MAP2, Synaptophysin Immunostaining in Rat Brain and Behavioral Modifications after Cerebral Postischemic Reperfusion

Martinez, G; Giacomo, Claudia Di; Carnazza, Maria Luisa; Sorrenti, Valeria; Castana, R; Barcellona, Maria Luisa; Perez‐Polo, J. Regino; Vanella, A.

doi:10.1159/000111243

Cited by 25 publications

(11 citation statements)

References 19 publications

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“…BCCA occlusion causes reduction in blood flow to diverse regions of brain and contributes to associated behavioral and cognitive deficits (Tsuchiya et al 1993;Martinez et al 1997). Res (2011) 20:379-386 383 In the present study, a significant decrease (72.54%) in locomotor activity and an increase (189.59%) in beam walking latency have been observed after ischemia reperfusion, which was reversed by embelin pretreatment (25 and 50 mg/kg p.o.)…”

Section: Discussionsupporting

confidence: 51%

Protective Effect of Embelin from Embelia ribes Burm. Against Transient Global Ischemia-Induced Brain Damage in Rats

Thippeswamy¹,

Nagakannan²,

Shivasharan³

et al. 2011

Neurotox Res

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Embelia ribes is being used in Indian traditional herbal medicine for the treatment of mental disorders and as brain tonic. The present study was designed to investigate the protective effects of embelin from E. ribes on global ischemia/reperfusion-induced brain injury in rats. Transient global ischemia was induced by occluding bilateral common carotid arteries for 30 min followed by 24-h reperfusion. Neurological functions were measured using sensorimotor tests. Ischemia/reperfusion-induced neuronal injury was assessed by cerebral infarct area, biochemical and histopathological examination. Pretreatment of embelin (25 and 50 mg/kg, p.o.) significantly increased locomotor activity and hanging latency time and decreased beam walking latency when compared with ischemic control. The treatment also reduced significantly the lipid peroxidation and increased the total thiol content and glutathione-S-transferase activity in brain homogenates. The decreased cerebral infarction area in embelin-treated groups and histopathological observations confirmed the above findings. These observations suggested that embelin is a neuroprotective agent and may prove to be useful adjunct in the treatment of stroke.

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Section: Discussionsupporting

confidence: 51%

Protective Effect of Embelin from Embelia ribes Burm. Against Transient Global Ischemia-Induced Brain Damage in Rats

Thippeswamy¹,

Nagakannan²,

Shivasharan³

et al. 2011

Neurotox Res

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“…Decrease in the synaptophysin IR is associated with brain injury and aging, possibly reflecting functional disturbances of synaptic transmission (13). The neuronal MAP2 determines stability and arrangement of neuronal microtubules.…”

mentioning

confidence: 99%

Cognition- and Anxiety-Related Behavior, Synaptophysin and MAP2 Immunoreactivity in the Adult Rat Treated with a Single Course of Antenatal Betamethasone

et al. 2006

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ABSTRACT:We investigated the effects of a single course of antenatal betamethasone on cognition-and anxiety-related behavior and synaptophysin and microtubule-associated protein 2 (MAP2) immunoreactivity in the adult rat hippocampus. On d 20 of gestation, pregnant rats were injected with either 1) 170 g/kg body weight of betamethasone ("clinically equivalent dose," equivalent to 12 mg twice, 24 h apart); 2) half this dose; or 3) vehicle. Cognition-and anxiety-related behavior of the offspring was analyzed at an age of 5 mo using the Morris water maze, object recognition task, and open field test. Subsequently, synaptophysin and MAP2 immunoreactivity were measured in the hippocampus. We report no detrimental effects of antenatal betamethasone on cognition-and anxiety-related behavior and synaptophysin immunoreactivity in the adult rat. On the other hand, MAP2 immunoreactivity was decreased by betamethasone in males, suggesting a permanent impairment in the hippocampus. Interestingly, the lower dose appears to have less influence in terms of growth restriction, known to be associated with an increased risk of disease in adulthood. Further research might elucidate whether the betamethasone effect on hippocampal neurons persists later in life and could affect the aging process increasing the risk for neuropathology of the adult. A ntenatal glucocorticoids are widely used to prevent respiratory distress syndrome in case of threat of preterm delivery (1). Although beneficial for lung maturation, this treatment causes a wide range of side effects in humans, including a reduction in weight and head circumference at birth (2), and in impairment in both circulating glucocorticoid bioactivity (3) and cortisol response to stressors (4). Animal studies showed that antenatal glucocorticoids affect the hypothalamic-pituitary-adrenal (HPA) axis (5), an impairment of which has been linked to the development of anxiety and mood disorders (6). Further, this treatment has been reported to reduce DNA content (7), cell proliferation rate (8), synaptic density (9), and neurotrophic factor concentrations within the neonatal brain (10) and induces neural degeneration within the developing hippocampus (11). However, little is known about the consequences for later life, in particular, the effects on cognition-and anxiety-related behavior are unclear (5,12).The presynaptic marker protein synaptophysin is a calciumbinding protein that plays an important role in the generation and maintenance of small vesicle membranes and their interaction with cytoskeletal elements. Decrease in the synaptophysin IR is associated with brain injury and aging, possibly reflecting functional disturbances of synaptic transmission (13). The neuronal MAP2 determines stability and arrangement of neuronal microtubules. Loss of MAP2 IR after brain injury correlates with neuronal degeneration (14) and is associated with age-related impairment of synaptic plasticity, cognition, and memory functions. Interestingly, both synaptophysin IR and MAP2 IR have been reported ...

