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Search Results: 1 - 10 of 47417 matches for " ca1 cell loss "
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Magnesium chloride alone or in combination with diazepam fails to prevent hippocampal damage following transient forebrain ischemia
Milani, H.;Lepri, E.R.;Giordani, F.;Favero-Filho, L.A.;
Brazilian Journal of Medical and Biological Research , 1999, DOI: 10.1590/S0100-879X1999001000016
Abstract: in the central nervous system, magnesium ion (mg2+) acts as an endogenous modulator of n-methyl-d-aspartate (nmda)-coupled calcium channels, and may play a major role in the pathomechanisms of ischemic brain damage. in the present study, we investigated the effects of magnesium chloride (mgcl2, 2.5, 5.0 or 7.5 mmol/kg), either alone or in combination with diazepam (dz), on ischemia-induced hippocampal cell death. male wistar rats (250-300 g) were subjected to transient forebrain ischemia for 15 min using the 4-vessel occlusion model. mgcl2 was applied systemically (sc) in single (1x, 2 h post-ischemia) or multiple doses (4x, 1, 2, 24 and 48 h post-ischemia). dz was always given twice, at 1 and 2 h post-ischemia. thus, ischemia-subjected rats were assigned to one of the following treatments: vehicle (0.1 ml/kg, n = 34), dz (10 mg/kg, n = 24), mgcl2 (2.5 mmol/kg, n = 10), mgcl2 (5.0 mmol/kg, n = 17), mgcl2 (7.5 mmol/kg, n = 9) or mgcl2 (5 mmol/kg) + dz (10 mg/kg, n = 14). seven days after ischemia the brains were analyzed histologically. fifteen minutes of ischemia caused massive pyramidal cell loss in the subiculum (90.3%) and ca1 (88.4%) sectors of the hippocampus (p<0.0001, vehicle vs sham). compared to the vehicle-treated group, all pharmacological treatments failed to attenuate the ischemia-induced death of both subiculum (lesion: 86.7-93.4%) and ca1 (lesion: 85.5-91.2%) pyramidal cells (p>0.05). both dz alone and dz + mgcl2 reduced rectal temperature significantly (p<0.05). no animal death was observed after drug treatment. these data indicate that exogenous magnesium, when administered systemically post-ischemia even in different multiple dose schedules, alone or with diazepam, is not useful against the histopathological effects of transient global cerebral ischemia in rats.
Magnesium chloride alone or in combination with diazepam fails to prevent hippocampal damage following transient forebrain ischemia
Milani H.,Lepri E.R.,Giordani F.,Favero-Filho L.A.
Brazilian Journal of Medical and Biological Research , 1999,
Abstract: In the central nervous system, magnesium ion (Mg2+) acts as an endogenous modulator of N-methyl-D-aspartate (NMDA)-coupled calcium channels, and may play a major role in the pathomechanisms of ischemic brain damage. In the present study, we investigated the effects of magnesium chloride (MgCl2, 2.5, 5.0 or 7.5 mmol/kg), either alone or in combination with diazepam (DZ), on ischemia-induced hippocampal cell death. Male Wistar rats (250-300 g) were subjected to transient forebrain ischemia for 15 min using the 4-vessel occlusion model. MgCl2 was applied systemically (sc) in single (1x, 2 h post-ischemia) or multiple doses (4x, 1, 2, 24 and 48 h post-ischemia). DZ was always given twice, at 1 and 2 h post-ischemia. Thus, ischemia-subjected rats were assigned to one of the following treatments: vehicle (0.1 ml/kg, N = 34), DZ (10 mg/kg, N = 24), MgCl2 (2.5 mmol/kg, N = 10), MgCl2 (5.0 mmol/kg, N = 17), MgCl2 (7.5 mmol/kg, N = 9) or MgCl2 (5 mmol/kg) + DZ (10 mg/kg, N = 14). Seven days after ischemia the brains were analyzed histologically. Fifteen minutes of ischemia caused massive pyramidal cell loss in the subiculum (90.3%) and CA1 (88.4%) sectors of the hippocampus (P<0.0001, vehicle vs sham). Compared to the vehicle-treated group, all pharmacological treatments failed to attenuate the ischemia-induced death of both subiculum (lesion: 86.7-93.4%) and CA1 (lesion: 85.5-91.2%) pyramidal cells (P>0.05). Both DZ alone and DZ + MgCl2 reduced rectal temperature significantly (P<0.05). No animal death was observed after drug treatment. These data indicate that exogenous magnesium, when administered systemically post-ischemia even in different multiple dose schedules, alone or with diazepam, is not useful against the histopathological effects of transient global cerebral ischemia in rats.
