Evels of AEA measured two h after single administration of URB597 improved within the hippocampus (t = four.342, df = ten, p \ 0.01), dorsal striatum (t = three.172, df = 10, p \ 0.01), and cerebellum (t = four.515, df = 10, p \ 0.01) (Table 2).2-AG IMI (15 mg/kg) remedy resulted inside a change within the 2-AG levels in the frontal cortex (F(two,21) = six.385; p = 0.0068), dorsal striatum (F(2,21) = 11.37; p = 0.0005), and cerebellum (F(two,21) = 7.035; p = 0.0046). The 2-AG levels either improved within the frontal cortex (p \ 0.05) or decreased in the cerebellum (p \ 0.05) soon after acuteadministration of IMI. IMI administered chronically evoked a rise of 2-AG levels inside the frontal cortex (p \ 0.01) and dorsal striatum (p \ 0.001), even though inside the cerebellum (p \ 0.01) lowered 2-AG levels were reported (Fig. 3). A 10-day washout period following chronic therapy of IMI restored the levels of 2-AG towards the levels of vehicletreated animals in all structures (Fig. 4). Administration of ESC (ten mg/kg) resulted in potent alterations inside the 2-AG concentration inside the prefrontal cortex (F(2,21) = six.169; p = 0.0078), frontal cortex (F(2,21) = eight.656; p = 0.0018), hippocampus (F(two,21) = 3.447; p = 0.0508), dorsal striatum (F(two,21) = three.848; p = 0.0377), and cerebellum (F(two,21) = 3.843; p = 0.0378). ESC administered acutely decreased the 2-AG levels in the frontal cortex (p \ 0.05). Chronic administration of ESC brought on a reduction in the 2-AG levels within the prefrontal cortex (p \ 0.01), frontal cortex (p \ 0.01), and cerebellum (p \ 0.05), while a rise of 2-AG concentration was observed inside the hippocampus (p \ 0.05) and dorsal striatum (p \ 0.05) (Fig. three). After 10-day drug-free period an increase of 2-AG levels was noted only within the hippocampus (t = two.272, df = 14, p \ 0.05) and dorsal striatum (t = 3.062, df = 14, p \ 0.01) (Fig. 4).Neurotox Res (2014) 26:190Fig. 2 AEA levels in rat brain structures following chronic drug/ compound administration and 10-day washout period. AEA anandamide, IMI(15) imipramine hydrochloride (15 mg/kg), ESC(10) escitalopram oxalate, TIA(ten) tianeptine sodium, NAC(100) N-acetylcysteine, URB597(0.3) cyclohexylcarbamic acid 3-carbamoylbiphenyl-3-yl ester,PFCTX prefrontal cortex, FCTX frontal cortex, HIP hippocampus, DSTR dorsal striatum, NAc nucleus accumbens, CER cerebellum. All data are expressed as the mean SEM. N = eight rats/group. *p \ 0.05 versus corresponding vehicleTIA (10 mg/kg) brought on changes inside the 2-AG levels in the frontal cortex (F(two,21) = 6.997; p = 0.0047) and dorsal striatum (F(two,21) = four.073; p = 0.032). Repeated each day injections of TIA resulted in an increase of 2-AG levels in the frontal cortex (p \ 0.TCEP Data Sheet 01) and dorsal striatum (p \ 0.Lamivudine salicylate 05), although TIA administered acutely did not alter the 2-AG levels (Fig.PMID:24202965 three). 10-day drug-free period triggered reduction inside the 2-AG levels inside the frontal cortex (t = five.294, df = 14, p \ 0.001) (Fig. 4). NAC (one hundred mg/kg) therapy evoked changes within the prefrontal cortex (F(2,20) = 9.116; p = 0.0015), frontal cortex (F(two,21) = 26.09; p \ 0.0001), dorsal striatum (F(2,21) = 22.26; p \ 0.0001), nucleus accumbens (F(2,21) = 8.139; p = 0.0024), and cerebellum (F(two,21) = five.187; p = 0.0148). NAC administered acutely brought on a decrease of 2-AG levels in the prefrontal cortex (p \ 0.01) and cerebellum (p \ 0.05). Just after chronic administration of NAC a reduce of 2-AG concentration was seen within the prefrontal cortex (p \ 0.05), nucleus accumbens (p \ 0.01) and cerebellum (p \ 0.05) and a rise of 2-AG concentration was noted i.