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Psychopharmacological characterisation of the successive negative contrast effect in rats.

Phelps CE, Mitchell EN, Nutt DJ, Marston HM, Robinson ES - Psychopharmacology (Berl.) (2015)

Bottom Line: The α2-adrenoceptor antagonist, yohimbine, increased premature responding but had no specific effect on SNC.These data suggest that the SNC effect is mediated, at least in part, by dopamine signalling.The SNC effect may also be attenuated by benzodiazepine anxiolytics.

View Article: PubMed Central - PubMed

Affiliation: School of Physiology and Pharmacology, University of Bristol, Medical Sciences Building, University Walk, Bristol, BS8 1TD, UK.

ABSTRACT

Rationale: Successive negative contrast (SNC) describes a change in the behaviour of an animal following a downshift in the quantitative or qualitative value of an expected reward. This behavioural response has been hypothesised to be linked to affective state, with negative states associated with larger and/or prolonged shifts in behaviour.

Objective: This study has investigated whether different psychopharmacological treatments have dissociable actions on the SNC effect in rats and related these findings to their actions on different neurotransmitter systems and affective state.

Methods: Animals were trained to perform a nose-poke response to obtain a high-value food reward (four pellets). SNC was quantified during devalue sessions in which the reward was reduced to one pellet. Using a within-subject study design, the effects of acute treatment with anxiolytic, anxiogenic, antidepressant and dopaminergic drugs were investigated during both baseline (four pellets) or devalue sessions (one pellet).

Results: The indirect dopamine agonist, amphetamine, attenuated the SNC effect whilst the D1/D2 antagonist, alpha-flupenthixol, potentiated it. The antidepressant citalopram, anxiolytic buspirone and anxiogenic FG7142 had no specific effects on SNC, although FG7142 induced general impairments at higher doses. The α2-adrenoceptor antagonist, yohimbine, increased premature responding but had no specific effect on SNC. Results for the anxiolytic diazepam were mixed with one group showing an attenuation of the SNC effect whilst the other showed no effect.

Conclusions: These data suggest that the SNC effect is mediated, at least in part, by dopamine signalling. The SNC effect may also be attenuated by benzodiazepine anxiolytics.

No MeSH data available.


Effects of systemic treatment with diazepam (0.0–1.0 mg/kg, i.p.) on performance variables in operant SNC in the second cohort of rats tested. There was a significant main effect of SESSION for correct latency, collection latency and omissions. Diazepam (0.3 mg/kg) significantly attenuated the SNC effect on correct latency. There was no effect of DOSE on the other variable parameters. Results are shown as mean ± SEM, n = 12 animals per group, within-subject, *p < 0.05, **p < 0.01, ***p < 0.001 pairwise comparison between baseline and devalue session following vehicle pretreatment. #p < 0.05 pairwise comparisons vehicle vs drug on baseline or devalue sessions
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Fig2: Effects of systemic treatment with diazepam (0.0–1.0 mg/kg, i.p.) on performance variables in operant SNC in the second cohort of rats tested. There was a significant main effect of SESSION for correct latency, collection latency and omissions. Diazepam (0.3 mg/kg) significantly attenuated the SNC effect on correct latency. There was no effect of DOSE on the other variable parameters. Results are shown as mean ± SEM, n = 12 animals per group, within-subject, *p < 0.05, **p < 0.01, ***p < 0.001 pairwise comparison between baseline and devalue session following vehicle pretreatment. #p < 0.05 pairwise comparisons vehicle vs drug on baseline or devalue sessions

Mentions: Diazepam showed a tendency to attenuate the devalue effect. In both cohorts of animals tested, there was an effect of devaluation with a main effect of SESSION for correct latency (F(1, 11) = 12.23, p = 0.005, Fig. 1a; F(1, 10) = 28.872, p < 0.001, Fig. 2a) and collection latency (F(1, 11) = 38.65, p < 0.001, Fig. 1b; F(1, 10) = 66.41, p < 0.001, Fig. 2b). Post hoc pairwise comparisons revealed a devalue effect between vehicle-treated baseline and vehicle-treated devalue sessions with increases in both correct (p = 0.007, Fig. 1a; p = 0.001, Fig. 2a) and collection (p = 0.002, Fig. 1b; p < 0.001, Fig. 2b) latencies (Figs. 1b and 2b). There was a trend towards a main effect of SESSION in the first group for omissions (F(1, 11) = 4.48, p = 0.058, Fig. 1d) and a main effect of SESSION in the second group (F(1, 10) = 5.54, p = 0.040, Fig. 2d). Post hoc pairwise comparisons for the second group showed a significant devalue effect under vehicle treatment (p = 0.02).Fig. 1


Psychopharmacological characterisation of the successive negative contrast effect in rats.

