Agonists and Antagonists of Metabotropic Glutamate Receptors: Anticonvulsants and Antiepileptogenic Agents?

Tang, Feng Ru

doi:10.2174/157015905774322525

Cited by 16 publications

(13 citation statements)

References 73 publications

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“…In the present study, the general down-regulation of CCR7, CCR9 and CCR10 in the hippocampal neurons during status epilepticus from 10 min to 2 h DPISE may weaken the neuroprotective mechanism, increase the presynaptic glutamate release, leading to over-excitation (which was supported by upregulation of c-fos expression in the principal cells) and delayed loss of hippocampal neurons. Down-regulation of CCR7 and CCR8 in some hippocampal interneurons occurred earlier than in principal cells, which may explain why, in this model, delayed loss of interneurons always occurs much earlier than principal cells after status epilepticus as observed in our previous studies (Tang et al 2004a,b;Tang 2005). At 1 week APISE, loss of CA1 pyramidal neurons (including those of CCR7-10 immunopositive) becomes obvious, suggesting that neurodegeneration has already been irreversible in the latent period after status epilepticus.…”

Section: Discussionsupporting

confidence: 62%

“…Down‐regulation of CCR7 and CCR8 in some hippocampal interneurons occurred earlier than in principal cells, which may explain why, in this model, delayed loss of interneurons always occurs much earlier than principal cells after status epilepticus as observed in our previous studies (Tang et al . 2004a,b; Tang 2005). At 1 week APISE, loss of CA1 pyramidal neurons (including those of CCR7–10 immunopositive) becomes obvious, suggesting that neurodegeneration has already been irreversible in the latent period after status epilepticus.…”

Section: Discussionmentioning

confidence: 99%

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CCR7, CCR8, CCR9 and CCR10 in the mouse hippocampal CA1 area and the dentate gyrus during and after pilocarpine‐induced status epilepticus

Liu

Cao

Tang

et al. 2006

Journal of Neurochemistry

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The present study showed CCR7, CCR8, CCR9 and CCR10 in the normal Swiss mouse hippocampus at both protein and mRNA levels. CCR7, CCR9 and CCR10 were mainly localized in hippocampal principal cells and some interneurons. CCR9 was also found in the mossy fibres and/or terminals, suggesting an axonal or presynaptic localization, and CCR10 in apical dendrites of pyramidal neurons in the CA1 area. CCR8 was observed in interneurons. Double-labelling immunocytochemistry revealed that most of calbindin (CB)-, calretinin (CR)-and parvalbumin (PV)-immunopositive neurons expressed CCR7-10, except CR-immunopositive cells in which only 10 to 12% expressed CCR8. During and after pilocarpineinduced status epilepticus, progressive changes of each of CCR7, CCR8, CCR9 and CCR10 proteins occurred in different patterns at various time points. Sensitive real-time PCR showed similar change patterns at mRNA level. At the chronic stage, i.e. at 2 months after pilocarpine-induced status epilepticus, significant reduction of CCR7-10 expression in CB-, CR-and PV-immunpositive interneurons may suggest the phenotype change of surviving interneurons. Double labelling of CCR7, CCR8 and CCR9 with glial fibrillary acidic protein (GFAP) at the chronic stage may suggest an induced expression in reactive astrocytes. The present study may, therefore, for the first time, provide evidence that CCR7-10 may be involved in normal hippocampal activity. The demonstration of the progressive changes of CCR7-10 during and after status epilepticus may open a new area to reveal the mechanism of neuronal loss after status epilepticus and of epileptogenesis. Keywords: CCR7-10, epilepsy, hippocampus, status epilepticus. J. Neurochem. (2007) 100, 1072-1088.The chemokine receptor ligand family has been not only well known to be inductively expressed in different cell types in the CNS in animal models of neurological disorders such as autoimmune encephalomyelitis (Ransohoff et al. 1993;Berman et al. 1996), HTLV-I-associated myelopathy (Umehara et al. 1996), trauma (Berman et al. 1996), acquired immunodeficiency syndrome (AIDS) dementia (Nuovo and Alfieri 1996), stroke or ischaemia (Gourmala et al. 1997;Spleiss et al. 1998), demyelinating multiple sclerosis (Sorensen et al. 1999;Van Der Voorn et al. 1999), tumour (Arenberg et al. 1996, and in patients with Alzheimer's disease (Xia et al. 1998(Xia et al. , 2000, but also shown in neurons in physiological brain (Bajetto et al. 2001;Cartier et al. 2005). The latter favours the view that the chemokine receptor ligand family may have an important role in physiological cellular communication within the adult mammalian CNS. However, previous studies have provided far less information for understanding the physiological role of the chemokine Received April 5, 2006; revised manuscript received July 7, 2006; accepted October 3, 2006. Address correspondence and reprint requests to Dr Feng-Ru Tang, Epilepsy Research Laboratory, National Neuroscience Institute, 11 Jalan Tan Tock Seng, Singapore 308433. E-mail: Feng_Ru...

