The Experts below are selected from a list of 42 Experts worldwide ranked by ideXlab platform
Antanas Kuras - One of the best experts on this subject based on the ideXlab platform.
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Muscarinic inhibition of recurrent glutamatergic excitation in frog tectum column prevents NMDA receptor activation on Efferent Neuron
Experimental Brain Research, 2011Co-Authors: Armantas Baginskas, Antanas KurasAbstract:It is widely recognized that Neuronal network activity can be modulated via activation of nicotinic and muscarinic acetylcholine receptors located pre- and postsynaptically. It was established in our earlier study that the activation of presynaptic nicotinic receptors greatly facilitates the retinotectal glutamatergic transmission. In the present study, we have determined a transmitter of tectal recurrent excitation and explored the effects of muscarinic acetylcholine receptor activation on the recurrent excitation and the activity of frog tectum column in vivo. Discharge of a single retinal ganglion cell was elicited by a minimal electrical stimulation of the retina. Evoked activity of the tectum column was recorded using the carbon-fiber microelectrode inserted into the tectum layer F. We found the following: 1. The recurrent excitation in the tectum column was not affected by d-tubocurarine (10 μM) and was greatly depressed by the kynurenic acid (500 μM), demonstrating glutamatergic nature of the recurrent excitation. 2. The glutamatergic recurrent excitation was largely reduced by carbamylcholine (100 μM) and oxotremorine-M (10 μM), demonstrating that the activation of muscarinic receptors, located, presumably, on the presynaptic terminals of recurrent pear-shaped Neurons, inhibits the recurrent excitation in the tectum column. 3. The muscarinic inhibition of glutamatergic recurrent transmission had critical influence on the activity of the tectum column, preventing the generation of an output signal through suppression of the NMDA receptor activation and establishing necessary conditions for returning of the network to its resting state.
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L-Type Ca^2+ current in frog tectal recurrent Neurons determines the NMDA receptor activation on Efferent Neuron
Experimental Brain Research, 2008Co-Authors: Armantas Baginskas, Antanas KurasAbstract:The activity patterns of a Neuronal network originate from the intrinsic properties and synaptic interactions of the constituent Neurons. Our recent studies support this view, showing that the discharge of a single frog retina ganglion cell brings an elementary Neuronal network of the tectum (tectum column) to a suprathreshold activity of two distinct levels that are related to the activation of the slow L-type calcium current in dendrites of the recurrent pear-shaped Neurons (lower level) and the NMDA receptors in Neurons (higher level) of the tectum column. We show in the present study that the dendritic slow L-type calcium current is necessary for the NMDA receptor activation in the tectum column. A small decrease of this current prevents the NMDA receptor activation and, hence, the transition of the network to the higher activity level, at which the Efferent Neuron of the network fires. So, the activity of the frog tectum column can be effectively controlled through the intrinsic properties of the recurrent pear-shaped Neurons of the column.
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L-Type Ca2+ current in frog tectal recurrent Neurons determines the NMDA receptor activation on Efferent Neuron
Experimental Brain Research, 2008Co-Authors: Armantas Baginskas, Antanas KurasAbstract:The activity patterns of a Neuronal network originate from the intrinsic properties and synaptic interactions of the constituent Neurons. Our recent studies support this view, showing that the discharge of a single frog retina ganglion cell brings an elementary Neuronal network of the tectum (tectum column) to a suprathreshold activity of two distinct levels that are related to the activation of the slow L-type calcium current in dendrites of the recurrent pear-shaped Neurons (lower level) and the NMDA receptors in Neurons (higher level) of the tectum column. We show in the present study that the dendritic slow L-type calcium current is necessary for the NMDA receptor activation in the tectum column. A small decrease of this current prevents the NMDA receptor activation and, hence, the transition of the network to the higher activity level, at which the Efferent Neuron of the network fires. So, the activity of the frog tectum column can be effectively controlled through the intrinsic properties of the recurrent pear-shaped Neurons of the column.
Armantas Baginskas - One of the best experts on this subject based on the ideXlab platform.
