Depression is a highly complex psychiatric disorder owing in part to the great variability
in patient symptoms; treatment response; and, presumably, underlying biological mechanisms
(
1
). This complexity as well as the inherent difficulty in studying mental symptoms in
rodents has made depression very difficult to model in the laboratory. Chronic social
defeat stress (CSDS) offers construct, face, and predictive validity; it induces many
of the core symptoms of depression that are measurable in rodents. This ethologically
relevant stressor involves forcing a rodent to intrude on the home cage of a larger,
more aggressive rodent, which overpowers it until a rapidly submissive phenotype emerges
(a process that is repeated typically for ≥10 days). Anhedonia, the lack of interest
in pleasurable or rewarding stimuli, is one of the most common symptoms of depression.
In rodents, anhedonia is often characterized by a reduction in preference for sucrose.
Anhedonia reportedly is induced by CSDS, yet results from sucrose preference tests
are inconsistent among studies. The test is vulnerable to various factors that may
influence an animal’s behavior, such as neophobia or a state of satiety. A promising
solution to this conundrum is intracranial self-stimulation (ICSS), a powerful assay
used to assess reward sensitivity that appears unaffected by confounds often seen
in other reward-related tests. In this issue of Biological Psychiatry, two studies, for the first time, combine CSDS with ICSS to determine whether 1)
CSDS produces anhedonia as reflected in changing thresholds for ICSS, 2) CSDS produces
maladaptive changes in brain reward processing, and 3) antidepressant treatment can
reverse CSDS-induced deficits in reward functioning.To read this article in full you will need to make a payment
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References
- Animal models of neuropsychiatric disorders.Nat Neurosci. 2010; 13: 1161-1169
- Enduring deficits in brain reward function after chronic social defeat in rats: Susceptibility, resilience, and antidepressant response.Biol Psychiatry. 2014; 76: 542-549
- Effects of striatal ΔFosB overexpression and ketamine on social defeat stress-induced anhedonia in mice.Biol Psychiatry. 2014; 76: 550-558
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Article info
Publication history
Published online: May 06, 2014
Accepted:
April 17,
2014
Received:
April 17,
2014
Identification
Copyright
© 2014 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
ScienceDirect
Access this article on ScienceDirectLinked Article
- Effects of Striatal ΔFosB Overexpression and Ketamine on Social Defeat Stress–Induced Anhedonia in MiceBiological PsychiatryVol. 76Issue 7
- PreviewChronic social defeat stress (CSDS) produces persistent behavioral adaptations in mice. In many behavioral assays, it can be difficult to determine if these adaptations reflect core signs of depression. We designed studies to characterize the effects of CSDS on sensitivity to reward because anhedonia (reduced sensitivity to reward) is a defining characteristic of depressive disorders in humans. We also examined the effects of striatal ΔFosB overexpression and the N-methyl-D-aspartate receptor antagonist ketamine, both of which promote resilience, on CSDS-induced alterations in reward function and social interaction.
- Full-Text
- Preview
- Enduring Deficits in Brain Reward Function after Chronic Social Defeat in Rats: Susceptibility, Resilience, and Antidepressant ResponseBiological PsychiatryVol. 76Issue 7
- PreviewAnhedonia, or diminished interest or pleasure in rewarding activities, characterizes depression and reflects deficits in brain reward circuitries. Social stress induces anhedonia and increases risk of depression, although the effect of social stress on brain reward function is incompletely understood.
- Full-Text
- Preview
