Activation of Metabotropic Glutamate Receptor Subtype 1/Protein Kinase C/Mitogen-Activated Protein Kinase Pathway Is Required for Postischemic Long-Term Potentiation in the Striatum
Excessive stimulation of glutamate receptors is believed to contribute substantially in determining neuronal vulnerability to ischemia. However, how this pathological event predisposes neurons to excitotoxic insults is still largely unknown. By using electrophysiological recordings from single stria...
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| Veröffentlicht in: | Molecular pharmacology 2001-10, Vol.60 (4), p.808-815 |
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| container_title | Molecular pharmacology |
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| creator | Calabresi, Paolo Saulle, Emilia Marfia, Girolama A. Centonze, Diego Mulloy, Roseann Picconi, Barbara Hipskind, Robert A. Conquet, François Bernardi, Giorgio |
| description | Excessive stimulation of glutamate receptors is believed to contribute substantially in determining neuronal vulnerability to ischemia. However, how this pathological event predisposes neurons to excitotoxic insults is still largely unknown. By using electrophysiological recordings from single striatal neurons, we demonstrate in a corticostriatal brain-slice preparation that in vitro ischemia (glucose and oxygen deprivation) activates a complex chain of intracellular events responsible for a dramatic and irreversible increase in the sensitivity of striatal neurons to synaptically released glutamate. This process follows the stimulation of both N-methyl-d-aspartate and metabotropic glutamate receptors and involves the activation of the mitogen-activated protein kinase ERK via protein kinase C. This pathological form of synaptic plasticity might play a role in the cell type-specific neuronal vulnerability in the striatum, because it is selectively expressed in neuronal subtypes that are highly sensitive to both acute and chronic disorders involving this brain area. |
| doi_str_mv | 10.1016/S0026-895X(24)12309-7 |
| format | Article |
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However, how this pathological event predisposes neurons to excitotoxic insults is still largely unknown. By using electrophysiological recordings from single striatal neurons, we demonstrate in a corticostriatal brain-slice preparation that in vitro ischemia (glucose and oxygen deprivation) activates a complex chain of intracellular events responsible for a dramatic and irreversible increase in the sensitivity of striatal neurons to synaptically released glutamate. This process follows the stimulation of both N-methyl-d-aspartate and metabotropic glutamate receptors and involves the activation of the mitogen-activated protein kinase ERK via protein kinase C. 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| subjects | Animals Calcium - metabolism Corpus Striatum - enzymology Corpus Striatum - metabolism Disease Models, Animal Electrophysiology Enzyme Inhibitors - pharmacology Interneurons - enzymology Interneurons - physiology Ischemia - enzymology Ischemia - metabolism Long-Term Potentiation - drug effects Long-Term Potentiation - physiology Mice Mitogen-Activated Protein Kinases - antagonists & inhibitors Mitogen-Activated Protein Kinases - metabolism Protein Kinase C - metabolism Rats Receptors, Metabotropic Glutamate - metabolism Receptors, Metabotropic Glutamate - physiology Receptors, N-Methyl-D-Aspartate - physiology Spinal Cord - enzymology Spinal Cord - physiology |
| title | Activation of Metabotropic Glutamate Receptor Subtype 1/Protein Kinase C/Mitogen-Activated Protein Kinase Pathway Is Required for Postischemic Long-Term Potentiation in the Striatum |
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