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Muscarinic inhibition of recurrent glutamatergic excitation in frog tectum column prevents NMDA receptor activation on Efferent Neuron
Experimental Brain Research, 2011Co-Authors: Armantas Baginskas, Antanas KurasAbstract:It is widely recognized that Neuronal network activity can be modulated via activation of nicotinic and muscarinic acetylcholine receptors located pre- and postsynaptically. It was established in our earlier study that the activation of presynaptic nicotinic receptors greatly facilitates the retinotectal glutamatergic transmission. In the present study, we have determined a transmitter of tectal recurrent excitation and explored the effects of muscarinic acetylcholine receptor activation on the recurrent excitation and the activity of frog tectum column in vivo. Discharge of a single retinal ganglion cell was elicited by a minimal electrical stimulation of the retina. Evoked activity of the tectum column was recorded using the carbon-fiber microelectrode inserted into the tectum layer F. We found the following: 1. The recurrent excitation in the tectum column was not affected by d-tubocurarine (10 μM) and was greatly depressed by the kynurenic acid (500 μM), demonstrating glutamatergic nature of the recurrent excitation. 2. The glutamatergic recurrent excitation was largely reduced by carbamylcholine (100 μM) and oxotremorine-M (10 μM), demonstrating that the activation of muscarinic receptors, located, presumably, on the presynaptic terminals of recurrent pear-shaped Neurons, inhibits the recurrent excitation in the tectum column. 3. The muscarinic inhibition of glutamatergic recurrent transmission had critical influence on the activity of the tectum column, preventing the generation of an output signal through suppression of the NMDA receptor activation and establishing necessary conditions for returning of the network to its resting state.
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L-Type Ca^2+ current in frog tectal recurrent Neurons determines the NMDA receptor activation on Efferent Neuron
Experimental Brain Research, 2008Co-Authors: Armantas Baginskas, Antanas KurasAbstract:The activity patterns of a Neuronal network originate from the intrinsic properties and synaptic interactions of the constituent Neurons. Our recent studies support this view, showing that the discharge of a single frog retina ganglion cell brings an elementary Neuronal network of the tectum (tectum column) to a suprathreshold activity of two distinct levels that are related to the activation of the slow L-type calcium current in dendrites of the recurrent pear-shaped Neurons (lower level) and the NMDA receptors in Neurons (higher level) of the tectum column. We show in the present study that the dendritic slow L-type calcium current is necessary for the NMDA receptor activation in the tectum column. A small decrease of this current prevents the NMDA receptor activation and, hence, the transition of the network to the higher activity level, at which the Efferent Neuron of the network fires. So, the activity of the frog tectum column can be effectively controlled through the intrinsic properties of the recurrent pear-shaped Neurons of the column.
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L-Type Ca2+ current in frog tectal recurrent Neurons determines the NMDA receptor activation on Efferent Neuron
Experimental Brain Research, 2008Co-Authors: Armantas Baginskas, Antanas KurasAbstract:The activity patterns of a Neuronal network originate from the intrinsic properties and synaptic interactions of the constituent Neurons. Our recent studies support this view, showing that the discharge of a single frog retina ganglion cell brings an elementary Neuronal network of the tectum (tectum column) to a suprathreshold activity of two distinct levels that are related to the activation of the slow L-type calcium current in dendrites of the recurrent pear-shaped Neurons (lower level) and the NMDA receptors in Neurons (higher level) of the tectum column. We show in the present study that the dendritic slow L-type calcium current is necessary for the NMDA receptor activation in the tectum column. A small decrease of this current prevents the NMDA receptor activation and, hence, the transition of the network to the higher activity level, at which the Efferent Neuron of the network fires. So, the activity of the frog tectum column can be effectively controlled through the intrinsic properties of the recurrent pear-shaped Neurons of the column.
Kristen A. Keefe - One of the best experts on this subject based on the ideXlab platform.
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Disruption of subcellular Arc/Arg 3.1 mRNA expression in striatal Efferent Neurons following partial monoamine loss induced by methamphetamine
Journal of neurochemistry, 2012Co-Authors: Melissa Barker-haliski, Katharina Oldenburger, Kristen A. KeefeAbstract:The immediate-early gene Arc (activity-regulated cytoskeleton-associated protein) is provocative in the context of neuroplasticity because of its experience-dependent regulation and mRNA transport to and translation at activated synapses. Normal rats have more preproenkephalin-negative (ppe-neg; presumed striatonigral) Neurons with cytoplasmic Arc mRNA than ppe-positive (ppe-pos; striatopallidal) Neurons, despite equivalent numbers of these Neurons showing novelty-induced transcriptional activation of Arc. Furthermore, rats with partial monoamine loss induced by methamphetamine (METH) show impaired Arc mRNA expression in both ppe-neg and ppe-pos Neurons relative to normal animals following response-reversal learning. In this study, Arc expression induced by exposure to a novel environment was used to assess transcriptional activation and cytoplasmic localization of Arc mRNA in striatal Efferent Neuron subpopulations subsequent to METH-induced neurotoxicity. Partial monoamine depletion significantly altered Arc expression. Specifically, basal Arc expression was elevated, but novelty-induced transcriptional activation was abolished. Without novelty-induced Arc transcription, METH-pre-treated rats also had fewer Neurons with cytoplasmic Arc mRNA expression, with the effect being greater for ppe-neg Neurons. Thus, METH-induced neurotoxicity substantially alters striatal Efferent Neuron function at the level of Arc transcription, suggesting a long-term shift in basal ganglia neuroplasticity processes subsequent to METH-induced neurotoxicity. Such changes potentially underlie striatally based learning deficits associated with METH-induced neurotoxicity.