Phelps CE, Mitchell EN, Nutt DJ, Marston HM, Robinson ES - Psychopharmacology (Berl.) (2015)

Effects of systemic treatment with diazepam (0.0–1.0 mg/kg, i.p.) on performance variables in operant SNC in the second cohort of rats tested. There was a significant main effect of SESSION for correct latency, collection latency and omissions. Diazepam (0.3 mg/kg) significantly attenuated the SNC effect on correct latency. There was no effect of DOSE on the other variable parameters. Results are shown as mean ± SEM, n = 12 animals per group, within-subject, *p < 0.05, **p < 0.01, ***p < 0.001 pairwise comparison between baseline and devalue session following vehicle pretreatment. #p < 0.05 pairwise comparisons vehicle vs drug on baseline or devalue sessions
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4502301&req=5

Fig2: Effects of systemic treatment with diazepam (0.0–1.0 mg/kg, i.p.) on performance variables in operant SNC in the second cohort of rats tested. There was a significant main effect of SESSION for correct latency, collection latency and omissions. Diazepam (0.3 mg/kg) significantly attenuated the SNC effect on correct latency. There was no effect of DOSE on the other variable parameters. Results are shown as mean ± SEM, n = 12 animals per group, within-subject, *p < 0.05, **p < 0.01, ***p < 0.001 pairwise comparison between baseline and devalue session following vehicle pretreatment. #p < 0.05 pairwise comparisons vehicle vs drug on baseline or devalue sessions
Mentions: Diazepam showed a tendency to attenuate the devalue effect. In both cohorts of animals tested, there was an effect of devaluation with a main effect of SESSION for correct latency (F(1, 11) = 12.23, p = 0.005, Fig. 1a; F(1, 10) = 28.872, p < 0.001, Fig. 2a) and collection latency (F(1, 11) = 38.65, p < 0.001, Fig. 1b; F(1, 10) = 66.41, p < 0.001, Fig. 2b). Post hoc pairwise comparisons revealed a devalue effect between vehicle-treated baseline and vehicle-treated devalue sessions with increases in both correct (p = 0.007, Fig. 1a; p = 0.001, Fig. 2a) and collection (p = 0.002, Fig. 1b; p < 0.001, Fig. 2b) latencies (Figs. 1b and 2b). There was a trend towards a main effect of SESSION in the first group for omissions (F(1, 11) = 4.48, p = 0.058, Fig. 1d) and a main effect of SESSION in the second group (F(1, 10) = 5.54, p = 0.040, Fig. 2d). Post hoc pairwise comparisons for the second group showed a significant devalue effect under vehicle treatment (p = 0.02).Fig. 1

Bottom Line: The α2-adrenoceptor antagonist, yohimbine, increased premature responding but had no specific effect on SNC.These data suggest that the SNC effect is mediated, at least in part, by dopamine signalling.The SNC effect may also be attenuated by benzodiazepine anxiolytics.

View Article: PubMed Central - PubMed

Affiliation: School of Physiology and Pharmacology, University of Bristol, Medical Sciences Building, University Walk, Bristol, BS8 1TD, UK.

ABSTRACT

Rationale: Successive negative contrast (SNC) describes a change in the behaviour of an animal following a downshift in the quantitative or qualitative value of an expected reward. This behavioural response has been hypothesised to be linked to affective state, with negative states associated with larger and/or prolonged shifts in behaviour.

Objective: This study has investigated whether different psychopharmacological treatments have dissociable actions on the SNC effect in rats and related these findings to their actions on different neurotransmitter systems and affective state.

Methods: Animals were trained to perform a nose-poke response to obtain a high-value food reward (four pellets). SNC was quantified during devalue sessions in which the reward was reduced to one pellet. Using a within-subject study design, the effects of acute treatment with anxiolytic, anxiogenic, antidepressant and dopaminergic drugs were investigated during both baseline (four pellets) or devalue sessions (one pellet).

Results: The indirect dopamine agonist, amphetamine, attenuated the SNC effect whilst the D1/D2 antagonist, alpha-flupenthixol, potentiated it. The antidepressant citalopram, anxiolytic buspirone and anxiogenic FG7142 had no specific effects on SNC, although FG7142 induced general impairments at higher doses. The α2-adrenoceptor antagonist, yohimbine, increased premature responding but had no specific effect on SNC. Results for the anxiolytic diazepam were mixed with one group showing an attenuation of the SNC effect whilst the other showed no effect.

Conclusions: These data suggest that the SNC effect is mediated, at least in part, by dopamine signalling. The SNC effect may also be attenuated by benzodiazepine anxiolytics.

No MeSH data available.