Distribution of metabotropic glutamate receptor mGluR3 in the mouse CNS: differential location relative to pre- and postsynaptic sites

Tamaru, Yoshinao; Nomura, Sakashi; Mizuno, Noboru; Shigemoto, Ryuichi

doi:10.1016/s0306-4522(01)00305-0

Cited by 320 publications

(301 citation statements)

References 69 publications

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“…Thus, mGlu2 receptors have an important regulatory role in preventing pathological glutamate excitation from occurring, but play less of a role in physiological excitatory transmission per se. mGlu2 and/or mGlu3 receptors are also present post-synaptically, where they hyperpolarize cells thus decreasing excitability (Tamaru et al, 2001). mGlu3 receptors have been identified on glial cells where their function is less understood (Schoepp, 2001).…”

Section: Ly354740 Plasma Concentrationsmentioning

confidence: 99%

Efficacy and Tolerability of an mGlu2/3 Agonist in the Treatment of Generalized Anxiety Disorder

Dunayevich

Erickson

Levine

et al. 2007

Neuropsychopharmacol

171

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Section: Ly354740 Plasma Concentrationsmentioning

confidence: 99%

Efficacy and Tolerability of an mGlu2/3 Agonist in the Treatment of Generalized Anxiety Disorder

Dunayevich

Erickson

Levine

et al. 2007

Neuropsychopharmacol

171

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“…mGluR 3 is expressed on both pre-and postsynaptic sites in the NAc and the caudate-putamen (Ohishi et al, 1993b;Tamaru et al, 2001). mGluR 2 in these brain areas is selectively expressed on presynaptic sites (Testa et al, 1998;Richards et al, 2005).…”

Section: Neuronal Mechanisms Underlying the Effect Of Ly379268 Nac Inmentioning

confidence: 99%

“…mGluR 2 are expressed primarily on presynaptic glutamate (and GABA) neurons, and when activated they provide negative feedback to decrease evoked neurotransmitter release (Anwyl, 1999;Schoepp, 2001). mGluR 3 are expressed on both postsynaptic and presynaptic neurons and on glia, but their functional role is unknown (Schoepp, 2001;Tamaru et al, 2001). The VTA is the cell body region of the mesolimbic dopamine system and there is evidence that glutamate transmission in this brain area is involved in conditioned and unconditioned reinforcing effects of opiate drugs (Carlezon et al, 1997;Xi and Stein, 2002;Harris et al, 2004) and relapse to drug seeking, as measured in a reinstatement model (Vorel et al, 2001;Sun et al, 2005;Wang et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…mGluR 2 and mGluR 3 are expressed in the NAc (Ohishi et al, 1993a, b;Tamaru et al, 2001;Richards et al, 2005), and this brain area receives glutamatergic projections from the prefrontal cortex, thalamus, basolateral amygdala, and hippocampus (Brog et al, 1993;Heimer et al, 1997;Groenewegen et al, 1999b). Infusions of an mGluR 2/3 agonist into the NAc decrease glutamate release .…”

Section: Introductionmentioning

confidence: 99%

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Activation of Group II Metabotropic Glutamate Receptors in the Nucleus Accumbens Shell Attenuates Context-Induced Relapse to Heroin Seeking

Bossert

Gray

Lü

et al. 2005

Neuropsychopharmacol

216

173

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Using a rat relapse model, we previously reported that re-exposing rats to a drug-associated context, following extinction of operant responding in a different context, reinstates heroin seeking. In an initial pharmacological characterization, we found that the mGluR 2/3 agonist LY379268, which acts centrally to reduce evoked glutamate release, attenuates context-induced reinstatement of heroin seeking when injected systemically or into the ventral tegmental area, the cell body region of the mesolimbic dopamine system. Here, we tested whether injections of LY379268 into the nucleus accumbens (NAc), a terminal region of the mesolimbic dopamine system, would also attenuate context-induced reinstatement of heroin seeking. Rats were trained to self-administer heroin; drug infusions were paired with a discrete tone-light cue. Subsequently, lever pressing was extinguished in the presence of the discrete cue in a context that differed from the drug self-administration context in terms of visual, auditory, tactile, and circadian cues. After extinction of responding, LY379268 was injected to different groups of rats into the NAc core or shell or into the caudate-putamen, a terminal region of the nigrastriatal dopamine system. Injections of LY379268 into the NAc shell (0.3 or 1.0 mg) dose-dependently attenuated context-induced reinstatement of heroin seeking. Injections of 1.0 mg of LY379268 into the NAc core had no effect, while a higher dose (3.0 mg) decreased this reinstatement. Injections of LY379268 (3.0 mg) 1.5 mm dorsal from the NAc core into the caudate-putamen were ineffective. Results suggest an important role of glutamate transmission in the NAc shell in context-induced reinstatement of heroin seeking.

