Journal: European Journal of Psychotraumatology

Article Title: Modelling post-traumatic stress disorder–major depressive disorder comorbidity in rats: impaired α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor signalling is consistent with synergistic behavioural and cognitive deficits

doi: 10.1080/20008066.2026.2645520

Figure Lengend Snippet: Paroxetine (PRX) administration improved the behavioural abnormalities in rats (1) ( n = 10/group). (A) Sucrose preference (%) was calculated as sucrose intake divided by total fluid intake. Sucrose preference showed a significant main effect of drug administration ( F (1,72) = 32.93, p < .0001). The interaction between modelling treatment and administration ( F (3,72) = 0.877, p = .4571) and the main effect of modelling treatment ( F (3,72) = 2.351, p = .0794) were not significant. (B) The interaction between modelling treatment × administration ( F (3,72) = 9.362, p < .0001), modelling treatment ( F (3,72) = 6.648, p = .0005), and administration ( F (1,72) = 42.49, p < .0001) had significant effects on the cognitive index of rats. (C) The total distance of open field test (OFT) movement was significantly affected by modelling × administration ( F (3,72) = 20.29, p < .0001) and administration ( F (1,72) = 15.47, p = .0002), but not by modelling ( F (3,72) = 0.8, p = .4979). (D) The interaction effect of modelling treatment × administration ( F (3,72) = 10.80, p < .001) was the number of times that rats entered the centre of the open field, while modelling ( F (3,72) = 2.505, p = .0658) and administration ( F (1,72) = 1.105, p = .2967) had no significant effect. (E) The modelling treatment × administration ( F (3,72) = 20.18, p < .0001) and administration ( F (1,72) = 7.95, p = .0062) significantly affected the percentage of movement distance in the central open field, while modelling treatment had no significant effect ( F (3,72) = 1.98, p = .1246). (F) Modelling treatment × administration ( F (3,72) = 11.26, p < .0001) was the main effect of the number of upright times in the open field, while modelling treatment ( F (3,72) = 1.36, p = .2608) and administration ( F (1,72) = 2.46, p = .1209) had no significant effect. (G) Schematic representation of the trajectories of rats in the open field after saline administration. (H) Schematic representation of the trajectories of rats in the open field after PRX administration. CON = control; Sal = saline; SPS&S = single prolonged stress and shock; CUMS = chronic unpredictable mild stress; S + C = SPS&S + CUMS. Data are presented as mean ± SEM . Statistical comparisons were performed using two-way analysis of variance followed by post-hoc tests. * p < .05, ** p < .01, *** p < .001, **** p < .0001.

Article Snippet: In Phase 2, data from the eight treatment groups were analysed by two-way ANOVA, with model and drug as independent factors (Kuang et al., ).

Techniques: Saline, Control

Journal: European Journal of Psychotraumatology

Article Title: Modelling post-traumatic stress disorder–major depressive disorder comorbidity in rats: impaired α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor signalling is consistent with synergistic behavioural and cognitive deficits

doi: 10.1080/20008066.2026.2645520

Figure Lengend Snippet: Paroxetine (PRX) administration improved the behavioural abnormalities in rats (2) ( n = 10/group). (A) The interaction of modelling treatment × administration ( F (3,72) = 2.922, p = .0397), modelling treatment ( F (3,72) = 5.029, p = .0032), and administration ( F (1,72) = 17.69, p <.0001) had a significant effect on the percentage of time spent in the open arm. (B) The interaction of modelling treatment × administration ( F (3,72) = 4.282, p = .0077), modelling treatment ( F (3,72) = 5.426, p = .0020), and administration ( F (1,72) = 31.58, p < .0001) had significant effects on the percentage of movement distance in the open arm. (C) The interaction of modelling treatment × administration ( F (3,72) = 0.604, p = .6146) and modelling treatment ( F (3,72) = 2.473, p = .0685) had no significant effect on the number of rats entering the open arm, while administration ( F (1,72) = 19.56, p < .0001) had a significant effect. (D) Modelling × administration ( F (3,72) = 22.16, p < .0001), modelling ( F (3,72) = 24.01, p < .0001), and administration ( F (1,72) = 86.79, p < .0001) had significant effects on the immobility time of rats. (E) Modelling × administration ( F (3,72) = 14.03, p < .0001), modelling ( F (3,72) = 126.3, p < .0001), and administration ( F (1,72) = 12.55, p = .0007) had significant effects on the weight gain of rats. (F) Schematic representation of the trajectories of rats in the elevated plus maze after saline administration. (G) Schematic representation of the trajectories of rats in the elevated plus maze after PRX administration. CON = control; Sal = saline; SPS&S = single prolonged stress and shock; CUMS = chronic unpredictable mild stress; S + C = SPS&S + CUMS. Data are presented as mean ± SEM . Statistical comparisons were performed using two-way analysis of variance followed by post-hoc tests. * p < .05, ** p < .01, **** p < .0001.

