of neural stem cells enhances expression of synaptic protein and promotes functional recovery in a rat model of traumatic brain injury

Preclinical and Clinical Development of Low Dose Methamphetamine for the Treatment of Traumatic Brain Injury

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