Modulation of the glutamatergic receptors (AMPA and NMDA) and of glutamate vesicular transporter 2 in the rat facial nucleus after axotomy

Eleore, Lyndell; Vassias, Isabelle; Vidal, Pierre‐Paul; Waele, Catherine de

doi:10.1016/j.neuroscience.2005.06.026

Cited by 23 publications

(32 citation statements)

References 58 publications

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“…Ionotropic NMDA receptor, as heteromeric proteins, consists of two distinct classes of subunits. The NR1 is the ligand binding subunit and seems to be constitutive, and four NR2 subunits (NR2A-2D) and/or NR3 can potentiate and differentiate NMDA receptor responses by heteromeric assemblies with NR1 [3] . Another ionotropic receptors AMPA, comprised of subunits GluR1-4, in which GluR2 mRNA expresses mainly (63.9+/-4.8%), and are mostly in edited form [3,12] .…”

Section: Discussionmentioning

confidence: 99%

“…The NR1 is the ligand binding subunit and seems to be constitutive, and four NR2 subunits (NR2A-2D) and/or NR3 can potentiate and differentiate NMDA receptor responses by heteromeric assemblies with NR1 [3] . Another ionotropic receptors AMPA, comprised of subunits GluR1-4, in which GluR2 mRNA expresses mainly (63.9+/-4.8%), and are mostly in edited form [3,12] . In our study, total RNA was extracted from brain tissue containing facial nucleus, and the expression of NMDAR2A and GluR2 mRNA were confirmed after amplification, which was in agreement with previously reported results [3] .…”

Section: Discussionmentioning

confidence: 99%

“…NR2A is responsible for Ca 2+ -sensitivity and NMDAR blockage by extracellular Mg 2+ [3,11,17] . Predominant expression of NMDAR2A and 2B subunits in motoneurons activates fast excitatory post-synaptic currents (EPSC), and reduces the potential impact of NMDA-mediated Ca 2+ -influx on repetitive firing (through activation of I K-Ca ) [11,17] .…”

Section: Discussionmentioning

confidence: 99%

“…Its functional status can affect the facial nerve regeneration and recovery. Previous studies reported a series of changes in morphology, biochemistry, metabolism and gene expression in facial motor neurons after axotomy, but little was known about changes in faical anastomosis models [1][2][3][4][5][6] . Using the immunohistochemistry and transmission electronic microscopy (TEM), synaptic remodelling of facial motorneurons was observed, and expression of neurotransmitter receptor subunits were examined by RT-PCR, with an attempt to identify the possible relations between excitatory synaptic remodeling and recovery of motor function.…”

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confidence: 99%

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Plastic changes of synapses and excitatory neurotransmitter receptors in facial nucleus following facial-facial anastomosis

Chen

Song

Luo

et al. 2008

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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The remodeling process of synapses and neurotransmitter receptors of facial nucleus were observed. Models were set up by facial-facial anastomosis in rat. At post-surgery day (PSD) 0, 7, 21 and 60, synaptophysin (p38), NMDA receptor subunit 2A and AMPA receptor subunit 2 (GluR2) were observed by immunohistochemical method and semi-quantitative RT-PCR, respectively. Meanwhile, the synaptic structure of the facial motorneurons was observed under a transmission electron microscope (TEM). The intensity of p38 immunoreactivity was decreased, reaching the lowest value at PSD day 7, and then increased slightly at PSD 21. Ultrastructurally, the number of synapses in nucleus of the operational side decreased, which was consistent with the change in P38 immunoreactivity. NMDAR2A mRNA was down-regulated significantly in facial nucleus after the operation (P<0.05), whereas AMPAR2 mRNA levels remained unchanged (P>0.05). The synapses innervation and the expression of NMDAR2A and AMPAR2 mRNA in facial nucleus might be modified to suit for the new motor tasks following facial-facial anastomosis, and influenced facial nerve regeneration and recovery.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Plastic changes of synapses and excitatory neurotransmitter receptors in facial nucleus following facial-facial anastomosis

