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The Unpredictable Chronic Mild Stress Protocol for Inducing Anhedonia in Mice
Published on: October 24, 2018
Early-life adversity facilitates acquisition of cocaine self-administration and induces persistent anhedonia
Jessica L Bolton1, Christina M Ruiz2, Neggy Rismanchi1
1Department of Anatomy & Neurobiology, University of California, Irvine, USA.
Insights
Early-life adversity, modeled by limited nesting (LBN), reduces reward responses to natural and drug rewards like cocaine. This adversity impacts brain circuits involved in reward and stress, contributing to anhedonia and altered drug-seeking behaviors.
Area of Science:
- Neuroscience
- Psychiatry
- Behavioral Science
Background:
- Early-life adversity is a risk factor for emotional disorders like depression and schizophrenia.
- Anhedonia, a core feature of these disorders, is modeled in rodents using limited bedding and nesting (LBN).
- Comorbidity of drug addiction with psychiatric disorders featuring anhedonia necessitates understanding LBN's effects on drug-seeking behavior and related neural circuits.
Purpose of the Study:
- To investigate the impact of LBN on cocaine intake and seeking behaviors in a rodent model.
- To assess the effects of LBN on neuronal activation within reward and stress circuits following cocaine exposure.
- To compare the effects of LBN on cocaine reward with its effects on natural reward (chocolate intake).
Main Methods:
- Utilized a rodent model of early-life adversity (LBN) involving restricted nesting conditions.
- Employed a battery of behavioral tests to measure distinct aspects of cocaine reward, including self-administration and reinstatement.
- Examined Fos expression in brain regions (nucleus accumbens, amygdala, habenula, hypothalamus) and orexin neuron activation post-cocaine exposure.
Main Results:
- LBN reduced spontaneous intake of palatable chocolate, indicating anhedonia-like behavior.
- LBN rats self-administered lower doses of cocaine under low-effort conditions, suggesting a reduced hedonic set-point.
- While not affecting anxiety or motivation for cocaine, LBN altered neuronal activation in reward and stress circuits, notably attenuating hypothalamic orexin neuron response to cocaine.
Conclusions:
- Early-life adversity (LBN) has enduring effects on both reward and fear/anxiety neural circuits.
- LBN induces anhedonia-like reductions in the consumption of natural and drug rewards.
- These findings highlight the neurobiological impact of early adversity on vulnerability to psychiatric and addictive disorders.
Abstract:
Early-life adversity increases the risk for emotional disorders such as depression and schizophrenia. Anhedonia, thought to be a core feature of these disorders, is provoked by our naturalistic rodent model of childhood adversity (i.e., rearing pups for one week in cages with limited bedding and nesting, LBN). Drug use and addiction are highly comorbid with psychiatric disorders featuring anhedonia, yet effects of LBN on drug-seeking behavior and the reward and stress-related circuits that underlie it remain unknown. Here we examined the effects of LBN on cocaine intake and seeking, using a battery of behavioral tests measuring distinct aspects of cocaine reward, and for comparison, chocolate intake. We also examined activation of neurons within the pleasure/reward and stress circuits following cocaine in LBN and control rats. Early-life adversity reduced spontaneous intake of palatable chocolate, extending prior reports of sucrose and social-play anhedonia. In a within-session cocaine behavioral economic test, LBN rats self-administered lower dosages of cocaine under low-effort conditions, consistent with a reduced hedonic set-point for cocaine, and potentially anhedonia. In contrast, cocaine demand elasticity was not consistently affected, indicating no major changes in motivation to maintain preferred cocaine blood levels. These changes were selective, as LBN did not cause an overt anxiety-like phenotype, nor did it affect sensitivity to self-administered cocaine dose, responding for cocaine under extinction conditions, cocaine- or cue-induced reinstatement of cocaine seeking, or locomotor response to acute cocaine. However, high Fos expression was seen after cocaine in both reward- and stress-related brain regions of LBN rats, including nucleus accumbens core, central amygdala, and lateral habenula. In contrast, hypothalamic orexin neuron activation after cocaine was significantly attenuated in LBN rats. Together, these findings demonstrate enduring effects of early-life adversity on both reward- and fear/anxiety-related neural circuits, as well as anhedonia-like reductions in consumption of natural and drug rewards.
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