Role of glutamate transporters in corticostriatal synaptic transmission

Autor: Gilles Bonvento, Corinne Beurrier, Paolo Gubellini, L. Kerkerian-Le Goff
Přispěvatelé: Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)
Rok vydání: 2009
Předmět:
Male
Patch-Clamp Techniques
Synaptic cleft
Amino Acid Transport System X-AG
Green Fluorescent Proteins
Biophysics
Glycine
Glutamic Acid
[SDV.BC]Life Sciences [q-bio]/Cellular Biology
In Vitro Techniques
Neurotransmission
Biology
Synaptic Transmission
03 medical and health sciences
Glutamatergic
0302 clinical medicine
Transduction
Genetic
Neural Pathways
Animals
Drug Interactions
ComputingMilieux_MISCELLANEOUS
030304 developmental biology
Cerebral Cortex
Neurons
Aspartic Acid
0303 health sciences
General Neuroscience
Glutamate receptor
Excitatory Postsynaptic Potentials
Corpus Striatum
Electric Stimulation
Rats
nervous system
Rats
Inbred Lew
Metabotropic glutamate receptor
Synapses
Synaptic plasticity
Excitatory postsynaptic potential
NMDA receptor
Excitatory Amino Acid Antagonists
Neuroscience
030217 neurology & neurosurgery
Zdroj: Neuroscience
Neuroscience, 2009, 158, pp.1608-1615
Neuroscience, Elsevier-International Brain Research Organization, 2009, 158, pp.1608-1615
ISSN: 0306-4522
1873-7544
Popis: High-affinity glutamate transporters (GTs) play a major role in controlling the extracellular level of this excitatory neurotransmitter in the CNS. Here we have characterized, by means of in vitro patch-clamp recordings from medium spiny neurons (MSNs), the role of GTs in regulating corticostriatal glutamatergic synaptic transmission in the adult rat. Charge transfer and decay-time, but not amplitude, of excitatory postsynaptic currents (EPSCs) were enhanced by dl -threo-β-benzyloxyaspartate (TBOA), a broad inhibitor of GTs. Moreover, TBOA also potentiated currents induced by high-frequency stimulation (HFS) protocols. Interestingly, the effect of TBOA on EPSCs was lost when MSNs were clamped at +40 mV, a condition in which neuronal GTs, that are voltage-dependent, are blocked. However, in this condition TBOA was still able to enhance HFS-induced currents, suggesting that glial GT's role is to regulate synaptic transmission when glutamate release is massive. These data suggest that neuronal GTs, rather than glial, shape EPSCs' kinetics and modulate glutamate transmission at corticostriatal synapse. Moreover, the control of glutamate concentration in the synaptic cleft by GTs may play a role in a number of degenerative disorders characterized by the hyperactivity of corticostriatal pathway, as well as in synaptic plasticity.
Databáze: OpenAIRE
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