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BackgroundThe nucleus accumbens (NAc) plays a principal role in drug reward. It has been reported that metabotropic glutamate receptors (mGluRs) play a key role in the rewarding pathway(s). Previous studies have shown the vast allocation of the different types of mGluRs, including mGluR8, in regions that are associated with opioid rewards, such as the NAc. The aim of the present study was to evaluate the role of mGlu8 receptors within the NAc in the acquisition and expression phases of morphine induced conditioned place preference (CPP). Adult male Wistar rats were bilaterally implanted by two cannulas' in the NAc and were evaluated in a CPP paradigm. Selective mGluR8 allosteric agonist (S-3,4-DCPG) was administered at doses of 0.03, 0.3, and 3μg/0.5 μL saline per side into the NAc on both sides during the 3 days of morphine (5 mg/kg) conditioning (acquisition) phase, or before place preference test, or post-conditioning (expression) phase of morphine-induced CPP. ResultsThe results revealed that intra-accumbal administration of S-3,4-DCPG (0.3 and 3 μg) markedly decreased the acquisition in a dose-dependent manner but had no effect on expression of morphine-induced CPP. ConclusionsThe findings suggest that activation of mGlu8 receptors in the NAc dose-dependently blocks the establishment of morphine-induced CPP and reduces the rewarding properties of morphine which may be related to the glutamate activity into the NAc and/or synaptic plasticity of this system in reward pathway(s).

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Background High-fat diets (HFDs) adversely influence glutamate metabolism and neurotransmission. The precise role of the group II metabotropic glutamate receptors (mGluR2/3) antagonist on spatial memory deficit following consumption of HFD has not yet been clarified. Therefore, in this study, we examined the effects of post-training administration of mGluR2/3 antagonism; LY341495 on spatial memory in rats fed with HFD by using Morris Water Maze (MWM) task. Intraperitoneal injection (i.p) injection of LY341495 was done 30 minutes before retention test. Results Our results showed that HFD did not have any effect on memory acquisition. There were not significant differences in escape latency and swimming distance between experimental groups (P>0.05, Two-way ANOVA). Our finding showed that consumption of an HFD leads to spatial memory impairment. There were significant differences in time spent in target zone between experimental groups [F (3, 20) = 7.031, P=0.0021, one-way ANOVA]. Also, LY341495 improved HFD-induced reference memory impairment. HFD animals treated with LY341495 spent more time in the target zone in compare with HFD animals (P= 0.0449). Conclusions Our results suggested that prolonged consumption of high-fat diet has no effects on the acquisition of spatial learning, but can impair memory retention of the adult male rats and post-training administration of LY341495 can improve HFD-induced reference memory impairment.

Aged heart is defined via structural and mitochondrial dysfunction of the heart. However, there is still no impressive compound to suppress and improve the abnormal alterations in cardiac function result from aging. Gallic acid (GA) is known to be an effective agent in improving cardiovascular disorders. In the present study, we exhibit the protective effects of GA against cardiac aging. Male Wistar rats were randomly divvied into four groups: Control, Control treated with GA at 25 mg/kg (GA25), aged rats induced by D-galactose (D-GAL), aged rats treated with GA at 25 mg/kg (D-GAL + GA25).Aging induced by D-GAL at 150 mL/kg via intraperitoneal injection for eight weeks. Aged rats treated with GA at 25 mg/kg (D-GAL GA25) by gavage for eight weeks. The blood samples were used to assessment biochemical factors and heart tissue was assessed for evaluating oxidative stress and the gene expression of molecular parameters. Histological examination of the heart was occurred. The D-GAL rats indicated cardiac hypertrophy, which was associated with reduced antioxidant activity of enzyme, increased oxidative marker and alterations in Sirtuin 1 (SIRT1), Peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1alpha and Transcription Factor A, Mitochondrial (TFAM) genes expression in comparison to the control animals. Co-treatment with GA improved all these alterations. Taken together, GA could protect the heart against D-GAL-induced aging via antioxidant effects, and the enhancement of SIRT1, PGC-1α, and TFAM genes expression.