Metabotropic glutamate receptors 2 and 3 expressed by astrocytes in rat ventrobasal thalamus
Section snippets
Acknowledgements
We thank Dr. A. Rustioni for supporting every step of this research, Dr. R. Weinberg for his critical review of the manuscript, and K. Phend for her expert technical assistance. This work was supported by grants USPHS NS 16246 and HFSP R6–2/95 (to A. Rustioni).
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Astrocytes modulate thalamic sensory processing via mGlu2 receptor activation
2017, NeuropharmacologyCitation Excerpt :This duality in glutamatergic signalling would suggest a state-dependent reciprocal role of glutamate within the VB-TRN complex, which may act in concert to support complex behaviours. It is important to note that there is also evidence from ultrastructural studies that indicate both Group II mGlu receptors may be localised on glial processes surrounding the TRN-VB synapse (Ralston, 1983; Ohara and Lieberman, 1993; Liu et al., 1998; Mineff and Valtschanoff, 1999). However, due to a lack of commercially available mGlu3 selective ligands, we are unable to investigate whether there is an mGlu3 astrocytic component to the overall Group II mGlu receptor effect on sensory-evoked inhibition in the VB.
Metabotropic glutamate receptors and neurodegenerative diseases
2017, Pharmacological ResearchCitation Excerpt :mGluR8 expression is observed in the olfactory bulb, certain regions of the cerebral cortex, pontine nuclei and lateral reticular nucleus of the medulla oblongata [39–41]. mGluRs are mainly expressed in neuronal cells, although mGluR3 and mGluR5 are also vastly expressed in glial cells throughout the brain [26–30,36,42–45]. Notably, mGluR3 and mGluR5 expression was shown to be up-regulated in reactive astrocytes [46–48].
MGlu3 receptor and astrocytes: Partners in neuroprotection
2013, NeuropharmacologyActions of Xanthurenic Acid, a putative endogenous Group II metabotropic glutamate receptor agonist, on sensory transmission in the thalamus
2013, NeuropharmacologyCitation Excerpt :Indeed, activation of both mGlu2 and mGlu3 receptors can reduce TRN-evoked inhibitory postsynaptic potentials in vitro (Turner and Salt, 2003), and blockade of inhibitory transmission from the TRN by the GABA antagonist bicuculline can produce a similar effect on neuronal responses upon execution of the same sensory stimulation protocol in vivo (Salt, 1989). This attenuation of inhibition is likely achieved by activation of Group II receptors localised on presynaptic TRN axons (Tamaru et al., 2001), and on glial processes surrounding GABAergic terminals (Liu et al., 1998; Mineff and Valtschanoff, 1999). Presynaptic Group II mGlu receptors have been demonstrated to reduce synaptic transmission (Anwyl, 1999; Niswender and Conn, 2010), and modulate non-vesicular glutamate release from glial cells via the cysteine-glutamate transporter (Baker et al., 2008; Moran et al., 2003; Xi et al., 2002) in multiple brain regions.
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2009, Neurochemistry InternationalMetabotropic glutamate receptors as a strategic target for the treatment of epilepsy
2006, Epilepsy Research