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CRF1 receptor antagonists do not reverse pharmacological disruption of prepulse inhibition in rodents

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Abstract

Rationale

As enhanced corticotropin-releasing factor (CRF) transmission is associated with induction of sensorimotor gating deficits, CRF1 receptor antagonists may reverse disrupted prepulse inhibition (PPI), an operational measure of sensorimotor gating.

Objectives

To determine the effects of CRF1 receptor antagonists in pharmacological models of disrupted PPI and to determine if long-term elevated central CRF levels alter sensitivity towards PPI disrupting drugs.

Methods

CP154,526 (10–40 mg/kg), SSR125543 (3–30 mg/kg) and DMP695 (40 mg/kg) were tested on PPI disruption provoked by d-amphetamine (2.5, 3 mg/kg), ketamine (5, 30 mg/kg) and MK801 (0.2, 0.5 mg/kg) in Wistar rats, C57Bl/6J and CD1 mice, and on spontaneously low PPI in Iffa Credo rats and DBA/2J mice. PPI-disrupting effects of d-amphetamine (2.5–5 mg/kg) and MK801 (0.3–1 mg/kg) were examined in CRF-overexpressing (CRFtg) mice, which display PPI deficits. Finally, we determined the influence of CP154,526 on d-amphetamine-induced dopamine outflow in nucleus accumbens and prefrontal cortex of CRFtg mice using in vivo microdialysis.

Results

No CRF1−antagonists improved PPI deficits in any test. CRFtg mice showed blunted PPI disruption in response to MK801, but not d-amphetamine. Further, d-amphetamine-induced dopamine release was less pronounced in CRFtg versus wild-type mice, a response normalized by pretreatment with CP154,526.

Conclusion

The inability of CRF1 receptor antagonists to block pharmacological disruption of sensorimotor gating suggests that the involvement of CRF1 receptors in the modulation of dopaminergic and glutamatergic neurotransmission relevant for sensory gating is limited. Furthermore, the alterations observed in CRFtg mice support the notion that long-term elevated central CRF levels induce changes in these neurotransmitter systems.

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Acknowledgements

We thank Gerdien Korte-Bouws for conducting and analyzing the HPLC studies and Elisabeth Y Bijlsma for valuable discussions regarding the content of this manuscript.

Conflicts of interest

The authors have no conflicts of interest to disclose. In the past 5 years, LG received research grants/support from PsychoGenics Inc. and Servier. BO received research grants/support from Emotional Brain, PsychoGenics Inc., Sepracor and Lundbeck and acted as advisor for Lundbeck. MJM is a full-time employee of Servier, BD and GG are full-time employees of Sanofi.

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Authors and Affiliations

  1. Department of Pharmacology, Utrecht Institute for Pharmaceutical Sciences and Brain Center Rudolf Magnus, Utrecht, The Netherlands

    T. N. Douma, P. M. Verdouw, K. G. Westphal, B. Olivier & L. Groenink

  2. Department of Psychopharmacology, Institut de Recherches SERVIER, Croissy-sur-Seine, France

    M. J. Millan

  3. Sanofi R&D, Exploratory Unit, Chilly-Mazarin, France

    D. Boulay & G. Griebel

  4. Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA

    B. Olivier

  5. Utrecht University, Universiteitsweg 99, Utrecht, The Netherlands

    L. Groenink

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  1. T. N. Douma
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Correspondence to L. Groenink.

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Douma, T.N., Millan, M.J., Boulay, D. et al. CRF1 receptor antagonists do not reverse pharmacological disruption of prepulse inhibition in rodents. Psychopharmacology 231, 1289–1303 (2014). https://doi.org/10.1007/s00213-013-3315-2

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