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“…Eight known subtypes of mGlu receptors can be divided into three groups (Group I: mGlu1,5;Group II: mGlu2,3;Group III: mGlu4,6,7,8) based on their molecular structure, second messenger system, and pharmacological profile (Conn and Pin, 1997;Schoepp et al, 1999a). Group II mGlu receptors are localized presynaptically outside the active zone of axon terminals, and also in postsynaptic neurons and glia (mGlu3 receptor) (Shigemoto et al, 1997;Tamaru et al, 2001). Electrophysiological studies have demonstrated that the activation of presynaptic mGlu2/3 receptors negatively modulates the release of glutamate providing feedback that prevents excessive glutamate release (reviewed by Anwyl, 1999;Cartmell and Schoepp, 2000).…”

Section: Introductionmentioning

confidence: 99%

Anxiolytic Activity of the MGLU2/3 Receptor Agonist LY354740 on the Elevated Plus Maze is Associated with the Suppression of Stress-Induced c-Fos in the Hippocampus and Increases in c-Fos Induction in Several Other Stress-Sensitive Brain Regions

Lindén

Greene

Bergeron

et al. 2003

Neuropsychopharmacol

101

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LY354740 is a potent and selective agonist for group II metabotropic glutamate (mGlu) receptors, mGlu2 and mGlu3 receptors, with anxiolytic activity in several animal models of anxiety, including the elevated plus maze (EPM) test. Here, we studied neuronal activation in mouse brain after EPM exposure in saline-and LY354740-treated mice using c-Fos immunoreactivity as a marker. The effect of LY354740 on c-Fos expression was also studied in cage control (no EPM) mice. Pretreatment with LY354740 (20 mg/kg, s.c.) produced robust anxiolytic behavior on the EPM. LY354740 administration decreased EPM-induced increases in c-Fos expression in the CA3 of the hippocampus, while having no significant effects on basal c-Fos expression in the hippocampus. LY354740 administration significantly increased c-Fos expression in specific limbic regions, including the lateral division of the central nucleus of the amygdala (CeL), lateral parabrachial nucleus, locus coeruleus, and Edinger-Westphal nucleus, whether or not animals were exposed to the EPM. Moreover, LY354740 administration per se significantly increased c-Fos expression in regions processing sensory information, including the paraventricular and lateral geniculate nucleus of the thalamus as well as the nucleus of the optic tract and superior colliculus. In particular, the suppression of fear-evoked neuronal activity in the hippocampus and drug-induced increases in neuronal activation in the CeL have been previously linked to the anxiolytic effects of clinically effective drugs such as benzodiazepines, and thus may contribute to anxiolytic actions of LY354740 in animal models and human anxiety patients.

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Distribution of metabotropic glutamate receptor mGluR3 in the mouse CNS: differential location relative to pre- and postsynaptic sites

Cited by 320 publications

References 69 publications

Efficacy and Tolerability of an mGlu2/3 Agonist in the Treatment of Generalized Anxiety Disorder

Efficacy and Tolerability of an mGlu2/3 Agonist in the Treatment of Generalized Anxiety Disorder

Activation of Group II Metabotropic Glutamate Receptors in the Nucleus Accumbens Shell Attenuates Context-Induced Relapse to Heroin Seeking

Anxiolytic Activity of the MGLU2/3 Receptor Agonist LY354740 on the Elevated Plus Maze is Associated with the Suppression of Stress-Induced c-Fos in the Hippocampus and Increases in c-Fos Induction in Several Other Stress-Sensitive Brain Regions

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