Chen

Song

Luo

et al. 2008

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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“…In all cases, massive activation of microglia (Graeber et al, 1988) and a deafferentation (synaptic loss) of the motoneurons is observed in the brainstem facial nucleus during the first week postaxotomy (Blinzinger and Kreutzberg, 1968). Several weeks after axotomy, neosynaptogenesis is observed on the soma of the remaining motoneurons (Eleore et al, 2005). Again, the precise role of microglia is not known in the reafferentation process, but it should be noted that upon axotomy activated microglia secrete thrombospondin (Chamak et al, 1995;Moller et al, 1996) which is known to be important for synaptogenesis (Christophersen et al, 2005).…”

Section: Functional Crosstalk Between Neurons and Microgliamentioning

confidence: 95%

Microglial control of neuronal death and synaptic properties

Bessis

Béchade

Bernard

et al. 2006

Glia

406

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Microglia have long been characterized by their immune function in the nervous system and are still mainly considered in a beneficial versus detrimental dialectic. However a review of literature enables to shed novel lights on microglial function under physiological conditions. It is now relevant to position these cells as full time partners of neuronal function and more specifically of synaptogenesis and developmental apoptosis. Indeed, microglia can actively control neuronal death. It has actually been shown in retina that microglial nerve growth factor (NGF) is necessary for the developmental apoptosis to occur. Similarly, in cerebellum, microglia induces developmental Purkinje cells death through respiratory burst. Furthermore, in spinal cord, microglial TNFalpha commits motoneurons to a neurotrophic dependent developmental apoptosis. Microglia can also control synaptogenesis. This is suggested by the fact that a mutation in KARAP/DAP12, a key protein of microglial activation impacts synaptic functions in hippocampus, and synapses protein content. In addition it has been now demonstrated that microglial brain-derived neurotrophin factor (BDNF) directly regulates synaptic properties in spinal cord. In conclusion, microglia can control neuronal function under physiological conditions and it is known that neuronal activity reciprocally controls microglial activation. We will discuss the importance of this cross-talk which allows microglia to orchestrate the balance between synaptogenesis and neuronal death occurring during development or injuries.

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SynCAM1 expression correlates with restoration of central synapses on spinal motoneurons after two different models of peripheral nerve injury

Zelano

Berg

Thams

et al. 2009

J of Comparative Neurology

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SynCAM1 and neuroligins (NLGs) are adhesion molecules that govern synapse formation in vitro. In vivo, the molecules are expressed during synaptogenesis, and altered NLG function is linked to synapse dysfunction in autism. Less is known about SynCAM1 and NLGs in adult synapse remodeling. CNS synapse elimination occurs after peripheral nerve injury, which causes a transient decrease in synapse number on spinal motoneurons. Here we have studied the expression of SynCAM1 and NLGs in relation to changes in synaptic covering on spinal motoneurons. We performed sciatic nerve transection (SNT) or crush (SNC), axotomy models that result in poor or good conditions for axon regeneration, respectively. The two lesions resulted in similar synapse elimination and in poor (SNT) and good (SNC) return of synapses after 70 days. Functional recovery was good after SNC but absent after SNT. SynCAM1 mRNA decreased after 14 days in both models and was restored 70 days after SNC, but not after SNT. NLG2 and -3 mRNAs decreased to a smaller degree after SNC than after SNT. Synaptophysin immunoreactivity correlated with SynCAM1 mRNA 70 days after SNT and NLG2 mRNA 70 days after SNC. Surprisingly, an inverse correlation was seen between NLG3 mRNA and Vglut2, a marker for excitatory synapses, 70 days after SNT. We conclude that 1) SynCAM1 mRNA levels seem to reflect the loss and restoration of synapses on motoneurons, 2) down-regulation of NLGs is not a prerequisite for synapse elimination, and 3) expression of SynCAM1 and NLGs is regulated by different mechanisms during regeneration.

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Modulation of the glutamatergic receptors (AMPA and NMDA) and of glutamate vesicular transporter 2 in the rat facial nucleus after axotomy

Cited by 23 publications

References 58 publications

Plastic changes of synapses and excitatory neurotransmitter receptors in facial nucleus following facial-facial anastomosis

Plastic changes of synapses and excitatory neurotransmitter receptors in facial nucleus following facial-facial anastomosis

Microglial control of neuronal death and synaptic properties

SynCAM1 expression correlates with restoration of central synapses on spinal motoneurons after two different models of peripheral nerve injury

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