Electrochemical behaviour of gamma hydroxybutyric acid at a platinum electrode in acidic medium

The electrooxidation of Gamma Hydroxybutyric Acid (GHB) on a polycrystalline platinum electrode is studied by cyclic voltammetry in acidic medium. Two oxidation peaks, A and B, are obtained in the positive scan within the potential range of the double layer region and of the platinum oxide region, respectively. In the negative going potential sweep an inverted oxidation peak with an onset partially overlapping with the tail of the cathodic peak for the reduction of the platinum oxide formed during the anodic scan is obtained (peak C). This inverted peak can be observed at a potential close to +0.2 V (vs Ag/AgCl at pH 2) and separated 0.4 and 0.8 V from the two other oxidation peaks obtained during the anodic scan and in such conditions that the surface is particularly activated to favour this electrochemical process. The response obtained in the electronic current for the different peaks when GHB concentration and scan rate were changed to allows inferring that these are the result of a potential dependent mechanism. The behaviour observed is according with the oxidation of the alcohol group to the corresponding aldehyde and carboxylic acid (succinic acid) as main products

Study of the electro-oxidation of a recreational drug GHB (gamma hydroxybutyric acid) on a platinum catalyst-type electrode through chronoamperometry and spectro-electrochemistry

The electro-oxidation of gamma-hydroxybutyric acid (GHB) on a polycrystalline platinum electrode in acidic medium has been studied using chronoamperometry. The study has been performed in a wide interval of potentials and at different concentrations. It was found that at longer times the density currents reached stationary values at more anodic potentials, whereas it is zero at lower potentials. These characteristics in the j-t curves suggest a different mechanism for the electro-oxidation of GHB, potential dependent, with a catalytic process at high potentials and an adsorption process controlled by mass transport at low potential. The change in the stationary current obtained at +0.9 V with variable GHB concentrations also suggests an oxidation mechanism catalysed by the platinum surface with platinum hydroxides acting as reaction intermediates to make the final oxidation product for GHB. The results obtained using chronoamperometry are in good agreement with those obtained using cyclic voltammetry where the alcohol group is oxidised at different potentials. In situ Surface Enhanced Raman Scattering (SERS) spectra corresponding to GHB intermediates and water adsorbed species being formed/consumed at the potentialdependent adsorption processes have been analyzed using spectro-electrochemistry. A peak at 1590 cm-1, corresponding to the asymmetric stretching of carboxylic group in a bridge configuration, increases with the potential. This supports the hypothesis of a mechanism of formation of the succinic acid on the platinum surface as reaction product under the experimental conditions studied

Cannabigerol is a novel, well-tolerated appetite stimulant in pre-satiated rats

Rationale The appetite-stimulating properties of cannabis are well documented and have been predominantly attributed to the hyperphagic activity of the psychoactive phytocannabinoid, ∆9-tetrahydrocannabinol (∆9-THC). However, we have previously shown that a cannabis extract devoid of ∆9-THC still stimulates appetite, indicating that other phytocannabinoids also elicit hyperphagia. One possible candidate is the non-psychoactive phytocannabinoid cannabigerol (CBG), which has affinity for several molecular targets with known involvement in the regulation of feeding behaviour. Objectives The objective of the study was to assess the effects of CBG on food intake and feeding pattern microstructure. Methods Male Lister hooded rats were administered CBG (30–120 mg/kg, per ora (p.o.)) or placebo and assessed in open field, static beam and grip strength tests to determine a neuromotor tolerability profile for this cannabinoid. Subsequently, CBG (at 30–240 mg/kg, p.o.) or placebo was administered to a further group of pre-satiated rats, and hourly intake and meal pattern data were recorded over 2 h. Results CBG produced no adverse effects on any parameter in the neuromotor tolerability test battery. In the feeding assay, 120–240 mg/kg CBG more than doubled total food intake and increased the number of meals consumed, and at 240 mg/kg reduced latency to feed. However, the sizes or durations of individual meals were not significantly increased. Conclusions Here, we demonstrate for the first time that CBG elicits hyperphagia, by reducing latency to feed and increasing meal frequency, without producing negative neuromotor side effects. Investigation of the therapeutic potential of CBG for conditions such as cachexia and other disorders of eating and body weight regulation is thus warranted