Article Snippet: In Phase 2, data from the eight treatment groups were analysed by two-way ANOVA, with model and drug as independent factors (Kuang et al., ).

Techniques: Saline, Control

Journal: European Journal of Psychotraumatology

Article Title: Modelling post-traumatic stress disorder–major depressive disorder comorbidity in rats: impaired α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor signalling is consistent with synergistic behavioural and cognitive deficits

doi: 10.1080/20008066.2026.2645520

Figure Lengend Snippet: Paroxetine (PRX) intervention improved the abnormal changes in the relative expression of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-related proteins and mRNA in rat hippocampus (HIP). (A) The interaction between modelling treatment × administration ( F (3,32) = 1.681, p = .1908) and modelling had no significant effect on glutamate receptor A1 (GluA1) protein expression in rats ( F (3,32) = 0.496, p = .6876), while administration had effect ( F (1,32) = 31.40, p < .0001). (B) The interaction of modelling treatment × administration ( F (3,32) = 6.769, p = .0012) and administration ( F (1,32) = 23.83, p < .0001) had a significant effect on the expression of GluA2 protein in rats, while modelling treatment ( F (3,32) = 2.225, p = .1043) had no significant effect. (C) The interaction of modelling treatment × administration ( F (3,32) = 1.129, p = .3522) and modelling ( F (3,32) = 1.749, p = .1767) had no significant effect on the expression of GluA3 protein in rats, but administration ( F (1,32) = 21.06, p < .0001) had a significant effect. (D) The interaction of modelling treatment × administration ( F (3,32) = 1.873, p = .1541) and modelling ( F (3,32) = 0.524, p = .6687) had no significant effect on the expression of mammalian target of rapamycin (mTOR) protein in rats, but administration ( F (1,32) = 23.73, p < .0001) had a significant effect. (E) The interaction of modelling treatment × administration ( F (3,32) = 2.938, p = .0481), modelling ( F (3,32) = 4.350, p = .0112), and administration ( F (1,32) = 38.08, p < .0001) had significant effects on the relative expression of GluA1 mRNA in rats. (F) The relative expression of GluA2 mRNA in rats was significantly affected by modelling × administration ( F (3,32) = 5.838, p = .0027), modelling ( F (3,32) = 21.58, p < .0001), and administration ( F (1,32) = 23.38, p < .0001). (G) Administration ( F (1,32) = 11.02, p = .0023) had a significant effect on the relative expression of GluA3 mRNA in rats, but modelling treatment × administration ( F (3,32) = 0.484 p = .6955) and modelling ( F (3,32) = 2.809, p = .0552) had no significant effect. (H) Administration ( F (1,32) = 35.36, p < .0001) had a significant effect on the relative expression of mTOR mRNA in rats, but modelling treatment × administration ( F (3,32) = 1.956, p = .1405) and modelling ( F (3,32) = 1.141, p = .3472) had no significant effect. CON = control; Sal = saline; SPS&S = single prolonged stress and shock; CUMS = chronic unpredictable mild stress; S + C = SPS&S + CUMS. Data are presented as mean ± SEM . Statistical comparisons were performed using two-way analysis of variance. * p < .05, ** p < .01, *** p < .001.

Article Snippet: In Phase 2, data from the eight treatment groups were analysed by two-way ANOVA, with model and drug as independent factors (Kuang et al., ).

Techniques: Expressing, Control, Saline

Journal: European Journal of Psychotraumatology

Article Title: Modelling post-traumatic stress disorder–major depressive disorder comorbidity in rats: impaired α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor signalling is consistent with synergistic behavioural and cognitive deficits