Resistance of CA1 Pyramidal Cells to STZ-Induced Diabetes in Young Rats
Fazeli,Seyyed Amirhossein; Gharravi,Anneh Mohammad; Jahanshahi,Mehrdad; Ghafari,Soraya; Behnampour,Naser; Golalipour,Mohammad Jafar;
International Journal of Morphology , 2009, DOI: 10.4067/S0717-95022009000400006
Abstract: the pyramidal cell density of ca1 hippocampal subfield following stz-induced diabetes in young rats were studied. 12 male albino 6-week wistar rats were allocated equally in groups of normal and diabetic. hyperglycemia induced by streptozotocin (80 mg/kg) in animals of diabetic group. after 5 weeks of study, all the rats were sacrificed and coronal sections were taken from dorsal hippocampal formation of the right cerebral hemispheres and stained with crysel violet. the area densities of the ca1 pyramidal cells were measured and compared among two groups. no significant difference between the densities of two experimental groups was found. the results can arise from the short period of diabetes and also the possible regenerative processes in developing brain of the young diabetic rats which compensated significant diabetes-induced neuronal loss.
GluA2-lacking AMPA receptors in hippocampal CA1 cell synapses: evidence from gene-targeted mice
Andrei Rozov,Peter H. Seeburg
Frontiers in Molecular Neuroscience , 2012, DOI: 10.3389/fnmol.2012.00022
Abstract: The GluA2 subunit in heteromeric alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor channels restricts Ca2+ permeability and block by polyamines, rendering linear the current-voltage relationship of these glutamate-gated cation channels. Although GluA2-lacking synaptic AMPA receptors occur in GABA-ergic inhibitory neurons, hippocampal CA1 pyramidal cell synapses are widely held to feature only GluA2 containing AMPA receptors. A controversy has arisen from reports of GluA2-lacking AMPA receptors at hippocampal CA3-to-CA1 cell synapses and a study contesting these findings. Here we sought independent evidence for the presence of GluA2-lacking AMPA receptors in CA1 pyramidal cell synapses by probing the sensitivity of their gated cation channels in wild-type (WT) mice and gene-targeted mouse mutants to philanthotoxin, a specific blocker of GluA2-lacking AMPA receptors. The mutants either lacked GluA2 for maximal philanthotoxin sensitivity, or, for minimal sensitivity, expressed GluA1 solely in a Q/R site-edited version or not at all. Our comparative electrophysiological analyses provide incontrovertible evidence for the presence in wild-type CA1 pyramidal cell synapses of GluA2-less AMPA receptor channels. This article is part of a Special Issue entitled “Calcium permeable AMPARs in synaptic plasticity and disease.”
Resistance of CA1 Pyramidal Cells to STZ-Induced Diabetes in Young Rats Resistencia de las Células Piramidales CA1 a Diabetes Inducida por STZ en Ratas Jóvenes
Seyyed Amirhossein Fazeli,Anneh Mohammad Gharravi,Mehrdad Jahanshahi,Soraya Ghafari
International Journal of Morphology , 2009,
Abstract: The pyramidal cell density of CA1 hippocampal subfield following STZ-induced diabetes in young rats were studied. 12 male albino 6-week Wistar rats were allocated equally in groups of normal and diabetic. Hyperglycemia induced by Streptozotocin (80 mg/kg) in animals of diabetic group. After 5 weeks of study, all the rats were sacrificed and coronal sections were taken from dorsal hippocampal formation of the right cerebral hemispheres and stained with crysel violet. The area densities of the CA1 pyramidal cells were measured and compared among two groups. No significant difference between the densities of two experimental groups was found. The results can arise from the short period of diabetes and also the possible regenerative processes in developing brain of the young diabetic rats which compensated significant diabetes-induced neuronal loss. La densidad de las células piramidales del subcampo CA1 hipocampal resultantes de diabetes inducida por STZ en ratas jóvenes fue estudiada. 12 ratas albinas Wistar macho, de 6 semanas fueron asignadas equitativamente en grupos normal y diabético. La hiperglicemia fue inducida por Streptozotocin (80 mg/kg) en los animales del grupo de diabéticos. Después de 5 semanas de estudio, todas las ratas se sacrificaron y se tomaron secciones coronales de la formación del hipocampo dorsal de los hemisferios cerebrales derecho y se ti eron con violeta crisol. Las áreas de densidad de las células piramidales CA1 fueron medidas y comparadas entre los dos grupos. No se encontraron diferencias significativas entre las densidades de los dos grupos experimentales. Los resultados pueden explicarse debido al corto periodo de diabetes y también por la posibilidad de procesos regenerativos del cerebro en desarrollo de las ratas jóvenes diabéticas los cuales compensan significativamente la pérdida neuronal en la diabetes inducida.
