Differential effects of NMDA and AMPA glutamate receptors on functional magnetic resonance imaging signals and evoked neuronal activity during forepaw stimulation of the rat
In: Journal of Neuroscience Journal of Neuroscience, Society for Neuroscience, 2006, 26 (33), pp.8409-16. ⟨10.1523/JNEUROSCI.4615-05.2006⟩ Journal of Neuroscience, 2006, 26 (33), pp.8409-16. ⟨10.1523/JNEUROSCI.4615-05.2006⟩; (2006-08-16)
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Zugriff:
Most of the currently used methods for functional brain imaging do not visualize neuronal activity directly but rather rely on the elicited hemodynamic and/or metabolic responses. Glutamate, the major excitatory neurotransmitter, plays an important role in the neurovascular/neurometabolic coupling, but the specific mechanisms are still poorly understood. To investigate the role of the two major ionotropic glutamate receptors [NMDA receptors (NMDA-Rs) and AMPA receptors (AMPA-Rs)] for the generation of functional magnetic resonance imaging (fMRI) signals, we used fMRI [measurements of blood oxygenation level-dependent (BOLD), perfusion-weighted imaging (PWI), and cerebral blood volume (CBV)] together with recordings of somatosensory evoked potentials (SEPs) during electrical forepaw stimulation in the α-chloralose anesthetized rat. Intravenous injection of the NMDA-R antagonist MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate] (0.06 mg/kg plus 3.6 μg · kg−1· h−1) significantly decreased BOLD (−51 ± 19%;n= 5) and PWI (−57 ± 26%;n= 5) responses but reduced the SEPs only mildly (approximately −10%). Systemic application of the AMPA-R antagonist GYKI-53655 [1-(4-aminophenyl)-3-methylcarbamyl-4-methyl7,8-methylenedioxy-3,4-dihydro-5H-2,3-benzodiazepine] significantly decreased both the hemodynamic response (BOLD, −49 ± 13 and −65 ± 15%; PWI, −22 ± 48 and −68 ± 4% for 5 and 7 mg/kg, i.v., respectively; CBV, −80 ± 7% for 7 mg/kg;n= 4) and the SEPs (up to −60%). These data indicate that the interaction of glutamate with its postsynaptic and/or glial receptors is necessary for the generation of blood flow and BOLD responses and illustrate the differential role of NMDA-Rs and AMPA-Rs in the signaling chain leading from increased neuronal activity to the hemodynamic response in the somatosensory cortex.
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Differential effects of NMDA and AMPA glutamate receptors on functional magnetic resonance imaging signals and evoked neuronal activity during forepaw stimulation of the rat
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Autor/in / Beteiligte Person: | Gsell, Willy ; Schwindt, Wolfram ; Burke, Michael ; Bonvento, Gilles ; Bührle, Christian ; Hoehn, Mathias ; Dauphin, François ; Wiedermann, Dirk ; Silva, Alfonso C. ; Laboratoire des Maladies Neurodégénératives - UMR 9199 (LMN) ; Service MIRCEN (MIRCEN) ; Université Paris-Saclay-Institut de Biologie François JACOB (JACOB) ; Direction de Recherche Fondamentale (CEA) (DRF (CEA)) ; Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)) ; Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Institut de Biologie François JACOB (JACOB) ; Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS) ; Groupe Mémoire et Plasticité comportementale (GMPc) ; Université de Caen Normandie (UNICAEN) ; Normandie Université (NU)-Normandie Université (NU) ; Radiology, Clinical ; Muenster University Hospital ; Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie François JACOB (JACOB) ; Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie François JACOB (JACOB) |
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Quelle: | Journal of Neuroscience Journal of Neuroscience, Society for Neuroscience, 2006, 26 (33), pp.8409-16. ⟨10.1523/JNEUROSCI.4615-05.2006⟩ Journal of Neuroscience, 2006, 26 (33), pp.8409-16. ⟨10.1523/JNEUROSCI.4615-05.2006⟩; (2006-08-16) |
Veröffentlichung: | HAL CCSD, 2006 |
Medientyp: | unknown |
ISSN: | 0270-6474 (print) ; 1529-2401 (print) |
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