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Mitochondrial superoxide production and MnSOD activity following exposure to an agonist and antagonists of ionotropic receptors in rat brain
Radenovi? Lidija Lj.,Selakovi? Vesna
Archives of Biological Sciences , 2005, DOI: 10.2298/abs0501001r
Abstract: The involvement of NMDA and AMPA/kainate receptors in the induction of superoxide production in the rat brain was examined after intrahippocampal injection of kainate, a non-NMDA receptor agonist; kainate plus CNQX, a selective AMPA/kainate receptor antagonist; or kainate plus APV, a selective NMDA receptor antagonist. The measurements took place at different times in the ipsi- and contralateral hippocampus, forebrain cortex, striatum, and cerebellum homogenates. The used glutamate antagonists both ensured sufficient neuroprotection in the sense of lowering superoxide production and raising MnSOD levels, but in the mechanisms and time dynamics of their effects were different. Our findings suggest that NMDA and AMPA/kainate receptors are differentially involved in superoxide production. UDC 612.815 612.82.
Nitric oxide production in the rat brain after kainate-induced seizure
Radenovi? Lidija Lj.,Jovanovi? Marina D.,Vasiljevi? Ivana D.,Ninkovi? Milica
Acta Veterinaria , 2002, DOI: 10.2298/avb0206319r
Abstract: We investigated the role of nitric oxide (NO) as a new neurotransmitter in the control of excitability and neurotoxicity of the hippocampus, forebrain cortex, striatum and cerebellum of the rat, as well as the possible functional interaction between NO and the glutamate system. Kainic acid is an endogenous excitotoxin acting on glutamate non-N-methyl-D-aspartate (non-NMDA) receptors, that leads to neurotoxic damage resembling the alterations observed in some neurological disorders. Stimulation of glutamate receptors induces neuronal NO release, which in turn modulates glutamate transmission. We also investigated the effects of 7-nitroindazole (7-NI), a selective neuronal nitric oxide synthase inhibitor in vivo, on nitrite concentration after kainic acid injection (0.5 mg/ml, pH 7.2) unilaterally into the CA3 region of the rat hippocampus. The accumulation of nitrite, the stable metabolite of NO, was measured by the Griess reaction at different times (5 min, 15 min, 2 h, 48 hand 7 days) following kainate injection in the ipsi- and contralateral hippocampus, forebrain cortex striatum and cerebellum homogenates. 7-NI (WOmicroM) can effectively inhibit NO synthesis in rat brain after kainate-induced intrahippocampal neurotoxicity, suppressed nitrite accumulation and attenuated neuronal damage induced by NMDA overactivity. All data showed that reduction of nitrite levels in the nervous system causes overactivity resulting from the absence of the NO-mediated modulatory action. The relatively transient nitric oxide synthase inhibitory effect of 7-NI following intracerebral injection should be taken into account when using this drug to evaluate the central effects of NO. The present results implicate neuronal NO generation in the pathogenesis of both direct and secondary excitotoxic neuronal injuries in vivo. As such they suggest that neuronal NO synthase inhibitors may be useful in the treatment of neurological diseases in which excitotoxic mechanisms play a role.
The Effect of Intrahippocampal Injection of Ascorbic Asid on Spatial Learning and Memory in Adult Male Rats
khadije esmaeilpour,mehdi abbasnejad,saeed esmaeili mahani,yaser masomi ardakani
Physiology and Pharmacology , 2010,
Abstract: Introduction: Ascorbic acid (AA) is present in high concentrations with heterogeneous distribution in the mammalian brain. Previous studies have shown that release of various neurotransmitters such as glutamate, acetylcholine and dopamine might be involved in the central AA release. On the other hand all of these neurotransmitters and the region CA1 of the hippocampus are involved in learning and memory. The aim of the present study was to evaluate the effects of ascorbic acid injection in the CA1 region on spatial learning and memory in adult male rats. Methods: 42 adult male NMRI rats (250-300 g) divided into 6 groups were used in this study. They included control group that received no injection, sham-operated group that received normal saline injection as vehicle and four groups that received different doses of ascorbic acid (6, 12, 24 and 48 μg/rat). All injections were given in 5 consecutive days and 30 min after each injection, the rats were tested in the Morris Water Maze test to measure learning and memory task. Spatial learning and memory parameters were subjected to analysis of variance (ANOVA). Results: The results indicated that intrahippocampal microinjection of AA (12 and 24 μg/rat) significantly increased some spatial learning and memory parameters such as escape latency and path length to reach the hidden platform. Conclusion: Our findings show that AA injection into the CA1 region has a negative effect on spatial learning and memory.