The Effect of Ethanol on the Neuronal Subserving of Behavior in the Hippocampus  [PDF]
Yuri I. Alexandrov, Yuri V. Grinchenko, Diana G. Shevchenko, Robert G. Averkin, Valentina N. Matz, Seppo Laukka, Mikko Sams
Journal of Behavioral and Brain Science (JBBS) , 2013, DOI: 10.4236/jbbs.2013.31011
Abstract:
We have previously shown that both acute and chronic ethanol treatment depresses neural activity, specifically in the cingulate cortex. Minor influences were found in the motor cortex. The acute effect of ethanol in the hippocampus was intermediate to those in the cingulate and motor cortices. In the present study, we concentrate on the chronic effects of ethanol on the hippocampus. We demonstrate how the neuronal activity underlying food-acquisition behavior is modified after chronic ethanol treatment, and how the hippocampus subserves formation of newly-formed alcohol-acquisition behavior. Neuronal activity in CA1 was more sensitive to chronic ethanol than the Dg area. Acute administration of ethanol had a normalizing effect on the chronically-treated animals: their performance and the hippocampal neural activity approached a normal range. The sets of neurons involved in food-acquisition behavior formed before chronic ethanol treatment, and those involved in alcohol-acquisition behavior formed after treatment significantly overlapped supporting the view that the neuronal mechanisms of pre-existing behavior provide the basis for the formation of new behavior. Additionally, we also discovered alcohol-acquisition selective neurons. Assuming that the formation of new neuronal specializations underlies learning, we believe that alcohol-selective neurons are specialized during the formation of alcohol-acquisition behavior. Our data demonstrate several new findings on the effect of acute and chronic ethanol on hippocampus activity, and how the neuronal activity relates to behavior before and after ethanol treatment.
8-精加压素(AVP)对海马CA1区长时程增强(LTP)诱导的影响
刘春龙
科学通报 , 1994,
Abstract: 早在60年代De Wied就报道了加压素对记忆巩固的易化作用,近年来我们又报道了加压素对学习过程的增强作用,但它的作用机制至今尚未阐明.我们实验室的工作表明,AVP对学习过程的增强作用主要是通过它对海马、隔核和杏仁等边缘系统核团功能的调节来实现的.我们还报道了AVP对海马脑电节律和单位放电的影响.另有工作报道,AVP可直接兴奋隔核的神经元,对隔区脑片的LTP的维持起着重要的作用,在海马内可能起着递质的作用.为了探讨AVP增强学习记忆的作用机制,本工作在大鼠海马脑片CA1区研究了AVP对LTP的作用.
