The Experts below are selected from a list of 11247 Experts worldwide ranked by ideXlab platform
Shigenori Watanabe - One of the best experts on this subject based on the ideXlab platform.
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A role of sigma receptors on hypoxia/hypoglycemia-induced decrease in CA1 Presynaptic fiber spikes in rat hippocampal slices
Brain research, 1995Co-Authors: Shigenobu Shibata, Yasuharu Yamamoto, Shigenori WatanabeAbstract:Abstract Effects of sigma receptor agonists or antagonists on hypoxia/hypoglycemia-induced decrease in CA1 Presynaptic fiber spikes elicited by the stimulation of Schaffer collaterals were investigated using rat hippocampal slices. Treatment with sigma receptor antagonists such as haloperidol. NE-100 and rimcazole produced a concentration-dependent attenuation of the hypoxia/hypoglycemia-induced decrease in CA1 Presynaptic fiber spikes. The order of potency of protection against hypoxia/hypoglycemia-induced reduction in CA1 Presynaptic Potential was: NE-100 = haloperidol > rimcazole. Treatment with sigma receptor agonist DTG potentiated the hypoxia/hypoglycemia-induced decrease in the CA1 Presynaptic Potential, whereas SKF10047 which possesses an affinity for phenycyclidine site attenuated the decrease of Potential. NE-100 antagonized a functional deficit induced by DTG, but unaffected the improving effect induced by SKF10047. The present results suggest a facilitatory role of sigma receptor stimulation in hypoxia/hypoglycemia-induced an impairment of neurophysiological functions in CA1 Presynaptic regions of hippocampal slices.
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involvement of d1 dopamine receptor mechanism in ischemia induced impairment of ca1 Presynaptic fiber spikes in rat hippocampal slices
Brain Research, 1994Co-Authors: Yasaharu Yamamoto, Shigenobu Shibata, Takeshi Tanaka, Shigenori WatanabeAbstract:The effect of dopamine (DA) receptor agonists and antagonists on hypoxia/hypoglycemia (ischemia)-induced decrease in CA1 Presynaptic fiber spikes elicited by the stimulation of Schaffer collateral were investigated using hippocampal slices. Treatment with D1 dopamine receptor antagonist, SCH23390 produced a concentration-dependent attenuation of the ischemia-induced decrease of Presynaptic Potentials. The magnitude of recovery of the CA1 Presynaptic Potential in SCH233390-treated slices at 10 and 100 microM was 28 and 54%, respectively. Whereas, treatment with D1 dopamine receptor agonist, SKF38393 exacerbated the ischemia-induced decrease in the CA1 Presynaptic Potential. The decrease of CA1 Presynaptic Potential by ischemia was affected by neither D2 dopamine receptor agonist, bromocriptin and quinpirole nor D2 dopamine receptor antagonist, sulpiride. The neuroprotective effect of SCH23390 was completely blocked by cotreatment with SKF38393. The present results demonstrated that the blockade of D1 dopamine receptor function played a neuroprotective role in ischemic damage, suggesting a facilitatory role of D1 dopamine receptor-operated function in ischemia-induced neuronal deficits.
Shigenobu Shibata - One of the best experts on this subject based on the ideXlab platform.
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A role of sigma receptors on hypoxia/hypoglycemia-induced decrease in CA1 Presynaptic fiber spikes in rat hippocampal slices
Brain research, 1995Co-Authors: Shigenobu Shibata, Yasuharu Yamamoto, Shigenori WatanabeAbstract:Abstract Effects of sigma receptor agonists or antagonists on hypoxia/hypoglycemia-induced decrease in CA1 Presynaptic fiber spikes elicited by the stimulation of Schaffer collaterals were investigated using rat hippocampal slices. Treatment with sigma receptor antagonists such as haloperidol. NE-100 and rimcazole produced a concentration-dependent attenuation of the hypoxia/hypoglycemia-induced decrease in CA1 Presynaptic fiber spikes. The order of potency of protection against hypoxia/hypoglycemia-induced reduction in CA1 Presynaptic Potential was: NE-100 = haloperidol > rimcazole. Treatment with sigma receptor agonist DTG potentiated the hypoxia/hypoglycemia-induced decrease in the CA1 Presynaptic Potential, whereas SKF10047 which possesses an affinity for phenycyclidine site attenuated the decrease of Potential. NE-100 antagonized a functional deficit induced by DTG, but unaffected the improving effect induced by SKF10047. The present results suggest a facilitatory role of sigma receptor stimulation in hypoxia/hypoglycemia-induced an impairment of neurophysiological functions in CA1 Presynaptic regions of hippocampal slices.