Efects of intrahippocampal injection of scopolamine on behavior In the elevated plus-maze
Garcia Becerra, Andrea Milena
Suma Psicológica , 2009,
Abstract: In this study we aimed to investigate the effects of intrahippocampal injection of scopolamine (an antagonist of M1 muscarinic receptors with amnesic effects) on the behavior of rats evaluated on elevated plus-maze. The animals were tested in the plus-maze immediately after the drug injection and re-tested after 24 h without the drug effect. We analyzed the open and closed arms exploration in each session, and also the behavioral profile in each session using the minute by minute analyses. The results showed increases in the open arms exploration to the scopolamine animals in the first session. The minute by minute analyses in this session showed a maintenance of the exploration during the session, conversely to the observed in the saline animals when in the third minute is showed a significant reduction in comparison to the first minute. These results show that the scopolamine leads to impair the mechanism of acquisition and consolidation of the information during the session, without altering the long term memory processes.
Effect of Intrahippocampal Injection of Aluminum on Active Avoidance Learning in Adult Male Rats
A. Sarkaki,S. Zahedi Asl,R. Assaei
Pakistan Journal of Biological Sciences , 2009,
Abstract: Aim of this research was to study the effect of intrahippocampal injection of different doses of AlCl3 in adult male rats on active avoidance learning. Thirty five adult male Wistar rats (250-300 g) were used into five groups: (1) Control, (2) Test-I received daily 1 μL AlCl3 1%, pH = 7.2, 3); Test-II received daily 1 μL AlCl3 0.5%, pH = 3.4, 4); Sham-I received daily 1 μL aCSF, pH = 7.2, 5); Sham-II received daily 1 μL aCSF, pH = 3.4. All rats in test and sham groups treated 10 min before training. Animals were anaesthetized with ketamine HCl/xylazine (90/10 mg kg-1 b.wt-1, i.p.) and underwent a stereotaxic surgery for implant of two stainless steel guide cannula into the hippocampus bilaterally. Every day 10 min after above treatments all rats were used to assess the spatial learning performing using Y-maze. Criterion Correct Response (CCR) was 90% in last session of training. There were no significant differences between training sessions to receiving CCR in control, Sham-I and Sham-II groups. Cognition in animals received AlCl3 1%, pH = 7.2 was impaired significantly with compare to other groups (*p<0.0001). Present results show that intrahippocampal injection of AlCl3 1%, causes active avoidance learning impairment significantly. The exact mechanism of Al3 effect on brain and cognition is remains unknown.
Exendin-4 Protected against Cognitive Dysfunction in Hyperglycemic Mice Receiving an Intrahippocampal Lipopolysaccharide Injection  [PDF]
Hei-Jen Huang, Yen-Hsu Chen, Keng-Chen Liang, Yu-Syuan Jheng, Jhih-Jhen Jhao, Ming-Tsan Su, Guey-Jen Lee-Chen, Hsiu Mei Hsieh-Li
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0039656
Abstract: Background Chronic hyperglycemia-associated inflammation plays critical roles in disease initiation and the progression of diabetic complications, including Alzheimer’s disease (AD). However, the association of chronic hyperglycemia with acute inflammation of the central nervous system in the progression of AD still needs to be elucidated. In addition, recent evidence suggests that Glucagon-like peptide-1 receptor (GLP-1R) protects against neuronal damage in the brain. Therefore, the neuroprotective effects of the GLP-1R agonist exendin-4 (EX-4) against hyperglycemia/lipopolysaccharides (LPS) damage were also evaluated in this study. Methodology/Principal Findings Ten days after streptozotocin (STZ) or vehicle (sodium citrate) treatment in mice, EX-4 treatment (10 μg/kg/day) was applied to the mice before intrahippocampal CA1 injection of LPS or vehicle (saline) and continued for 28 days. This study examined the molecular alterations in these mice after LPS and EX4 application, respectively. The mouse cognitive function was evaluated during the last 6 days of EX-4 treatment. The results showed that the activation of NF-κB-related inflammatory responses induced cognitive dysfunction in both the hyperglycemic mice and the mice that received acute intrahippocampal LPS injection. Furthermore, acute intrahippocampal LPS injection exacerbated the impairment of spatial learning and memory through a strong decrease in monoaminergic neurons and increases in astrocytes activation and apoptosis in the hyperglycemic mice. However, EX-4 treatment protected against the cognitive dysfunction resulting from hyperglycemia or/and intrahippocampal LPS injection. Conclusions/Significance These findings reveal that both hyperglycemia and intrahippocampal LPS injection induced cognitive dysfunction via activation of NF-κB-related inflammatory responses. However, acute intrahippocampal LPS injection exacerbated the progression of cognitive dysfunction in the hyperglycemic mice via a large increase in astrocytes activation-related responses. Furthermore, EX-4 might be considered as a potential adjuvant entity to protect against neurodegenerative diseases.
