Abstract
γ-Hydroxybutyric acid (GHB) reduces (a) alcohol intake and alcohol motivational properties in alcohol-preferring rats and (b) alcohol drinking and craving for alcohol in human alcoholics. The present study was designed to extend to relapse-like drinking the capacity of GHB to suppress different alcohol-related behaviors in alcohol-preferring rats. The “alcohol deprivation effect,” defined as the temporary increase in alcohol intake occurring in laboratory animals after a period of alcohol deprivation, was used as model of alcohol relapse. Acute administration of non-sedative doses of GHB (0, 100, 200, and 300 mg/kg, i.p.) resulted in the complete suppression of the extra-amount of alcohol consumed by Sardinian alcohol-preferring rats during the first hour of re-access to alcohol after a 14-day period of deprivation. These data demonstrate that GHB suppressed relapse-like drinking in a rat model of excessive alcohol consumption.
Highlights
The short-chain fatty acid, γ-hydroxybutyric acid (GHB; see Snead and Gibson, 2005; Agabio et al, 2010), has been used for years – in some European Countries – in the treatment of alcohol dependence
Post hoc analysis indicated that all doses of GHB suppressed alcohol deprivation effect” (ADE), as alcohol intake in all GHBtreated alcohol-deprived rat groups was significantly lower than that recorded in vehicle-treated alcohol-deprived rats (Figure 1); Alcohol intake (g/kg)
The results of the present study indicate that acute treatment with GHB suppressed the extra-amount of alcohol (ADE) voluntarily consumed by alcohol-preferring Sardinian alcohol-preferring (sP) rats after a 2-week period of forced abstinence from alcohol
Summary
The short-chain fatty acid, γ-hydroxybutyric acid (GHB; see Snead and Gibson, 2005; Agabio et al, 2010), has been used for years – in some European Countries – in the treatment of alcohol dependence. A small double-blind study (Gallimberti et al, 1992) and some subsequent open studies (Addolorato et al, 1996, 1998; Moncini et al, 2000; Maremmani et al, 2001; Caputo et al, 2003, 2007, 2011) indicated that treatment with GHB was effective in reducing alcohol drinking, promoting abstinence, and controlling craving for alcohol (for review, see Agabio and Gessa, 2002; Addolorato et al, 2009). Three double-blind studies (Gallimberti et al, 1989; Addolorato et al, 1999a; Nimmerrichter et al, 2002) and some additional open studies (Nava et al, 2007; Elsing et al, 2009) reported that treatment with GHB was effective in suppressing the symptomatology of alcohol withdrawal syndrome (for review, see Agabio and Gessa, 2002; Addolorato et al, 2009). As predictable on the basis of a number of clinical and preclinical observations (see Nicholson and Balster, 2001; Drasbek et al, 2006), the major limitation of the therapeutic use of GHB appears to be its abuse potential: a portion of patients undergoing GHB treatment voluntarily increased their daily GHB dosage ( some of these self-administered increases were made in an attempt to achieve more effective therapeutic doses) (Addolorato et al, 1996; Gallimberti et al, 2000; Glisson and Norton, 2002; Caputo et al, 2011) and some patients even developed dependence on GHB (Addolorato et al, 1999b; see Caputo et al, 2009)
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