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Serotonin1A receptor deletion does not interact with maternal separation-induced increases in startle reactivity and prepulse inhibition deficits.

Groenink L, Bijlsma EY, van Bogaert MJ, Oosting RS, Olivier B - Psychopharmacology (Berl.) (2010)

Bottom Line: These effects of MS were independent of genotype.MS had no effect on the other readouts.Serotonin(1A) receptor deletion does not enhance vulnerability to the effects of MS on startle plasticity.

View Article: PubMed Central - PubMed

Affiliation: Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Sorbonnelaan 16, 3584 CA, Utrecht, The Netherlands. l.groenink@uu.nl

ABSTRACT

Rationale: Early life stress is a risk factor for the development of psychopathology in later life. Consequences of adverse life events, however, may depend on the genetic makeup of an individual. Reduced serotonin(1A) receptor function may predispose to the development of anxiety disorders.

Objective: Determine susceptibility of serotonin(1A) receptor knockout (1AKO) mice on different background strains to the effects of maternal separation (MS) by assessing startle plasticity in adulthood.

Methods: 1AKO mice on a 129S6 and a Swiss Webster (SW) background were used. MS groups were separated daily from their mother for 180 min/day from postnatal days 2 to 14. Control groups underwent normal animal facility rearing. In adulthood, effects on acoustic startle response, habituation, prepulse inhibition (PPI), and foot shock sensitization were determined.

Results: MS increased startle reactivity and reduced PPI in 129S6 mice. These effects of MS were independent of genotype. MS had no effect on the other readouts. In SW mice, MS had no consistent effect on startle reactivity and did not alter startle plasticity in wild type or in 1AKO mice. 1AKO mice did not differ from wild-type mice in startle plasticity.

Conclusion: Serotonin(1A) receptor deletion does not enhance vulnerability to the effects of MS on startle plasticity. The life-long increase in startle reactivity and PPI deficit induced by MS are strain-dependent. Further, the use of startle reactivity and plasticity may have added value in translational studies relating to early life stress.

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PPI of the acoustic startle response. Effect of MS (gray bars) on percent PPI measured at different prepulse intensities, in 129S6 (a, b, c) and SW mice (d, e). White bars show the response of AFR mice (control, white bars). In panela, the effects on wild-type and 1AKO 129S6 mice are taken together, as the effects of MS were independent of genotype. Panelsb–e show the effect of MS for the separate genotypes. Differences between wild-type and 1AKO mice can be inferred by comparing the white bars in panelsb and c for 129S6, and white bars in panelsd and e for SW. Pearson’s correlation showed that startle magnitude and mean PPI levels were not correlated (r = -0.17, NS, n = 63). Data represent means ± SEM. *p < 0.05 relative to corresponding control
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Fig3: PPI of the acoustic startle response. Effect of MS (gray bars) on percent PPI measured at different prepulse intensities, in 129S6 (a, b, c) and SW mice (d, e). White bars show the response of AFR mice (control, white bars). In panela, the effects on wild-type and 1AKO 129S6 mice are taken together, as the effects of MS were independent of genotype. Panelsb–e show the effect of MS for the separate genotypes. Differences between wild-type and 1AKO mice can be inferred by comparing the white bars in panelsb and c for 129S6, and white bars in panelsd and e for SW. Pearson’s correlation showed that startle magnitude and mean PPI levels were not correlated (r = -0.17, NS, n = 63). Data represent means ± SEM. *p < 0.05 relative to corresponding control

Mentions: MS reduced percent PPI similarly in wild-type and 1AKO mice, but the effect of MS was dependent on prepulse intensity (F3,96 = 5.6, p = 0.001). As shown in Fig. 3a, the differences between AFR and MS mice were significant at 2 and 4 dB prepulse intensity. PPI in 1AKO mice did not differ from that of wild-type mice (see Fig. 3b, c). Startle magnitude was significantly higher in MS mice, irrespective of genotype (F1,32 = 12.6, p = 0.001; control mice 758 ± 88.7, MS mice 1150.2 ± 119).Fig. 3


Serotonin1A receptor deletion does not interact with maternal separation-induced increases in startle reactivity and prepulse inhibition deficits.