Effects of opiate receptor agonists and antagonists on spontaneuse seizure activity in hipocampal slices
M. H. Esmaeili,H. Haghdost,N. Gheybea
Koomesh , 2007,
Abstract: Introduction: Opiates have complex effects on seizure activity. They have both anti-andproconvulsive effects depend on their concentration. Low doses of morphine have anticonvulsanteffects, while high doses have proconvulsant effects. Sudden morphine withdrawal results in shorttermproconvulsant effects. In the present, the effects of opioid receptors agonists and antagonists onspontaneous seizure activity in epileptogenic hippocampal slices were evaluated.Materials and Methods: Hippocampal slices (400 μm) were prepared from young Wistar rats(P15-25). Seizure activity was induced by continuous perfusion of the slices with low-Mg2+ ACSF.Extra cellular recordings were performed in the hippocampal CA1 pyramidal cell layer. Seizureactivity was quantified by measuring the amplitude and duration of the ictal events as well as theirnumber after and prior to the application of the agonists and antagonists of the opioid receptors. Inaddition, the numbers of interictal spikes were determined to complement the analysis of seizuredischarges before and after drug application.Result: Our results show that DAMGO and Dyn-A (10 μM), as μ and κ-opioid receptor agonistrespectively, cause a significant increase in the incidence and amplitude & duration of ictal activityand these effects were completely reversed following the appilcation of B-FNA and nor-BNI (10 μM) as μ and κ opioid receptor antagonist respectively. DPDPE (10μM), a selective δ-opioid receptoragonist, caused a significant decrease in the incidence and duration of ictal activity and these effectswere completely reversed by the addition of NTI (10μM), a selective δ opioid receptor antagonist.Conclusion: Our finding showed that epileptic effects of morphine probably are established byactivation of μ and κ opioid receptors and due to the activation of δ opioid receptor, morphineproduces antiepileptic effects.
The effect of low protein diet on thalamic projections of hippocampus in rat
Bayat M,Hasanzadeh GR,Barzroodipour M,Javadi M
Neuroanatomy , 2005,
Abstract: Recent investigations show that protein malnutrition alters the structure and function of some areas of the hippocampal formation. We investigated therefore the effect of protein malnutrition on thalamic projections to the CA1 hippocampal area. In this study, the efferent projections from the thalamus to hippocampus in rat by horseradish peroxidase (HRP) neural tract tracing was investigated in two groups. The control group was fed with regular diet (18% protein) whereas the study group was fed with low protein diet (8% protein). In the control group we found that the whole anterior thalamic nuclei and nucleus reuniens send projections to the CA1 hippocampal region. Among these nuclei, the anteroventral nucleus (AV) had the highest amount of labelled neurons which sent projection to the CA1 hippocampal region. Anterior thalamus projected to both hippocampus. Number of HRP labelled neurons in the contralateral thalamus were less than the ipsilateral thalamus. As a result of the influence of low protein diet, efferent projection from the anterior thalamus and nucleus reuniens to the CA1 region of hippocampus had decreased (p<0.05) in the study group. The reason may be due to reduction of neuronal activity of thalamus and hippocampal formation under the influence of protein restriction or the affected progression of developmental programmes controlling synaptogenesis.
Stress-related factors in the emergence of transient global amnesia with hippocampal lesions
Juliane D?hring,Alexander Schmuck,Thorsten Bartsch
Frontiers in Behavioral Neuroscience , 2014, DOI: 10.3389/fnbeh.2014.00287
Abstract: The transient global amnesia (TGA) is a rare amnesic syndrome that is characterized by an acute onset episode of an anterograde and retrograde amnesia. Its origin is still debated, but there is evidence for psychological factors involved in TGA. In neuroimaging, selective lesions in the CA1 field of the hippocampus can be detected, a region that is particularly involved in the processing of memory, stress and emotion. The aim of this study was to assess the role of psychological stress in TGA by studying the prevalence of stress related precipitating events and individual stress-related personality profiles as well as coping strategies in patients. The hypothesis of a functional differentiation of the hippocampus in mnemonic and stress-related compartments was also evaluated. From all 113 patients, 18% (n = 24) patients experienced emotional and psychological stress episodes directly before the TGA. In a cohort of 21 acute patients, TGA patients tend to cope with stress less efficiently and less constructively than controls. Patients who experienced a stress related precipitant event exhibited a higher level of anxiety in comparison to non-stress patients and controls. However, there was no difference between the general experience of stress and the number of stress inducing life events. The majority of patients (73%) did show typical magnetic resonance imaging (MRI) lesions in the CA1 region of the hippocampal cornu ammonis. There was no clear association between stressful events, distribution of hippocampal CA1 lesions and behavioral patterns during the TGA. Disadvantageous coping strategies and an elevated anxiety level may increase the susceptibility to psychological stress which may facilitate the pathophysiological cascade in TGA. The findings suggest a role of emotional stress factors in the manifestation of TGA in a subgroup of patients. Stress may be one trigger involved in the emergence of transient lesions in the hippocampal CA1 region, which are thought to be the structural and functional correlate of TGA.
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