Chronic infusion of a CRH1 receptor antisense oligodeoxynucleotide into the central nucleus of the amygdala reduced anxiety-related behavior in socially defeated rats
Abstract
We studied the role of central amygdala CRH receptors in behavioral responses to an anxiogenic stimulus. An antisense oligodeoxynucleotide corresponding to the rat CRH1 receptor mRNA was infused chronically into the central amygdaloid nucleus of male rats via osmotic minipumps (0.25 micrograms/0.5 microliters/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 CRH1 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.
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The central amygdala nucleus (CEA) has been implicated in learning and expression of fear responses, as well as the expression of stress-induced anxiety behaviors.
“Functionally, CEA has been implicated in learning and expression of fear responses,105, 106, 107 as well as the expression of stress-induced anxiety behaviors.108, 109, 110, 111, 112, 113”
From Preferential loss of dorsal-hippocampus synapses underlies memory impairments provoked by short, multimodal stress (2014) · cites this paper as [109]
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- Authors
- Liebsch, G., Landgraf, R., Gerstberger, R., Probst, J. C., Wotjak, C. T., Engelmann, M., Holsboer, F., & Montkowski, A.
- Affiliations
- Max Planck Institute of Psychiatry (DE)
- Max Planck Society (DE)
- Corresponding author
- Montkowski, Alexandra
- Venue
- Regulatory Peptides
- Publisher
- Elsevier BV
- Published
- 1995-10
- Volume
- 59
- Issue
- 2
- Pages
- 229-239
- ISSN
- 0167-0115 (ISSN-L)
- OpenAlex
- W1967569415
- Cited by
- 220
- References
- 51
- Citations by year
- 2023: 2 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 3 · 2018: 2 · 2017: 1 · 2016: 4 · 2015: 7 · 2014: 5 · 2013: 10 · 2012: 3
- FWCI
- 3.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Regulatory Peptides (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Keywords
- central amygdala, antisense oligodeoxynucleotides, anxiety-like behavior, social defeat, elevated plus maze, social discrimination, gene silencing
- MeSH terms
- Amygdala, Animals, Anxiety, Autoradiography, Base Sequence, Behavior, Animal, Discrimination Learning, Infusions, Parenteral, Functional Laterality, Male, Molecular Sequence Data, Social Behavior, Oligonucleotides, Antisense, Rats, Wistar, In Situ Hybridization, Receptors, Corticotropin-Releasing Hormone, Maze Learning, Rats
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