2.2.2. Derecho Constitucional a la identidad personal
2.2.2.5. Definición
2.2.2.5.2. Características
7.3.2/ Effects of pCPA on the noradrenergic resp onse to CNS agents
The basal dialysate levels of noradrenaline (samples collected between T^o-To) were not affected by the pCPA treatment. Pooled data for the 3 groups of animals (6^-amphetamine, BTS 54 354 or atipamezole, alone, with and without pCPA) gave basal efflux of: frontal cortex: 9 ± 1 fmol/20 min in control and pCPA treated animals (F 1,61 = 0.57, P = 0.45); and hypothalamus: 8 ± 1 fmol/20 min and 9 ± 1 fmol/20 min in
control and pCPA treated animals, respectively (F 1,54 = 0.19, F = 0.67).
7.3.2.1/ Effects o f pCP4 on the noradrenergic response to Iocai infusion o f 6-amphetamine (10 fiM)
In the frontal cortex, administration of ^/-amphetamine increased noradrenaline efflux in both groups of rats (time effect between Tq-Tôo for control and pCPA treated rats: F 3 , 3 3 = 6.91, P < 0.01 and F 3,24 = 19.33, P < 0.001, respectively) (Figure 7.2 A; for basal levels refer to Table 7.2). The maximum increase was 19 ± 6 fmol/20 min (40 min after start of infusion) and 36 ± 5 fmol/20 min (100 min after start of infusion), in control and pCPA treated rats, respectively. Over the period T40-T220, this increase was greater in
rats that had been treated with pCPA (F i,ig = 7.97, P = 0.01). Also, in pCPA treated rats, there was no longer any attenuation of the response seen after T140 in control rats. Finally,
comparing the noradrenaline efflux after Two in animals receiving (/-amphetamine after administration of pCPA and animals receiving atipamezole and d-amphetamine (refer to Chapter 6), the increase was greater in the former group over the period T160-T200
(F 1,17 = 4.94, P < 0.05) (Figure 7.2 A).
Similarly, in the hypothalamus, administration of d-amphetamine increased noradrenaline efflux in both groups of rats (time effect for control and pCPA treated rats: T-40-T40, F4,4o = 4.07, P = 0.05 and Tq-Tôo, F3,24 = 27.28, P < 0.001, respectively)
(Figure 7.2 B; for basal levels refer to Table 7.2). The maximum increase was 24 ± 7 fmol/20 min (100 min after start of infusion) and 25 ± 4 fmol/20 min (80 min after start of infusion) in control and pCPA treated rats, respectively. There was no difference
received pCPA, there was no longer any attenuation of the noradrenaline efflux seen after Ti4o in control rats. The increase in noradrenaline efflux was greater than that seen in rats
not pretreated with pCPA over the period T160-T220 (F i.is = 8.36, P = 0.01). It was also
greater than that seen in animals receiving atipamezole and (/-amphetamine (refer to Chapter 6) over the period T160-T200 (F i,ig = 12,89, P < 0.01) (Figure 7.2 B).
N.B : Animals in the groups dAMP and Ati + dAMP are different from those discussed in Chapter 6. However, the same findings emerged from the data collected so they are not discussed further here.
Table 7.2 Basal efflux of noradrenaline in animals treated with 6-amphetamine. Basais (fmol/20min) T,40"To N FCx Hyp dAMP 6 ± 1 9 ± 2 . 12 pCPA/dAM P 11 ± 2 8 ± 1 9 Ati + dAMP 5 ± 1 5 ± 1 12
dAMP represents animals having received d-amphetamine only; pCPA / dAMP represents animals treated with pCPA and d-amphetamine; Ati + dAMP represents animals having received d-amphetamine after administration of atipamezole.
Values show mean ± s.e. mean noradrenaline basal efflux (fmol/20 min).
C hapter 7: Modulation of the noradrenergic response to local 6-amphetamine and sibutramine by the serotonergic system
■ dAMP
■ pCPA/dAMP
■ Ati + dAMP dAMP
1
FCx 50 - 'E' I 40- E 30 - X 3 20 - c 3 10 - -10 -60 0 60 120 180 240 ■ dAMP ■ pC PA/dAMP Time (min) dAMP Ad + dAMP 60 -1 Hyp 50 - 40 - 30 - 20 - 10 - -10 -60 0 60 120 180 240 Time (min)F igure 7.2. The effects ofipCPA on the noradrenaline ( ‘N A ') response to local infusion o f d-amphetamine ( ‘dAMP') 10 pM in the frontal cortex (FCx) or hypothalamus (Hyp) o f freely-moving rats.
‘dAMP’ is the control group. The group ‘pCPA / dAMP’ received a pretreatment of pCPA and the group ‘Ati -fdAMP’ received a systemic injection of the (%2-adrenoceptor antagonist,
atipamezole (‘Ati’, 1 mg/kg), 2h before the beginning of infusion. In the three groups of rats, infusion of ^/-amphetamine started at To and was maintained for the following 220 min, as indivated by = . Points show mean ± s.e. mean noradrenaline efflux in: A, the frontal cortex and, B, the hypothalamus. * F < 0.05, ** p < 0.01, c.f dAMP / pCPA dAMP.
7.3.2.2/Effects ofpCPA on the noradrenergic response to Iocai infusion of BTS 54 354 (50 pM)
In the frontal cortex, administration of BTS 54 354 increased noradrenaline efflux in control rats with a maximum increase of 14 ± 3 fmol/20 min (40 min after start of infusion) (Table 7.3 and Figure 7.3 A; for basal levels refer to Table 7.4). However, when rats were pretreated with pCPA, the response to BTS 54 354 was abolished. The efflux in control rats was greater than that in rats treated with /?CPA over the period T20-T240
(F 1,10 = 8.17, P < 0.05).
In the hypothalamus, administration of BTS 54 354 increased noradrenaline efflux in both groups of rats with a maximum increase o f 17 ± 5 fmol/20 min (80 min after start of infusion) and 13 ± 2 fmol/20 min (140 min after start of infusion) in control and pCPA treated rats, respectively (Table 7.3 and Figure 7.3 B; for basal levels refer to Table 7.4). There was no difference in the increase in noradrenaline efflux in animals that had or had not received pCPA (Figure 7.3 B).
Table 7.3 Statistics generated from split-plot ANOVA summarising the effects o f administration o f BTS 54 354 50 pM in control rats or in rats treated with pCPA on noradrenaline efflux, in the frontal cortex (FCx) and the hypothalamus (Hyp).
BTS 54 354 50 pM pCPA/BTS 54 354 50 pM FCx Hyp FCx Hyp Time Tao'Teo Fi,20= 66.76 P < 0.001 Fi^4= 10.60 P<0.01 Fi,io= 0.02 P = 0.B8 Fi,7= 26.27 P = 0.001 Tb0"Ti20 F i^ = 18.60 P < 0.001 Fu4= 10.62 P<0.01 Fi,io= 0.20 P = 0.67 Fi,7= 11.40 P < 0.05 Ti40‘Ti80 F i^ = 5.26 P< 0.05 Fu4 = 5.82 P < 0 .0 5 Fi,9= 1.76 P=0.22 Fi.7= 19.07 P<0.01 T200‘T240 F i^ = 5.04 P <0.05 Fi^ = 4.27 P < 0 .0 5 Fi,9=0.28 P = 0.61 Fi.7= 14.90 P<0.01
Noradrenaline efflux after each treatment was compared, over 1-h increments, with efflux in the cluster of basal samples (Refer to section 2.3.4). The significant differences are in bold.
Chapter 7: Modulation of the noradrenergic response to iocai 6-amphetamine and sibutramine by