Activity (P30): Analysis of activity over 4 repeated measurements showed an overall increase in A) locomotion [F(1,71) = 7.12, p = 9×10⁻³] and B) distance [F(1,71) = 7.36, p = 8.37×10^−<b>3</b>], but no change on C) speed [F(1,74) = 1.92, p = 1.69] in propofol treated animals.

<p>Propofol treatment did not alter D) anxiety related behavior in adolescent animals [F(1,74) = 0.02, p = 0.89]. An overall change in activity was observed over individual measurements, resulting in a significant decrease in locomotion [F(3,71) = 13.6, p = 4.08×10⁻⁷] and distance [F(3,71) = 5.35, p = 2.23×10⁻³] and a significant increase in speed [F(3,74) = 15.7, p = 5.53×10⁻⁸] and the index of anxiety [F(3,74) = 7.25, p = 3×10⁻⁴]. (n_controls = 12 animals, n_propofol = 8 animals).</p

Activity (P120): Analysis of activity over 4 repeated measurements showed no treatment effects on A) locomotion [F(1,73) = 0.94, p = 0.33], B) distance [F(1,74) = 1.86, p = 0.18], C) speed [F(1,74) = 0.44, p = 0.51] or D) anxiety related behavior [F(1,62) = 0.57, p = 0.45] in propofol treated animals.

<p>Apart from a transient effect on locomotion [F(3,71) = 5.92, p = 1.13×10⁻³], no significant changes over repeated measurements were observed in adult aged animals. (n_controls = 12 animals, n_propofol = 8 animals).</p

Impact of propofol on key proteins involved in apoptotic signalling.

<p>Densitometric quantifications of caspase-3 and AIF in cortex and thalamus of P6 rats as analysed by Western blotting. Values represent mean normalised ratios of the densities of caspase-3 and AIF bands compared to densities of the control group (n = 5–6/point+SE). There was an effect of propofol treatment on caspase-3 levels over time, which was significant after 24 hrs in the cortex [F(1,29) = 3.63, p = 0.06] and after 12 hrs in the thalamus [F(1,28) = 3.1, p = 0.09).</p

Impact of propofol on neurotrophins.

<p>Densitometric quantifications of mRNA levels of BDNF and NT-3 in cortex and thalamus of P6 rats, analysed by qRT-PCR. Values represent mean normalised ratios of the densities of BDNF and NT-3 bands compared to the density of the control group (n = 6–7/point+SE). There was an effect of propofol treatment with a decrease of BDNF levels over time, which was significant after 6 hrs in the cortex [F(1,30) = 66.5, p<0.001]. There was also a decrease in NT-3 levels, which was significant in the cortex after 6 hrs [F(1,28) = 12.7, p = 0.004] and after 12 hrs in the thalamus [F(1,24) = 3.5, p = 0.06].</p

Impact of propofol on survival promoting proteins.

<p>Densitometric quantifications of pAKT and pERK1/2 in the cortex and thalamus of P6 rats, analysed by Western blotting. Values represent mean normalised ratios of the densities of pAKT and pERK1/2 bands compared to the density of the control group (n = 6/point+SE). There was an effect of propofol treatment in decrease of pAKT levels over time in the thalamus, which was significant after 12 hrs [F(1,28) = 5.6, p = 0.06]. Post-hoc analysis showed most pronounced decrease after 12 hrs (2-sample t-test). In the cortex there was a significant decrease of pERK1/2 levels over the time, which was significant after 6, 12 and 24 hrs [F(1,29) = 12.7, p = 0.013].</p

Novel object recognition on P30 and P120: At the age of 30 days, both propofol treated animals (t(7) = 7.45, ***q = 4.3×10⁻⁴) and controls (t(10) = 6.30, ***q = 3.6×10⁻⁴) spent significantly more time with the novel object indicating their ability to discriminate the novel from the old object.

<p>Propofol (t(7) = −1.44, q = 0.192) as well as control animals (t(10) = −1.92, q = 0.168) failed to do so after a 24 hrs inter-trial interval. At P120 both groups spent a random amount of time with either of the objects after 6 hrs and also after a 24 hrs interval, indicating that they were unable to remember the old object. (n_controls = 12 animals, n_propofol = 8 animals).</p