Contributions of mGlu1 and mGlu5 receptors to interactions with N-methyl-d-aspartate receptor-mediated responses and nociceptive sensory responses of rat thalamic neurons

Salt, Thomas E.; Binns, K. E.

doi:10.1016/s0306-4522(00)00265-7

Cited by 78 publications

(58 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Therefore, mGlu1 receptors have a protective function against SWDs and a loss of this protective mechanism might contribute to the epileptic-prone phenotype of WAG/Rij rats while being a consequence of SWDs. Moreover, it has been shown that activation of mGlu5 receptors has an excitatory effect similar to that mediated by mGlu1 receptors and these receptors can participate in sensory responses of thalamic relay cells (Salt and Binns, 2000). Reduced expression and function of mGlu5 receptors in the thalamus has been observed in WAG/Rij rats both at 2 and 8 months of age, while an increased receptor expression in the sensorimotor cortex was described at the same ages Modulation of type-1 mGluRs has been suggested as a potential target for the treatment of absence seizures; this effect could be based on the dysregulation observed in the expression and function of these receptors along the CTC circuit since opposite effects of an orthosteric mGlu5R agonist had anti-absence action in the lethargic mice absence model (Chapman et al, 2000).…”

Section: Mglu Receptorsmentioning

confidence: 99%

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Russo

Citraro

Constanti³

et al. 2016

Neuroscience & Biobehavioral Reviews

128

View full text Add to dashboard Cite

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development.Neuroscience and Biobehavioral Reviews http://dx.doi.org/10. 1016/j.neubiorev.2016.09.017 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractThe WAG/Rij rat model has recently gathered attention as a suitable animal model of absence epileptogenesis. This latter term has a broad definition encompassing any possible cause that determines the development of spontaneous seizures; however, most of, if not all, preclinical knowledge on epileptogenesis is confined to the study of post-brain insult models such as traumatic brain injury or post-status epilepticus models. WAG/Rij rats, but also synapsin 2 knockout, Kv7 current-deficient mice represent the first examples of genetic models where an efficacious antiepileptogenic treatment (ethosuximide) was started before seizure onset. In this review, we have critically reconsidered all articles published regarding WAG/Rij rats, from the perspective that the period before SWD onset is considered as the latent period. In our new theory on seizure development, it is proposed that genes might be considered as the initial "insult" responsible for all plastic changes underpinning the development of spontaneous seizures. According to this idea, in WAG/Rij rats, genetic predisposition would lead to the development of abnormal bilateral cortical epileptic foci, which would then nongenetically stimulate the rest of the brain to rearrange networks in order to phenotypically develop seizures similarly to what happens during electrical kindling.

show abstract

Section: Mglu Receptorsmentioning

confidence: 99%

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Russo

Citraro

Constanti³

et al. 2016

Neuroscience & Biobehavioral Reviews

128

View full text Add to dashboard Cite

show abstract

“…In the ventrobasal complex, stimulation of mGlu1 receptors potentiate both AMPA and NMDA responses (Salt and Binns, 2000); hence, when the activation of mGlu1 receptors in the perisynaptic area of ventrobasal neurons is achieved by sustained activity of corticothalamic inputs, it would be able to exert a profound influence on ionotropic receptor-mediated responses (Salt, 2002). Intrathalamic injection of group I agonists enhances inflammatory pain behavior, whereas mGlu1 antagonists or gene targeting deletion of its primary intracellular effector PLC␤4 attenuates nociceptive behavior in the second phase of inflammatory pain induced by formalin injection (Miyata et al, 2003).…”

Section: Distribution and Role Of Metabotropic Glutamate 1 Receptors mentioning

confidence: 99%

Metabotropic Glutamate 1 Receptor: Current Concepts and Perspectives

Ferraguti

Crepaldi

Nicoletti³

2008

Pharmacol Rev

192

205

View full text Add to dashboard Cite

Almost 25 years after the first report that glutamate can activate receptors coupled to heterotrimeric G-proteins, tremendous progress has been made in the field of metabotropic glutamate receptors. Now, eight members of this family of glutamate receptors, encoded by eight different genes that share distinctive structural features have been identified. The first cloned receptor, the metabotropic glutamate ( mGlu) receptor mGlu1 has probably been the most extensively studied mGlu receptor, and in many respects it represents a prototypical subtype for this family of receptors. Its biochemical, anatomical, physiological, and pharmacological characteristics have been intensely investigated. Together with subtype 5, mGlu1 receptors constitute a subgroup of receptors that couple to phospholipase C and mobilize Ca(2+) from intracellular stores. Several alternatively spliced variants of mGlu1 receptors, which differ primarily in the length of their C-terminal domain and anatomical localization, have been reported. Use of a number of genetic approaches and the recent development of selective antagonists have provided a means for clarifying the role played by this receptor in a number of neuronal systems. In this article we discuss recent advancements in the pharmacology and concepts about the intracellular transduction and pathophysiological role of mGlu1 receptors and review earlier data in view of these novel findings. The impact that this new and better understanding of the specific role of these receptors may have on novel treatment strategies for a variety of neurological and psychiatric disorders is considered

show abstract

“…mGlu1/mGlu5) receptors in several brain areas (Fitzjohn et al 1996;Doherty et al 1997;Pisani et al 1997;Martin et al 1998;Holohean et al 1999), as has modulation of AMPA-receptor-mediated responses (Cerne & Randic 1992;Bond & Lodge 1995;Jones & Headley 1995;Dev & Henley 1998;Calabresi et al 1999). In the VB, activation of mGlu1 receptors potentiates responses mediated via either AMPA or NMDA receptors in vivo ( gure 2) (Salt & Binns 2000), and it is probable that this is due to the direct effects of mGlu1 activation on neuronal membrane potential and resistance (McCormick & Von Krosigk 1992;Turner & Salt 1998) rather than a speci c interaction at the receptor level, or that the potentiation seen is a combination of these factors (Salt & Binns 2000). Thus, although the isolated corticothalamic synaptic potential (which can be attributed to mGlu1 receptors in vitro) appears to be rather small (Turner & Salt 2000b), it would be able to exert a profound in uence on ionotropic receptor-mediated responses, if the sensory stimulus was appropriate to recruit activity in the corticothalamic output.…”

Section: Sensory Responses Of Thalmic Relay Neurons In Vivo: Recruitmmentioning

confidence: 99%

Glutamate receptor functions in sensory relay in the thalamus

Salt

2002

Phil. Trans. R. Soc. Lond. B

View full text Add to dashboard Cite

It is known that glutamate is a major excitatory transmitter of sensory and cortical afferents to the thalamus. These actions are mediated via several distinct receptors with postsynaptic excitatory effects predominantly mediated by ionotropic receptors of the a-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) and N-methyl-d-aspartate varieties (NMDA). However, there are also other kinds of glutamate receptor present in the thalamus, notably the metabotropic and kainate types, and these may have more complex or subtle roles in sensory transmission. This paper describes recent electrophysiological experiments done in vitro and in vivo which aim to determine how the metabotropic and kainate receptor types can in uence transmission through the sensory thalamic relay. A particular focus will be how such mechanisms might operate under physiological conditions.

show abstract

Contributions of mGlu1 and mGlu5 receptors to interactions with N-methyl-d-aspartate receptor-mediated responses and nociceptive sensory responses of rat thalamic neurons

Cited by 78 publications

References 40 publications

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Metabotropic Glutamate 1 Receptor: Current Concepts and Perspectives

Glutamate receptor functions in sensory relay in the thalamus

Contact Info

Product

Resources

About