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

CCR7, CCR8, CCR9 and CCR10 in the mouse hippocampal CA1 area and the dentate gyrus during and after pilocarpine‐induced status epilepticus

Liu

Cao

Tang

et al. 2006

Journal of Neurochemistry

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“…After all, extrasynaptic glutamate cannot only modulate synaptic transmission via activation of pre‐ and postsynaptic mGluRs, but it can also act on extrasynaptic NMDA receptors and as such increase neuronal excitability. In addition, several agonists and antagonists of respectively group II and group I mGluRs as well as antagonists of ionotropic glutamate receptors have been shown to exert anticonvulsive properties (for review, Tang ; Casillas‐Espinosa et al . ).…”

Section: Contribution Of System Xc− To Neurological Diseasementioning

confidence: 99%

Main path and byways: non‐vesicular glutamate release by system x_c⁻ as an important modifier of glutamatergic neurotransmission

Massie

Boillée

Hewett

et al. 2015

Journal of Neurochemistry

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System xc− is a cystine/glutamate antiporter that exchanges extracellular cystine for intracellular glutamate. Cystine is intracellularly reduced to cysteine, a building block of GSH. As such, system xc− can regulate the antioxidant capacity of cells. Moreover, in several brain regions, system xc− is the major source of extracellular glutamate. As such this antiporter is able to fulfill key physiological functions in the CNS, while evidence indicates it also plays a role in certain brain pathologies. Since the transcription of xCT, the specific subunit of system xc−, is enhanced by the presence of reactive oxygen species and inflammatory cytokines, system xc− could be involved in toxic extracellular glutamate release in neurological disorders that are associated with increased oxidative stress and neuroinflammation. System xc− has also been reported to contribute to the invasiveness of brain tumors and, as a source of extracellular glutamate, could participate in the induction of peritumoral seizures. Two independent reviews (Lewerenz et al. 2013, Bridges et al. 2012), approached from a different perspective, have recently been published on the functions of system xc− in the central nervous system. In this review, we highlight novel achievements and insights covering the regulation of system xc− as well as its involvement in emotional behavior, cognition, addiction, neurological disorders and glioblastomas, acquired in the past few years.

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“…Thus, in addition to the presence of postsynaptic ionotropic glutamate receptors, pre-and postsynaptic metabotropic receptors are frequently present to fine-tune the synaptic communication between neurons. The importance of metabotropic glutamate receptors (mGluRs) is highlighted by their linkage to numerous disorders including epilepsy and schizophrenia [1][2][3]. The mechanisms by which these receptors modulate synaptic communication have been the subject of ongoing study for decades, yet we are just beginning to understand how frequently the regulation of synaptic transmission by mGluRs dictates the output of a circuit.…”

Section: Introductionmentioning

confidence: 99%

mGluRs Modulate Strength and Timing of Excitatory Transmission in Hippocampal Area CA3

et al. 2011

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Excitatory transmission within hippocampal area CA3 stems from three major glutamatergic pathways: the perforant path formed by axons of layer II stellate cells in the entorhinal cortex, the mossy fiber axons originating from the dentate gyrus granule cells, and the recurrent axon collaterals of CA3 pyramidal cells. The synaptic communication of each of these pathways is modulated by metabotropic glutamate receptors that fine-tune the signal by affecting both the timing and strength of the connection. Within area CA3 of the hippocampus, group I mGluRs (mGluR1 and mGluR5) are expressed postsynaptically, whereas group II (mGluR2 and mGluR3) and III mGluRs (mGluR4, mGluR7, and mGluR8) are expressed presynaptically. Receptors from each group have been demonstrated to be required for different forms of pre- and postsynaptic long-term plasticity and also have been implicated in regulating short-term plasticity. A recent observation has demonstrated that a presynaptically expressed mGluR can affect the timing of action potentials elicited in the postsynaptic target. Interestingly, mGluRs can be distributed in a target-specific manner, such that synaptic input from one presynaptic neuron can be modulated by different receptors at each of its postsynaptic targets. Consequently, mGluRs provide a mechanism for synaptic specialization of glutamatergic transmission in the hippocampus. This review will highlight the variability in mGluR modulation of excitatory transmission within area CA3 with an emphasis on how these receptors contribute to the strength and timing of network activity within pyramidal cells and interneurons.

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Agonists and Antagonists of Metabotropic Glutamate Receptors: Anticonvulsants and Antiepileptogenic Agents?

Cited by 16 publications

References 73 publications

CCR7, CCR8, CCR9 and CCR10 in the mouse hippocampal CA1 area and the dentate gyrus during and after pilocarpine‐induced status epilepticus

CCR7, CCR8, CCR9 and CCR10 in the mouse hippocampal CA1 area and the dentate gyrus during and after pilocarpine‐induced status epilepticus

Main path and byways: non‐vesicular glutamate release by system x_c⁻ as an important modifier of glutamatergic neurotransmission

mGluRs Modulate Strength and Timing of Excitatory Transmission in Hippocampal Area CA3

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Agonists and Antagonists of Metabotropic Glutamate Receptors: Anticonvulsants and Antiepileptogenic Agents?

Cited by 16 publications

References 73 publications

CCR7, CCR8, CCR9 and CCR10 in the mouse hippocampal CA1 area and the dentate gyrus during and after pilocarpine‐induced status epilepticus

CCR7, CCR8, CCR9 and CCR10 in the mouse hippocampal CA1 area and the dentate gyrus during and after pilocarpine‐induced status epilepticus

Main path and byways: non‐vesicular glutamate release by system xc− as an important modifier of glutamatergic neurotransmission

mGluRs Modulate Strength and Timing of Excitatory Transmission in Hippocampal Area CA3

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Product

Resources

About

Main path and byways: non‐vesicular glutamate release by system x_c⁻ as an important modifier of glutamatergic neurotransmission