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WAG/Rij rats show a reduced expression of CB1 receptors in thalamic nuclei and respond to the CB1 receptor agonist, R(+)WIN55,212-2, with a reduced incidence of spike-wave discharges

EPILEPSIA, Issue 8 2010
Clementina M. Van Rijn
Summary Purpose:, Genetically epileptic WAG/Rij rats develop spontaneous absence-like seizures after 3 months of age. We used WAG/Rij rats to examine whether absence seizures are associated with changes in the expression of type-1 cannabinoid (CB1) receptors. Methods:, Receptor expression was examined by in situ hybridization and western blot analysis in various brain regions of "presymptomatic" 2-month old and "symptomatic" 8-month-old WAG/Rij rats relative to age-matched nonepileptic control rats. Furthermore, we examined whether pharmacologic activation of CB1 receptor affects absence seizures. We recorded spontaneous spike-wave discharges (SWDs) in 8-month old WAG/Rij rats systemically injected with the potent CB1 receptor agonist, R(+)WIN55,212-2 (3,12 mg/kg, s.c.), given alone or combined with the CB1 receptor antagonist/inverse agonist, AM251 (12 mg/kg, s.c.). Results:, Data showed a reduction of CB1 receptor mRNA and protein levels in the reticular thalamic nucleus, and a reduction in CB1 receptor protein levels in ventral basal thalamic nuclei of 8-month-old WAG/Rij rats, as compared with age-matched ACI control rats. In vivo, R(+)WIN55,212-2 caused a dose-dependent reduction in the frequency of SWDs in the first 3 h after the injection. This was followed by a late increase in the mean SWD duration, which suggests a biphasic modulation of SWDs by CB1 receptor agonists. Both effects were reversed or attenuated when R(+)WIN55,212-2 was combined with AM251. Discussion:, These data indicate that the development of absence seizures is associated with plastic modifications of CB1 receptors within the thalamic-cortical-thalamic network, and raise the interesting possibility that CB1 receptors are targeted by novel antiabsence drugs. [source]

Effect of Acute Ethanol Administration on the Release of Opioid Peptides From the Midbrain Including the Ventral Tegmental Area

ALCOHOLISM, Issue 6 2009
Samuel Jarjour
Background:, Experimental evidence suggests that ethanol alters the activity of the endogenous opioid peptide systems in a dose and brain-region dependent manner. These alterations may influence the processes of ethanol reward and reinforcement. Thus, it was the objective of this study to investigate the response of the 3 major opioid peptide systems (endorphins, enkephalins, and dynorphins) to acute ethanol administration, at the level of the midbrain including the ventral tegmental area (midbrain/VTA), a region important for drug, including ethanol reinforcement. Methods:, Using the in vivo microdialysis technique coupled with specific solid-phase radioimmunoassay for ,-endorphin, met-enkephalin, and dynorphin A1,8, changes in the extracellular concentration of theses peptides at the level of midbrain/VTA were determined at distinct time points following the administration of 0.0 (saline), 0.8, 1.2, 1.6, 2.0, and 2.4 g ethanol/kg B.Wt. Results:, A biphasic effect of ethanol on ,-endorphin release was found, with low to medium (1.2, 1.6, and 2.0 g) but not high (2.4 g) doses of ethanol, inducing a significant increase in the dialysate content of ,-endorphin. A late increase in the dialysate content of dynorphin A1,8 was observed in response to the 1.2 g ethanol dose. However, none of the ethanol doses tested significantly altered the content of met-enkephalin in the dialysate. Conclusions:, The present findings suggest that the ethanol-induced increase of ,-endorphin release at the level of midbrain/VTA may influence alcohol reinforcement. [source]

Postharvest response of ,Brown Turkey' figs (Ficus carica L.) to the inhibition of ethylene perception

JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 14 2005
Gabriel O Sozzi
Abstract The potential use of 1-methylcyclopropene (1-MCP) alone or as a supplement to cold storage to delay the softening of ,Brown Turkey' figs (Ficus carica L.) was studied. Figs were treated with 0, 0.25, 0.5 or 5 µl l,1 1-MCP at 25 °C for 8 h and stored at 20 °C until evaluated. Figs treated with 0.5 or 5 µl l,1 1-MCP had higher ethylene production and respiration rates but slower softening than untreated fruit and those treated with 0.25 µl l,1 1-MCP. Early-harvested firm figs and late-harvested soft figs were untreated or treated with 0.5 or 5 µl l,1 1-MCP at 25 °C and stored at 0 °C for 19 days. Firm figs treated with 1-MCP showed an early peak in ethylene synthesis, higher respiration rate and were firmer than control fruit. In contrast, soft figs did not respond to 1-MCP except for a late increase in respiration rates of fruit treated with 5 µl l,1 1-MCP. 1-MCP appeared to have a relatively limited effect on slowing ripening of ,Brown Turkey' figs and its effect was influenced by ripening stage. Copyright © 2005 Society of Chemical Industry [source]

Effects of a high-fat meal on resistance vessel reactivity and on indicators of oxidative stress in healthy volunteers

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 4 2001
Andreas Schinkovitz
High fat meals postprandially impair macrovascular endothelial function and a link to increased oxidative stress is suggested. Few information, on the other hand, exists on the effect of postprandial hyperlipidaemia on resistance vessel function. Under normal circumstances this vascular bed regulates tissue perfusion and, by controlling flow, impacts on macrovascular nitric oxide formation. The impact of a high fat meal (1200 kcal, 90 g fat, 46 g protein and 47 g carbohydrates) on postprandial resistance vessel reactivity and on indicators of oxidative stress was studied in 11 healthy subjects by venous-occlusion plethysmography using another six subjects as time control group. Ingestion of the test meal resulted in a pronounced increase of serum triglycerides from 1·05 ± 0·61 mmol l,1 in the fasting state to peak postprandial values of 1·94 ± 0·41 mmol l,1 (P < 0·001) reached after 4 h and a return to baseline after 8 h. Fasting peak reactive hyperaemia (RH) was 19·6 ± 2·4 ml min,1 (100 ml),1. Two hours after ingestion of the test meal peak RH was transiently reduced to 16·8 ± 2·2 ml min,1 (100 ml),1 (P < 0·05). No alteration of resting forearm perfusion was observed. The time course of peak RH suggested a potential biphasic effect of the test meal with an early impairment and a late increase of RH. Ingestion of a lipid rich test meal did not exert any influence on either total plasma antioxidant capacity given in trolox equivalents (513 ± 26 ,mol l,1 at baseline) or on plasma peroxides measured as H2O2 equivalents (469 ± 117 ,mol l,1). Our results suggest that ingestion of a meal containing 90 g of fat results in a transient impairment of reactive hyperaemia in healthy subjects but these vascular alterations are not accompanied by signs of systemically increased oxidative stress. [source]