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 |
Externí odkaz: |