Selective activation of group I metabotropic glutamate receptors upregulates preprodynorphin, substance P, and preproenkephalin mRNA expression in rat dorsal striatum

Antagonism of metabotropic glutamate receptor type 5 attenuates l‐DOPA‐induced dyskinesia and its molecular and neurochemical correlates in a rat model of Parkinson’s disease

“…Thus, our data indicate that mGluR5 is involved in the maladaptive molecular changes that induce and maintain a dyskinesia‐prone state. Although group I mGluRs have been reported to modulate striatal gene expression in different model systems (Mao and Wang 2001, 2002, 2003), this is the first report showing that l ‐DOPA‐induced gene expression can be inhibited by mGluR5 blockade. This data is particularly important in light of the fact that NMDA antagonists are reportedly unable to inhibit D 1 receptor dependent‐ and/or l ‐DOPA‐induced gene expression in DA‐denervated striatal neurons (Keefe and Gerfen 1996; Adams et al.…”

“…The blockade of l ‐DOPA‐induced PDyn gene up‐regulation by MTEP in this study indicates that the compound normalized the response to l ‐DOPA in striatal neurons of the ‘direct pathway’. Although the anatomical site of action of MTEP was not addressed, several independent studies performed in cell cultures and slice preparations have shown that pharmacological antagonists of mGluR5 can directly modulate gene expression and synaptic responses in striatal neurons by a local effect (Mao and Wang 2001, 2002, 2003; Voulalas et al. 2005).…”

Antagonism of metabotropic glutamate receptor type 5 attenuates l‐DOPA‐induced dyskinesia and its molecular and neurochemical correlates in a rat model of Parkinson’s disease

“…Thus, our data indicate that mGluR5 is involved in the maladaptive molecular changes that induce and maintain a dyskinesia‐prone state. Although group I mGluRs have been reported to modulate striatal gene expression in different model systems (Mao and Wang 2001, 2002, 2003), this is the first report showing that l ‐DOPA‐induced gene expression can be inhibited by mGluR5 blockade. This data is particularly important in light of the fact that NMDA antagonists are reportedly unable to inhibit D 1 receptor dependent‐ and/or l ‐DOPA‐induced gene expression in DA‐denervated striatal neurons (Keefe and Gerfen 1996; Adams et al.…”

“…The blockade of l ‐DOPA‐induced PDyn gene up‐regulation by MTEP in this study indicates that the compound normalized the response to l ‐DOPA in striatal neurons of the ‘direct pathway’. Although the anatomical site of action of MTEP was not addressed, several independent studies performed in cell cultures and slice preparations have shown that pharmacological antagonists of mGluR5 can directly modulate gene expression and synaptic responses in striatal neurons by a local effect (Mao and Wang 2001, 2002, 2003; Voulalas et al. 2005).…”

Phosphorylation of cAMP response element‐binding protein in cultured striatal neurons by metabotropic glutamate receptor subtype 5

“…Our recent data show that the non‐selective mGluR agonist ACPD increased c‐ fos and opioid peptide mRNA expression in striatal neurons (Wang 1998; Wang and McGinty 1998). Similarly, a group I agonist DHPG elevated opioid gene expression in vivo (Mao and Wang 2001a) and in vitro (Mao and Wang 2001b). It can be speculated that ACPD‐ and DHPG‐sensitive c‐ fos or opioid gene expression may be mediated via a pCREB‐regulated transcription, although it needs to be proven experimentally.…”

Slow excitatory synaptic potentials evoked by distension in myenteric descending interneurones of guinea‐pig ileum

“…Recently, Ren et al (2000) showed that some myenteric neurones respond to glutamate with slow depolarizations that are blocked by mGluR1 antagonists. However, the specific mGluR1 antagonist PHCCC, at concentrations (10 or 30 μ m ) well above those that have significant effects in the central nervous system (Mao & Wang, 2001), failed to affect the slow EPSP in response to either electrical stimulation or distension in six of seven NOS‐IR interneurones tested. It also had no effect on electrically evoked slow EPSPs in another two NOS‐IR interneurones.…”

Antagonism of metabotropic glutamate receptor type 5 attenuates l‐DOPA‐induced dyskinesia and its molecular and neurochemical correlates in a rat model of Parkinson’s disease

“…Thus, our data indicate that mGluR5 is involved in the maladaptive molecular changes that induce and maintain a dyskinesia‐prone state. Although group I mGluRs have been reported to modulate striatal gene expression in different model systems (Mao and Wang 2001, 2002, 2003), this is the first report showing that l ‐DOPA‐induced gene expression can be inhibited by mGluR5 blockade. This data is particularly important in light of the fact that NMDA antagonists are reportedly unable to inhibit D 1 receptor dependent‐ and/or l ‐DOPA‐induced gene expression in DA‐denervated striatal neurons (Keefe and Gerfen 1996; Adams et al.…”

