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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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Foot shock sensitization of the acoustic startle response. Mean startle magnitude (in arbitrary units ± SEM) before, after, and upon re-exposure to the context 24 h later. Left panel shows the effect in the 129S6 strain (wild-type and 1AKO together), while right panel shows the effect in the SW strain (wild-type and 1AKO mice together). Effects on wild-type and 1AKO mice are not shown separately, as the effects of foot shock and MS were independent of genotype. The significant overall effect of MS (black triangles) on startle reactivity in 129S6 mice is not indicated in the left panel, as the effect of foot shock was independent of rearing condition. * p < 0.05 relative to pre-shock for control and MS groups together
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Fig4: Foot shock sensitization of the acoustic startle response. Mean startle magnitude (in arbitrary units ± SEM) before, after, and upon re-exposure to the context 24 h later. Left panel shows the effect in the 129S6 strain (wild-type and 1AKO together), while right panel shows the effect in the SW strain (wild-type and 1AKO mice together). Effects on wild-type and 1AKO mice are not shown separately, as the effects of foot shock and MS were independent of genotype. The significant overall effect of MS (black triangles) on startle reactivity in 129S6 mice is not indicated in the left panel, as the effect of foot shock was independent of rearing condition. * p < 0.05 relative to pre-shock for control and MS groups together

Mentions: As shown in Fig. 4a, presentation of foot shocks increased the startle response (F2,80 = 23, p < 0.001), measured post-shock (F1,40 = 49.1, p < 0.001), and 24 h later (F1,40 = 13.2, p = 0.001). These effects of foot shock were independent of rearing condition and genotype. No significant differences were observed between wild-type and 1AKO mice in this procedure (see Table 2). Foot shock reactivity to the shocks per se was similar for all experimental groups (wt-control 1,536 ± 87.6, 1AKO-control 1,289 ± 72.8, wt-MS 1,346 ± 86.7, 1AKO-MS 1,324 ± 56.7).Table 2


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)

Foot shock sensitization of the acoustic startle response. Mean startle magnitude (in arbitrary units ± SEM) before, after, and upon re-exposure to the context 24 h later. Left panel shows the effect in the 129S6 strain (wild-type and 1AKO together), while right panel shows the effect in the SW strain (wild-type and 1AKO mice together). Effects on wild-type and 1AKO mice are not shown separately, as the effects of foot shock and MS were independent of genotype. The significant overall effect of MS (black triangles) on startle reactivity in 129S6 mice is not indicated in the left panel, as the effect of foot shock was independent of rearing condition. * p < 0.05 relative to pre-shock for control and MS groups together
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3045511&req=5

Fig4: Foot shock sensitization of the acoustic startle response. Mean startle magnitude (in arbitrary units ± SEM) before, after, and upon re-exposure to the context 24 h later. Left panel shows the effect in the 129S6 strain (wild-type and 1AKO together), while right panel shows the effect in the SW strain (wild-type and 1AKO mice together). Effects on wild-type and 1AKO mice are not shown separately, as the effects of foot shock and MS were independent of genotype. The significant overall effect of MS (black triangles) on startle reactivity in 129S6 mice is not indicated in the left panel, as the effect of foot shock was independent of rearing condition. * p < 0.05 relative to pre-shock for control and MS groups together
Mentions: As shown in Fig. 4a, presentation of foot shocks increased the startle response (F2,80 = 23, p < 0.001), measured post-shock (F1,40 = 49.1, p < 0.001), and 24 h later (F1,40 = 13.2, p = 0.001). These effects of foot shock were independent of rearing condition and genotype. No significant differences were observed between wild-type and 1AKO mice in this procedure (see Table 2). Foot shock reactivity to the shocks per se was similar for all experimental groups (wt-control 1,536 ± 87.6, 1AKO-control 1,289 ± 72.8, wt-MS 1,346 ± 86.7, 1AKO-MS 1,324 ± 56.7).Table 2

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