doi: 10.1080/20008066.2026.2645520

Figure Lengend Snippet: Paroxetine (PRX) intervention improved the abnormal changes in the relative expression of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-related proteins and mRNA in rat prefrontal cortex (PFC). (A) There was no significant difference in the expression of glutamate receptor A1 (GluA1) protein between modelling treatment × administration ( F (3,32) = 0.149, p = .9291) and modelling ( F (3,32) = 1.461, p = .2437), but there was a significant difference between modelling treatment × administration ( F (1,32) = 37.97, p < .0001). (B) There was no significant effect of modelling treatment × administration ( F (3,32) = 1.825, p = .1625), modelling ( F (3,32) = 0.875, p = .4643) and administration ( F (1,32) = 1.469, p = .2344) on the expression of GluA2 protein in rats. (C) There was no significant difference in the expression of GluA3 protein between modelling treatment × administration ( F (3,32) = 2.817, p = .0547) and modelling ( F (3,32) = 0.709, p = .5537), but administration ( F (1,32) = 5.483, p = .0256) had a significant effect. (D) The expression of mammalian target of rapamycin (mTOR) protein was significantly affected by modelling × administration ( F (3,32) = 4.443, p = .0102), modelling ( F (3,32) = 6.104, p = .0021), and administration ( F (1,32) = 18.89, p = .0001). (E) There was no significant difference in the relative expression of GluA1 mRNA between modelling treatment × administration ( F (3,32) = 2.049, p = .1267) and modelling ( F (3,32) = 0.447, p = .7214), but administration ( F (1,32) = 8.040, p = .0079) had a significant effect. (F) The relative expression of GluA1 mRNA in rats was not significantly affected by modelling treatment × administration ( F (3,32) = 1.665, p = .1940), but was significantly affected by modelling ( F (3,32) = 3.641, p = .0229) and administration ( F (1,32) = 28.66, p < .0001). (G) There was no significant effect of modelling treatment × administration ( F (3,32) = 0.343, p = .7942), modelling ( F (3,32) = 0.661, p = .5822), and administration ( F (1,32) = 0.104, p = .7491) on the relative expression of GluA3 mRNA in rats. (H) The relative expression of mTOR mRNA was significantly affected by modelling treatment × administration ( F (3,32) = 4.111, p = .0142) and administration ( F (1,32) = 14.47, p = .0006), but not by modelling ( F (3,32) = 2.424, p = .0839). CON = control; Sal = saline; SPS&S = single prolonged stress and shock; CUMS = chronic unpredictable mild stress; S + C = SPS&S + CUMS. Data are presented as mean ± SEM . Statistical comparisons were performed using two-way analysis of variance. * p < .05, ** p < .01.

Article Snippet: In Phase 2, data from the eight treatment groups were analysed by two-way ANOVA, with model and drug as independent factors (Kuang et al., ).

Techniques: Expressing, Control, Saline

Journal: European Journal of Psychotraumatology

Article Title: Modelling post-traumatic stress disorder–major depressive disorder comorbidity in rats: impaired α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor signalling is consistent with synergistic behavioural and cognitive deficits

doi: 10.1080/20008066.2026.2645520

Figure Lengend Snippet: Paroxetine (PRX) intervention improved the abnormal changes in the relative expression of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-related proteins and mRNA in rat amygdala (AMY). (A) There was no significant effect of modelling × administration ( F (3,32) = 2.398, p = .0863) on the expression of glutamate receptor A1 (GluA1) protein in rats, but there were significant effects of modelling ( F (3,32) = 3.811, p = .0192) and administration ( F (1,32) = 7.713, p = .0091). (B) The expression of GluA2 protein was significantly affected by modelling × administration ( F (3,32) = 2.920, p = .0490), modelling ( F (3,32) = 6.024, p = .0023, and administration ( F (1,32) = 9.133, p = .0049). (C) The expression of GluA3 protein was significantly affected by modelling × administration ( F (3,32) = 7.110, p = .0009) and modelling ( F (3,32) = 9.998, p < .0001), but not by administration ( F (1,32) = 3.287, p = .0792). (D) Neither modelling × administration ( F (3,32) = 2.621, p = .0677) nor modelling ( F (3,32) = 0.169, p = .9162) had a significant effect on mammalian target of rapamycin (mTOR) protein expression, while administration ( F (1,32) = 6.338, p = .0170) had a significant effect. (E) The relative expression of GluA1 mRNA was not significantly affected by modelling treatment × administration ( F (3,32) = 2.028, p = .1296), but was significantly affected by modelling ( F (3,32) = 6.011, p = .0023) and administration ( F (1,32) = 13.81, p = .0008). (F) The relative expression of GluA2 mRNA was significantly affected by modelling treatment × administration ( F (3,32) = 3.666, p = .0223) and modelling ( F (3,32) = 4.946, p = .0062), but not by administration ( F (1,32) = 1.052, p = .3128). (G) There was no significant effect of modelling treatment × administration ( F (3,32) = 0.573, p = .6371), modelling ( F (3,32) = 2.322, p = .0938), or administration ( F (1,32) = 0.062, p = .8047) on the relative expression of GluA3 mRNA. (H) The relative expression of mTOR mRNA was not significantly affected by modelling treatment × administration ( F (3,32) = 0.633, p = .5992), but was significantly affected by modelling ( F (3,32) = 5.880, p = .0026) and administration ( F (1,32) = 5.565, p = .0246). CON = control; Sal = saline; SPS&S = single prolonged stress and shock; CUMS = chronic unpredictable mild stress; S + C = SPS&S + CUMS. Data are presented as mean ± SEM . Statistical comparisons were performed using two-way analysis of variance. * p < .05.

Article Snippet: In Phase 2, data from the eight treatment groups were analysed by two-way ANOVA, with model and drug as independent factors (Kuang et al., ).

Techniques: Expressing, Control, Saline