6533b855fe1ef96bd12b1333
RESEARCH PRODUCT
Chelation of synaptic zinc induces overexcitation in the hilar mossy cells of the rat hippocampus.
Julio Poza-aznarF.j. Martínez-guijarroCarlos CrespoAna-isabel Marqués-maríJ.m. Blasco-ibáñezFrancisco-javier Gracia-llanessubject
medicine.medical_specialtyCentral nervous systemPresynaptic TerminalsWheat Germ Agglutinin-Horseradish Peroxidase ConjugateHippocampusAction PotentialsHSP72 Heat-Shock Proteinsc-FosHippocampusSynaptic TransmissionSeizuresInternal medicineNeural PathwaysmedicineAnimalsReceptors AMPAHeat-Shock ProteinsChelating AgentsbiologyGeneral NeuroscienceDentate gyrusGlutamate receptorColocalizationImmunohistochemistryRatsZincEndocrinologymedicine.anatomical_structurenervous systemDentate GyrusMossy Fibers Hippocampalbiology.proteinExcitatory postsynaptic potentialDitiocarbImmediate early geneProto-Oncogene Proteins c-fosdescription
Complete removal of synaptic zinc by the chelator dietyldithiocarbamate (DEDTC; 500 mg/kg i.p.) in rat was followed by convulsive behaviour including wet dog shakes alternating immobility. Histological analysis 1 day after DEDTC administration detected expression of heat shock protein in the hippocampus restricted to hilar cells. These cells colocalize the marker for neurons and the glutamate receptor GluR2/3 showing that they are excitatory neurons. Additionally, they projected to the contralateral dentate gyrus. Therefore, they correspond to hilar mossy cells. These data show that the synaptic zinc has a role in normal hippocampus avoiding overexcitation, that would impair functionality even in absence of pathological or exoexcitotoxic phenomena.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2004-01-20 | Neuroscience letters |