Mouse Breathalyzer

Abstract

Background The development of a relatively simple, noninvasive method for estimating blood ethanol concentrations in mice will be useful in behavioral studies related to alcoholism. This study validated such a method. Methods The apparatus consists of a body chamber fitted with a head stock through which the mouse head protrudes. This was fitted against a water-jacketed head-space chamber surrounding the mouse’s head. Rebreathed air maintained at 37°C in the head-space chamber was removed using a peristaltic pump and loaded into a 1-ml injection loop. Ethanol in the sample was quantified using gas chromatography. To validate this method, ethanol levels in breath samples were compared against those in tail blood samples collected immediately after the breath samples. Breath samples were collected at 5, 10, 20, 40, 80, 120, and 160 minutes after ethanol (0.4, 0.8, 1.2, 1.6, 2.4, and 3.2 g/kg) was administered to male C57BL/6J mice. Results Breath and blood ethanol levels were well correlated (r2 = 0.96) across time points on the descending ethanol–time curve at doses below 2.4 g/kg. Correlation for these doses on the ascending portion of the curve had greater variance, but was still well correlated (r2 = 0.92). Conclusions The mouse breathalyzer is an accurate, convenient, noninvasive and well-tolerated method for estimating blood ethanol concentrations in mice across a range of behaviorally relevant concentrations below 2.4 g/kg, especially on the descending limb of the ethanol–time curve. Although this procedure requires a gas chromatograph in the animal facility, the ability to estimate ethanol concentrations quickly and easily will be especially useful in behavioral studies where repeated blood sampling is not feasible.

FMRP regulates an ethanol-dependent shift in GABABR function and expression with rapid antidepressant properties

“…A concentration of 30 mM ethanol was chosen, as it has been shown to reduce NMDAR activity in hippocampal neurons and reflects that achieved in vivo following i.p. injection 9 33 . Acute ethanol exposure (30 mM, 2 h) increased the dendritic levels of GABA B R2 by ∼47%, but did not affect GABA B R1 levels ( Fig.…”

REVIEW: Ethanol consumption: how should we measure it? Achieving consilience between human and animal phenotypes

“…An alternative strategy, using a continuous access procedure in which the temporal pattern of intake is monitored, would be to collect blood samples shortly after bouts that meet some minimum level of intake per unit time. New noninvasive technologies to measure breath alcohol levels in rodents could be used (Javors et al, 2005; Ginsburg et al, 2008). Following up on initial work by Dole, Ho and Gentry (1985), computer programs could also be developed to estimate blood alcohol levels using data from systems that permit simultaneous microstructural analysis of the animals' alcohol and fluid intake (Boyle et al, 1997; Reidelberger et al, 1996).…”

Ethanol and a rapid-acting antidepressant produce overlapping changes in exon expression in the synaptic transcriptome

“…We reasoned that the molecular changes that occur within an hour at hippocampal synapses to mediate long-lasting antidepressant effects since rodent models show antidepressant-like behaviors and humans report reduced depressive symptoms with a single injection of NMDAR antagonists within this time frame(Workman et al, 2015; Workman et al, 2013; Zarate et al, 2006). While ethanol treatment within this time frame produces intoxication (2.5mg/kg estimated to produce an alcohol concentration of 0.215g/dl)(Ginsburg et al, 2008), we predict that similar molecular changes that support the antidepressant and reduced anxiety-like behaviors observed at 24 hours in Wolfe et al, are initiated similarly. We used RNA-Seq to analyze gene expression in hippocampal synaptoneurosomes isolated from mice treated with ethanol or Ro 25–6981.…”