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involvement of d1 dopamine receptor mechanism in ischemia induced impairment of ca1 Presynaptic fiber spikes in rat hippocampal slices
Brain Research, 1994Co-Authors: Yasaharu Yamamoto, Shigenobu Shibata, Takeshi Tanaka, Shigenori WatanabeAbstract:The effect of dopamine (DA) receptor agonists and antagonists on hypoxia/hypoglycemia (ischemia)-induced decrease in CA1 Presynaptic fiber spikes elicited by the stimulation of Schaffer collateral were investigated using hippocampal slices. Treatment with D1 dopamine receptor antagonist, SCH23390 produced a concentration-dependent attenuation of the ischemia-induced decrease of Presynaptic Potentials. The magnitude of recovery of the CA1 Presynaptic Potential in SCH233390-treated slices at 10 and 100 microM was 28 and 54%, respectively. Whereas, treatment with D1 dopamine receptor agonist, SKF38393 exacerbated the ischemia-induced decrease in the CA1 Presynaptic Potential. The decrease of CA1 Presynaptic Potential by ischemia was affected by neither D2 dopamine receptor agonist, bromocriptin and quinpirole nor D2 dopamine receptor antagonist, sulpiride. The neuroprotective effect of SCH23390 was completely blocked by cotreatment with SKF38393. The present results demonstrated that the blockade of D1 dopamine receptor function played a neuroprotective role in ischemic damage, suggesting a facilitatory role of D1 dopamine receptor-operated function in ischemia-induced neuronal deficits.
Dominique Debanne - One of the best experts on this subject based on the ideXlab platform.
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Dynamic Control of Neurotransmitter Release by Presynaptic Potential
Frontiers in Cellular Neuroscience, 2016Co-Authors: Mickael Zbili, Sylvain Rama, Dominique DebanneAbstract:Action Potentials (APs) in the mammalian brain are thought to represent the smallest unit of information transmitted by neurons to their postsynaptic targets. According to this view, neuronal signaling is all-or-none or digital. Increasing evidence suggests, however, that subthreshold changes in Presynaptic membrane Potential before triggering the spike also determines spike-evoked release of neurotransmitter. We discuss here how analog changes in Presynaptic voltage may regulate spike-evoked release of neurotransmitter through the modulation of biophysical state of voltage-gated potassium, calcium and sodium channels in the Presynaptic compartment. The contribution of this regulation has been greatly underestimated and we discuss the impact for information processing in neuronal circuits.
Mickael Zbili - One of the best experts on this subject based on the ideXlab platform.
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Dynamic Control of Neurotransmitter Release by Presynaptic Potential
Frontiers in Cellular Neuroscience, 2016Co-Authors: Mickael Zbili, Sylvain Rama, Dominique DebanneAbstract:Action Potentials (APs) in the mammalian brain are thought to represent the smallest unit of information transmitted by neurons to their postsynaptic targets. According to this view, neuronal signaling is all-or-none or digital. Increasing evidence suggests, however, that subthreshold changes in Presynaptic membrane Potential before triggering the spike also determines spike-evoked release of neurotransmitter. We discuss here how analog changes in Presynaptic voltage may regulate spike-evoked release of neurotransmitter through the modulation of biophysical state of voltage-gated potassium, calcium and sodium channels in the Presynaptic compartment. The contribution of this regulation has been greatly underestimated and we discuss the impact for information processing in neuronal circuits.
Sylvain Rama - One of the best experts on this subject based on the ideXlab platform.
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Dynamic Control of Neurotransmitter Release by Presynaptic Potential
Frontiers in Cellular Neuroscience, 2016Co-Authors: Mickael Zbili, Sylvain Rama, Dominique DebanneAbstract:Action Potentials (APs) in the mammalian brain are thought to represent the smallest unit of information transmitted by neurons to their postsynaptic targets. According to this view, neuronal signaling is all-or-none or digital. Increasing evidence suggests, however, that subthreshold changes in Presynaptic membrane Potential before triggering the spike also determines spike-evoked release of neurotransmitter. We discuss here how analog changes in Presynaptic voltage may regulate spike-evoked release of neurotransmitter through the modulation of biophysical state of voltage-gated potassium, calcium and sodium channels in the Presynaptic compartment. The contribution of this regulation has been greatly underestimated and we discuss the impact for information processing in neuronal circuits.