Neuroprotection, excitotoxicicity and nmda antagonists
GAGLIARDI, RUBENS JOSé;
Arquivos de Neuro-Psiquiatria , 2000, DOI: 10.1590/S0004-282X2000000300030
Abstract: purpose: to analyze the main aspects of neuroprotection and excitotoxicity. discussion: this is a significant theory on the pathophysiology of cerebral ischemia; it is based on the release of excitatory aminoacid (eaa), mainly glutamate. the sequence starts with a decrease of the blood flow and ends in neuronal death. the main stages of this reaction are herein presented and discussed. an in depth study of the effects of the excessive intracellular calcium is undertaken. neuroprotectors (np) are a group of drugs that reduce the excitotoxicity, opposing the excessive release of eaa and its intracellular effects. neuroprotectors represent a rational approach to stroke treatment and offer a number of potential advantages. they prevent or limit ischemia-induced damage. conclusion: there are many experimental and clinical np trials. a minimum of 800 trials are currently under study worldwide. the most important np subgroups are: n-methyl d-aspartate (nmda) antagonists, gamma-amino butyric acid (gaba) agonists, amino-hydroxy-methyl-isoxalone propionic acid (ampa) antagonists, reducers of intracellular ca++ inhibitors of nitric oxide modulation pathway free radicals scavengers, sodium channel antagonists, glutamate release inhibitor, growth factors, hypothermia and potassium channel activators.
Neuroprotection, excitotoxicicity and nmda antagonists
GAGLIARDI RUBENS JOSé
Arquivos de Neuro-Psiquiatria , 2000,
Abstract: PURPOSE: To analyze the main aspects of neuroprotection and excitotoxicity. DISCUSSION: This is a significant theory on the pathophysiology of cerebral ischemia; it is based on the release of excitatory aminoacid (EAA), mainly glutamate. The sequence starts with a decrease of the blood flow and ends in neuronal death. The main stages of this reaction are herein presented and discussed. An in depth study of the effects of the excessive intracellular calcium is undertaken. Neuroprotectors (NP) are a group of drugs that reduce the excitotoxicity, opposing the excessive release of EAA and its intracellular effects. Neuroprotectors represent a rational approach to stroke treatment and offer a number of potential advantages. They prevent or limit ischemia-induced damage. CONCLUSION: There are many experimental and clinical NP trials. A minimum of 800 trials are currently under study worldwide. The most important NP subgroups are: N-methyl D-aspartate (NMDA) antagonists, gamma-amino butyric acid (GABA) agonists, amino-hydroxy-methyl-isoxalone propionic acid (AMPA) antagonists, reducers of intracellular Ca++ inhibitors of nitric oxide modulation pathway free radicals scavengers, sodium channel antagonists, glutamate release inhibitor, growth factors, hypothermia and potassium channel activators.
7-nitroindazole, a selective neuronal nitric oxide synthase inhibitore in vivo, prevents kainate-induced intrahippocampal neurotoxicity
Radenovi? Lidija Lj.,Selakovi? Vesna,Bo?i? Biljana
Archives of Biological Sciences , 2005, DOI: 10.2298/abs0502075r
Abstract: We investigated the effects of 7-nitroindazole (7-NI), a selective neuronal nitric oxide synthase inhibitor in vivo, on nitrite concentration after kainic acid injection unilaterally into the CA3 region of the rat hippocampus. The accumulation of nitrite, the stable metabolite of NO, was measured by the Griess reaction at different times in hippocampus, forebrain cortex, striatum, and cerebellum homogenates. 7-nitroindazole can effectively inhibit NO synthesis in rat brain after kainate-induced neurotoxicity and suppressed nitrite accumulation. The present results suggest that neuronal NO synthase inhibitors may be useful in the treatment of neurological diseases in which excitotoxic mechanisms play a role.
Behavioral and electroencephalographic analysis of seizures induced by intrahippocampal injection of granulitoxin, a neurotoxic peptide from the sea anemone Bunodosoma granulifera
Santana, A.N.C.;Trindade-Filho, E.M.;Cunha, R.B.;Sousa, M.V.;Cavalheiro, E.A.;Carvalho, K.M.;
Brazilian Journal of Medical and Biological Research , 2001, DOI: 10.1590/S0100-879X2001000600016
Abstract: in this study, the behavioral and electroencephalographic (eeg) analysis of seizures induced by the intrahippocampal injection in rats of granulitoxin, a neurotoxic peptide from the sea anemone bunodosoma granulifera, was determined. the first alterations occurred during microinjection of granulitoxin (8 μg) into the dorsal hippocampus and consisted of seizure activity that began in the hippocampus and spread rapidly to the occipital cortex. this activity lasted 20-30 s, and during this period the rats presented immobility. during the first 40-50 min after its administration, three to four other similar short eeg seizure periods occurred and the rats presented the following behavioral alterations: akinesia, facial automatisms, head tremor, salivation, rearing, jumping, barrel-rolling, wet dog shakes and forelimb clonic movements. within 40-50 min, the status epilepticus was established and lasted 8-12 h. these results are similar to those observed in the acute phase of the pilocarpine model of temporal lobe epilepsy and suggest that granulitoxin may be a useful tool not only to study the sodium channels, but also to develop a new experimental model of status epilepticus.
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