Chronic treatment with the mGlu5R antagonist MPEP reduces the functional effects of the mGlu5R agonist CHPG in the striatum of 6-hydroxydopamine-lesioned rats: possible relevance to the effects of mGlu5R blockade in Parkinson's disease.

This study was designed to test whether chronic treatment with the metabotropic glutamate receptor 5 (mGlu5R) antagonist MPEP showed antiparkinsonian effects in rats unilaterally lesioned with 6-hydroxydopamine (6-OHDA) (a "classic" model of Parkinson's disease, PD), and to evaluate whether chronic MPEP influenced the functional properties and/or the expression of striatal mGlu5Rs. Wistar rats were lesioned with 6-OHDA and then treated with MPEP (3 mg/kg/day, i.p.

Potentiation of ischemia-related behavioral alterations by electro-acupuncture in gerbils.

Gerbils subjected to global ischemia or sham-ischemia received electro-acupuncture (EA) or sham EA at points 26 Du (Renzhong) and 8 Du (Junsuo). All animals were then tested for motor activity in an open field, and for spontaneous alternation in a T maze. Results show that EA alone did not affect any behavioral parameter.

Progressive behavioural changes in the spatial open-field in the quinolinic acid rat model of Huntington's disease.

Huntington's disease (HD) is a progressive neurodegenerative disorder, characterized by severe degeneration of basal ganglia, motor abnormalities, impaired cognitive functions and emotional disturbances. Intrastriatal injection of the excitotoxin quinolinic acid (QA), an N-methyl-D-aspartate receptor agonist, appears to reproduce in rats some of the clinical features of human HD, included motor and behavioural deficits. Aim of this study was to assess whether the behavioural alterations described in the QA rat model of HD progressed over time.

Neuroprotective effects of the mGlu5R antagonist MPEP towards quinolinic acid-induced striatal toxicity: involvement of pre- and post-synaptic mechanisms and lack of direct NMDA blocking activity.

The aim of this work was to investigate the potential neuroprotective effects of the metabotropic glutamate receptor 5 (mGlu5R) antagonist 2-Methyl-6-(phenylethynyl)-pyridine (MPEP) towards quinolinic acid (QA)-induced striatal excitoxicity. Intrastriatal MPEP (5 nmol/0.5 micro L) significantly attenuated the body weight loss, the electroencephalographic alterations, the impairment in spatial memory and the striatal damage induced by bilateral striatal injection of QA (210 nmol/0.

Study of the effects of electroacupuncture in a rodent model of cerebral ischaemia.

The effects of electroacupuncture (EA) has been studied in a model of global cerebral ischaemia performed in gerbils through the bilateral carotid artery occlusion (BCAO). Animals, under isofluorane anaesthesia, underwent 5 min of BCAO and were killed after 7 days. The effects of EA were evaluated both on functional (with electrophysiological recordings of synaptic potentials in hippocampal slices) and morphological parameters (by counting the number of survived neurons in CA1 area of the hippocampus).

Adenosine A(2A) antagonism increases striatal glutamate outflow in the quinolinic acid rat model of Huntington's disease.

In the quinolinic acid (QA)-rat model of Huntington's disease (HD), 15 days after QA injection, striatal glutamate, measured by in vivo microdialysis, was unchanged while a significant decrease in adenosine occurred. The decrease in adenosine may depend on QA-induced striatal cell loss. Probe perfusion of the adenosine A(2A) receptor antagonist SCH 58261 significantly increased striatal glutamate outflow, suggesting a potential detrimental effect of A(2A) antagonism at later stages of the neurodegenerative process induced by QA.

Metabotropic glutamate receptor 5 (mGluR5)-mediated phosphoinositide hydrolysis and NMDA-potentiating effects are blunted in the striatum of aged rats: a possible additional mechanism in striatal senescence.

The aim of the present work was to verify whether an impairment of subtype 5 metabotropic glutamate receptor-mediated neurotransmission did occur in the aged striatum. To this end, the ability of the subtype 5 metabotropic glutamate receptor agonist, RS-2-chloro-5-hydroxyphenylglycine, to stimulate phosphoinositide hydrolysis and to potentiate N-methyl-d-aspartate-induced effects in striatal slices from young (3 months) and aged (24 months) rats was compared. The ability of RS-2-chloro-5-hydroxyphenylglycine to induce maximal phosphoinositide turnover and to potentiate N-methyl-d-aspartate effects was significantly reduced in slices from old vs.

Involvement of adenosine A1 and A2A receptors in the motor effects of caffeine after its acute and chronic administration.

The involvement of adenosine A(1) and A(2A) receptors in the motor effects of caffeine is still a matter of debate. In the present study, counteraction of the motor-depressant effects of the selective A(1) receptor agonist CPA and the A(2A) receptor agonist CGS 21680 by caffeine, the selective A(1) receptor antagonist CPT, and the A(2A) receptor antagonist MSX-3 was compared. CPT and MSX-3 produced motor activation at the same doses that selectively counteracted motor depression induced by CPA and CGS 21680, respectively.

Blockade of striatal adenosine A2A receptor reduces, through a presynaptic mechanism, quinolinic acid-induced excitotoxicity: possible relevance to neuroprotective interventions in neurodegenerative diseases of the striatum.

The aim of the present study was to evaluate whether, and by means of which mechanisms, the adenosine A2A receptor antagonist SCH 58261 [5-amino-7-(2-phenylethyl)-2-(2-furyl)-pyrazolo[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine] exerted neuroprotective effects in a rat model of Huntington's disease. In a first set of experiments, SCH 58261 (0.01 and 1 mg/kg) was administered intraperitoneally to Wistar rats 20 min before the bilateral striatal injection of quinolinic acid (QA) (300 nmol/1 microl).