Groenink L, Bijlsma EY, van Bogaert MJ, Oosting RS, Olivier B - Psychopharmacology (Berl.) (2010)

PPI of the acoustic startle response. Effect of MS (gray bars) on percent PPI measured at different prepulse intensities, in 129S6 (a, b, c) and SW mice (d, e). White bars show the response of AFR mice (control, white bars). In panela, the effects on wild-type and 1AKO 129S6 mice are taken together, as the effects of MS were independent of genotype. Panelsb–e show the effect of MS for the separate genotypes. Differences between wild-type and 1AKO mice can be inferred by comparing the white bars in panelsb and c for 129S6, and white bars in panelsd and e for SW. Pearson’s correlation showed that startle magnitude and mean PPI levels were not correlated (r = -0.17, NS, n = 63). Data represent means ± SEM. *p < 0.05 relative to corresponding control
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3045511&req=5

Fig3: PPI of the acoustic startle response. Effect of MS (gray bars) on percent PPI measured at different prepulse intensities, in 129S6 (a, b, c) and SW mice (d, e). White bars show the response of AFR mice (control, white bars). In panela, the effects on wild-type and 1AKO 129S6 mice are taken together, as the effects of MS were independent of genotype. Panelsb–e show the effect of MS for the separate genotypes. Differences between wild-type and 1AKO mice can be inferred by comparing the white bars in panelsb and c for 129S6, and white bars in panelsd and e for SW. Pearson’s correlation showed that startle magnitude and mean PPI levels were not correlated (r = -0.17, NS, n = 63). Data represent means ± SEM. *p < 0.05 relative to corresponding control
Mentions: MS reduced percent PPI similarly in wild-type and 1AKO mice, but the effect of MS was dependent on prepulse intensity (F3,96 = 5.6, p = 0.001). As shown in Fig. 3a, the differences between AFR and MS mice were significant at 2 and 4 dB prepulse intensity. PPI in 1AKO mice did not differ from that of wild-type mice (see Fig. 3b, c). Startle magnitude was significantly higher in MS mice, irrespective of genotype (F1,32 = 12.6, p = 0.001; control mice 758 ± 88.7, MS mice 1150.2 ± 119).Fig. 3

Bottom Line: These effects of MS were independent of genotype.MS had no effect on the other readouts.Serotonin(1A) receptor deletion does not enhance vulnerability to the effects of MS on startle plasticity.

View Article: PubMed Central - PubMed

Affiliation: Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Sorbonnelaan 16, 3584 CA, Utrecht, The Netherlands. l.groenink@uu.nl

ABSTRACT

Rationale: Early life stress is a risk factor for the development of psychopathology in later life. Consequences of adverse life events, however, may depend on the genetic makeup of an individual. Reduced serotonin(1A) receptor function may predispose to the development of anxiety disorders.

Objective: Determine susceptibility of serotonin(1A) receptor knockout (1AKO) mice on different background strains to the effects of maternal separation (MS) by assessing startle plasticity in adulthood.

Methods: 1AKO mice on a 129S6 and a Swiss Webster (SW) background were used. MS groups were separated daily from their mother for 180 min/day from postnatal days 2 to 14. Control groups underwent normal animal facility rearing. In adulthood, effects on acoustic startle response, habituation, prepulse inhibition (PPI), and foot shock sensitization were determined.

Results: MS increased startle reactivity and reduced PPI in 129S6 mice. These effects of MS were independent of genotype. MS had no effect on the other readouts. In SW mice, MS had no consistent effect on startle reactivity and did not alter startle plasticity in wild type or in 1AKO mice. 1AKO mice did not differ from wild-type mice in startle plasticity.

Conclusion: Serotonin(1A) receptor deletion does not enhance vulnerability to the effects of MS on startle plasticity. The life-long increase in startle reactivity and PPI deficit induced by MS are strain-dependent. Further, the use of startle reactivity and plasticity may have added value in translational studies relating to early life stress.

Show MeSH
Related in: MedlinePlus