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“…The occurrence of this cascade of events was also demonstrated under in vivo experimental conditions of partial and transient cerebral ischemia in rats and was indirectly confirmed by protective effects observed following treatment with drugs acting with different molecular mechanisms [41–46]. Over recent years, neuroscientists have acquired a considerable body of evidence to support the fact that the mammalian brain can adapt to injurious insults such cerebral ischemia, thus increasing the chances of survival [47, 48]. So, sublethal ischemic insults may protect tissues from subsequent insults.…”

Section: Discussionmentioning

confidence: 92%

“…Our previous studies, carried out on the same experimental model of partial and transient cerebral ischemia, indicated that the environment of injured neurons seemed to determine the ability of axons to regenerate after injury [47, 72]. To this regard, endogenous mediators affecting vasculature such as endothelium-derived NO, inducing smooth muscle relaxation and then vasodilatation of brain vessels, might improve tissue perfusion, attenuating the ischemic insult and promoting functional recovery of the infarcted brain area.…”

Section: Discussionmentioning

confidence: 99%

Effect of Treatment with Cyanidin-3-O-β-D-Glucoside on Rat Ischemic/Reperfusion Brain Damage

Giacomo

Acquaviva

Santangelo

et al. 2012

Evidence-Based Complementary and Alternative Medicine

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This study investigated the effect of cyanidin-3-O-β-glucoside on an experimental model of partial/transient cerebral ischemia in the rats in order to verify the effectiveness of both pre- and posttreatments. Cyanidin-3-O-β-glucoside-pretreated rats were injected with 10 mg/Kg i.p. 1 h before the induction of cerebral ischemia; in posttreated rats, the same dosage was injected during reperfusion (30 min after restoring blood flow). Cerebral ischemia was induced by bilateral clamping of common carotid arteries for 20 min. Ischemic rats were sacrificed immediately after 20 min ischemia; postischemic reperfused animals were sacrificed after 3 or 24 h of restoring blood flow. Results showed that treatment with cyanidin increased the levels of nonproteic thiol groups after 24 h of postischemic reperfusion, significantly reduced the lipid hydroperoxides, and increased the expression of heme oxygenase and γ-glutamyl cysteine synthase; a significant reduction in the expression of neuronal and inducible nitric oxide synthases and the equally significant increase in the endothelial isoform were observed. Significant modifications were also detected in enzymes involved in metabolism of endogenous inhibitors of nitric oxide. Most of the effects were observed with both pre- and posttreatments with cyanidin-3-O-β-glucoside suggesting a role of anthocyanin in both prevention and treatment of postischemic reperfusion brain damage.

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MAP2, Synaptophysin Immunostaining in Rat Brain and Behavioral Modifications after Cerebral Postischemic Reperfusion

Cited by 25 publications

References 19 publications

Protective Effect of Embelin from Embelia ribes Burm. Against Transient Global Ischemia-Induced Brain Damage in Rats

Protective Effect of Embelin from Embelia ribes Burm. Against Transient Global Ischemia-Induced Brain Damage in Rats

Cognition- and Anxiety-Related Behavior, Synaptophysin and MAP2 Immunoreactivity in the Adult Rat Treated with a Single Course of Antenatal Betamethasone

Effect of Treatment with Cyanidin-3-O-β-D-Glucoside on Rat Ischemic/Reperfusion Brain Damage

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