“…The blockade of l ‐DOPA‐induced PDyn gene up‐regulation by MTEP in this study indicates that the compound normalized the response to l ‐DOPA in striatal neurons of the ‘direct pathway’. Although the anatomical site of action of MTEP was not addressed, several independent studies performed in cell cultures and slice preparations have shown that pharmacological antagonists of mGluR5 can directly modulate gene expression and synaptic responses in striatal neurons by a local effect (Mao and Wang 2001, 2002, 2003; Voulalas et al. 2005).…”

Phosphorylation of cAMP response element‐binding protein in cultured striatal neurons by metabotropic glutamate receptor subtype 5

“…Our recent data show that the non‐selective mGluR agonist ACPD increased c‐ fos and opioid peptide mRNA expression in striatal neurons (Wang 1998; Wang and McGinty 1998). Similarly, a group I agonist DHPG elevated opioid gene expression in vivo (Mao and Wang 2001a) and in vitro (Mao and Wang 2001b). It can be speculated that ACPD‐ and DHPG‐sensitive c‐ fos or opioid gene expression may be mediated via a pCREB‐regulated transcription, although it needs to be proven experimentally.…”

Slow excitatory synaptic potentials evoked by distension in myenteric descending interneurones of guinea‐pig ileum

“…Recently, Ren et al (2000) showed that some myenteric neurones respond to glutamate with slow depolarizations that are blocked by mGluR1 antagonists. However, the specific mGluR1 antagonist PHCCC, at concentrations (10 or 30 μ m ) well above those that have significant effects in the central nervous system (Mao & Wang, 2001), failed to affect the slow EPSP in response to either electrical stimulation or distension in six of seven NOS‐IR interneurones tested. It also had no effect on electrically evoked slow EPSPs in another two NOS‐IR interneurones.…”

Antagonism of metabotropic glutamate receptor type 5 attenuates l‐DOPA‐induced dyskinesia and its molecular and neurochemical correlates in a rat model of Parkinson’s disease

“…Thus, our data indicate that mGluR5 is involved in the maladaptive molecular changes that induce and maintain a dyskinesia‐prone state. Although group I mGluRs have been reported to modulate striatal gene expression in different model systems (Mao and Wang 2001, 2002, 2003), this is the first report showing that l ‐DOPA‐induced gene expression can be inhibited by mGluR5 blockade. This data is particularly important in light of the fact that NMDA antagonists are reportedly unable to inhibit D 1 receptor dependent‐ and/or l ‐DOPA‐induced gene expression in DA‐denervated striatal neurons (Keefe and Gerfen 1996; Adams et al.…”

“…The blockade of l ‐DOPA‐induced PDyn gene up‐regulation by MTEP in this study indicates that the compound normalized the response to l ‐DOPA in striatal neurons of the ‘direct pathway’. Although the anatomical site of action of MTEP was not addressed, several independent studies performed in cell cultures and slice preparations have shown that pharmacological antagonists of mGluR5 can directly modulate gene expression and synaptic responses in striatal neurons by a local effect (Mao and Wang 2001, 2002, 2003; Voulalas et al. 2005).…”

Phosphorylation of cAMP response element‐binding protein in cultured striatal neurons by metabotropic glutamate receptor subtype 5

“…Our recent data show that the non‐selective mGluR agonist ACPD increased c‐ fos and opioid peptide mRNA expression in striatal neurons (Wang 1998; Wang and McGinty 1998). Similarly, a group I agonist DHPG elevated opioid gene expression in vivo (Mao and Wang 2001a) and in vitro (Mao and Wang 2001b). It can be speculated that ACPD‐ and DHPG‐sensitive c‐ fos or opioid gene expression may be mediated via a pCREB‐regulated transcription, although it needs to be proven experimentally.…”

Slow excitatory synaptic potentials evoked by distension in myenteric descending interneurones of guinea‐pig ileum

“…Recently, Ren et al (2000) showed that some myenteric neurones respond to glutamate with slow depolarizations that are blocked by mGluR1 antagonists. However, the specific mGluR1 antagonist PHCCC, at concentrations (10 or 30 μ m ) well above those that have significant effects in the central nervous system (Mao & Wang, 2001), failed to affect the slow EPSP in response to either electrical stimulation or distension in six of seven NOS‐IR interneurones tested. It also had no effect on electrically evoked slow EPSPs in another two NOS‐IR interneurones.…”