Melissa Barker-haliski - One of the best experts on this subject based on the ideXlab platform.
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Disruption of subcellular Arc/Arg 3.1 mRNA expression in striatal Efferent Neurons following partial monoamine loss induced by methamphetamine
Journal of neurochemistry, 2012Co-Authors: Melissa Barker-haliski, Katharina Oldenburger, Kristen A. KeefeAbstract:The immediate-early gene Arc (activity-regulated cytoskeleton-associated protein) is provocative in the context of neuroplasticity because of its experience-dependent regulation and mRNA transport to and translation at activated synapses. Normal rats have more preproenkephalin-negative (ppe-neg; presumed striatonigral) Neurons with cytoplasmic Arc mRNA than ppe-positive (ppe-pos; striatopallidal) Neurons, despite equivalent numbers of these Neurons showing novelty-induced transcriptional activation of Arc. Furthermore, rats with partial monoamine loss induced by methamphetamine (METH) show impaired Arc mRNA expression in both ppe-neg and ppe-pos Neurons relative to normal animals following response-reversal learning. In this study, Arc expression induced by exposure to a novel environment was used to assess transcriptional activation and cytoplasmic localization of Arc mRNA in striatal Efferent Neuron subpopulations subsequent to METH-induced neurotoxicity. Partial monoamine depletion significantly altered Arc expression. Specifically, basal Arc expression was elevated, but novelty-induced transcriptional activation was abolished. Without novelty-induced Arc transcription, METH-pre-treated rats also had fewer Neurons with cytoplasmic Arc mRNA expression, with the effect being greater for ppe-neg Neurons. Thus, METH-induced neurotoxicity substantially alters striatal Efferent Neuron function at the level of Arc transcription, suggesting a long-term shift in basal ganglia neuroplasticity processes subsequent to METH-induced neurotoxicity. Such changes potentially underlie striatally based learning deficits associated with METH-induced neurotoxicity.
Jian Hu - One of the best experts on this subject based on the ideXlab platform.
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constraint induced movement therapy promotes contralesional oriented structural and bihemispheric functional neuroplasticity after stroke
Brain Research Bulletin, 2019Co-Authors: Ce Li, Bei Zhang, Zhijian Zhang, Yuyuan Wang, Jian HuAbstract:Abstract The mechanism behind constraint-induced movement therapy (CIMT) in promoting motor recovery after stroke remains unclear. We explored the bilateral structural and functional reorganization of the brain induced by CIMT after left middle cerebral artery occlusion (MCAO) in rats. CIMT started on the 8th day (D8) after MCAO surgery and lasted for 3 weeks. Skilled walking was assessed by Foot-Fault tests. The Efferent Neuron network innervating the paralyzed forelimb was labeled by pseudorabies virus (PRV) to explore Neuron recruitment. Synapsin Ⅰ was used as an indicator of the number of synapses. Additionally, C-fos expression 1 h after walking was detected to explore the activation of the brain. As a result, CIMT significantly improved skilled walking and elicited more Neuron recruitment into the innervating network of a paralyzed forelimb in the contralesional rather than the ipsilesional motor cortex and red nucleus. CIMT also increased the synapse number in the contralesional cortex but there was no corresponding effect in the intact ipsilesional cortex. Furthermore, MCAO decreased ipsilesional motor cortex activation, but CIMT partially compensated for this by increasing the number of activated Neurons (c-fos+) in both the left and right motor cortex. In conclusion, the contralesional motor cortex and red nucleus might play more important roles than corresponding ipsilesional regions in structural reorganization during CIMT-induced motor recovery after stroke. However, CIMT promotes bilateral motor cortex activity without a side preference.
