Chronic infusion of a CRH 1 receptor antisense oligodeoxynucleotide into the central nucleus of the amygdala reduced anxiety-related behavior in socially defeated rats

Chronic infusion of a CRH 1 receptor antisense oligodeoxynucleotide into the central nucleus of... We studied the role of central amygdala CRH receptors in behavioral responses to an anxiogenic stimulus. An antisense oligodeoxynucleotide corresponding to the rat CRH 1 receptor mRNA was infused chronically into the central amygdaloid nucleus of male rats via osmotic minipumps (0.25 μg/0.5 μl/h). Control groups received infusions of either a scrambled sequence oligodeoxynucleotide or vehicle. On the 4th day of treatment, rats were subjected to 10 min of social defeat and immediately afterwards tested on the elevated plus-maze. Antisense oligodeoxynucleotide-treated rats spent significantly more time exploring the open arms of the plus-maze than scrambled sequence- and vehicle-treated animals, both of which did not differ from each other. The social discrimination test, on the other hand, revealed no difference in juvenile recognition abilities among the treatment groups. Using in situ hybridization and receptor autoradiography, we were not able to detect clear signals of CRH 1 receptor mRNA and CRH binding sites in the central amygdaloid nucleus of either group, confirming the reportedly low expression and density of CRH receptors in this brain area. The present data support the view that CRH receptors in the central nucleus of the amygdala are involved in the mediation and expression of anxiety-related behavior, but simultaneously raise questions as to the mechanisms of antisense oligodeoxynucleotide action. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Regulatory Peptides Elsevier

Chronic infusion of a CRH 1 receptor antisense oligodeoxynucleotide into the central nucleus of the amygdala reduced anxiety-related behavior in socially defeated rats

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Publisher
Elsevier
Copyright
Copyright © 1995 Elsevier Ltd
ISSN
0167-0115
eISSN
1873-1686
DOI
10.1016/0167-0115(95)00099-W
Publisher site
See Article on Publisher Site

Abstract

We studied the role of central amygdala CRH receptors in behavioral responses to an anxiogenic stimulus. An antisense oligodeoxynucleotide corresponding to the rat CRH 1 receptor mRNA was infused chronically into the central amygdaloid nucleus of male rats via osmotic minipumps (0.25 μg/0.5 μl/h). Control groups received infusions of either a scrambled sequence oligodeoxynucleotide or vehicle. On the 4th day of treatment, rats were subjected to 10 min of social defeat and immediately afterwards tested on the elevated plus-maze. Antisense oligodeoxynucleotide-treated rats spent significantly more time exploring the open arms of the plus-maze than scrambled sequence- and vehicle-treated animals, both of which did not differ from each other. The social discrimination test, on the other hand, revealed no difference in juvenile recognition abilities among the treatment groups. Using in situ hybridization and receptor autoradiography, we were not able to detect clear signals of CRH 1 receptor mRNA and CRH binding sites in the central amygdaloid nucleus of either group, confirming the reportedly low expression and density of CRH receptors in this brain area. The present data support the view that CRH receptors in the central nucleus of the amygdala are involved in the mediation and expression of anxiety-related behavior, but simultaneously raise questions as to the mechanisms of antisense oligodeoxynucleotide action.

Journal

Regulatory PeptidesElsevier

Published: Oct 20, 1995

References

  • A new test for aggression in rats without aversive stimulation: differential effects of d-amphetamine and cocaine
    Miczek, K.A.
  • Simultaneous monitoring of intracerebral release and behavior: endogenous vasopressin improves social recognition
    Engelmann, M.; Ludwig, M.; Landgraf, R.
  • Rapid effect on suckling of an oxytocin antisense oligonucleotide administered into rat supraoptic nucleus
    Neumann, I.; Porter, D.W.F.; Landgraf, R.; Pittman, Q.J.

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