Corticotropin-Releasing Factor (CRF) circuit modulation of cognition and motivation

Hupalo, Sofiya; Bryce, Courtney A.; Bangasser, Debra A.; Berridge, Craig W.; Valentino, Rita J.; Floresco, Stan

doi:10.1016/j.neubiorev.2019.06.010

Cited by 69 publications

(47 citation statements)

References 151 publications

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“…CRF1R in the mPFC has also been shown to significantly contribute to stress-induced executive dysfunction [45], further supporting a role of the mPFC CRF system in modulating stress behavior such as that observed during withdrawal from chronic ethanol consumption. Important to the present work, mPFC CRF is further known to modulate cognitive function independent of stress as well as anxiety-like behavior in rodents [27,46]. Intra-mPFC infusions of CRF increased while infusion of a CRF1R antagonist attenuated anxiety-like behavior in male mice [29,47].…”

Section: Discussionmentioning

confidence: 99%

“…A subpopulation of mPFC gamma-Aminobutyric acid (GABA)-ergic neurons produce CRF and synapse onto both excitatory projection neurons and other interneuron populations [11,25,26]. Notably, CRF1R and CRF2R activation may differentially alter activity of distinct cell populations, potentially contributing to the opposing roles these two receptors play in a number of behaviors including consumption and anxiety [27]. For instance, within the dorsal raphe nucleus (DRN), CRF1R activation alters GABAerigc while CRF2R activation alters serotonergic signaling [28,29].…”

Section: Introductionmentioning

confidence: 99%

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Corticotropin Releasing Factor Type 1 and 2 Receptor Signaling in the Medial Prefrontal Cortex Modulates Binge-Like Ethanol Consumption in C57BL/6J Mice

2019

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Corticotropin releasing factor (CRF) signaling via limbic CRF1 and 2 receptors (CRF1R and CRF2R, respectively) is known to modulate binge-like ethanol consumption in rodents. Though CRF signaling in the medial prefrontal cortex (mPFC) has been shown to modulate anxiety-like behavior and ethanol seeking, its role in binge ethanol intake is unknown. Here, we used “drinking-in-the-dark” (DID) procedures in male and female C57BL/6J mice to address this gap in the literature. First, the role of CRF1R and CRF2R signaling in the mPFC on ethanol consumption was evaluated through site-directed pharmacology. Next, we evaluated if CRF1R antagonist reduction of binge-intake was modulated in part through CRF2R activation by co-administration of a CRF1R and CRF2R antagonist. Intra-mPFC inhibition of CRF1R and activation of CRF2R resulted in decreased binge-like ethanol intake. Further, the inhibitory effect of the CRF1R antagonist was attenuated by co-administration of a CRF2R antagonist. We provide novel evidence that (1) inhibition of CRF1R or activation of CRF2R in the mPFC reduces binge-like ethanol intake; and (2) the effect of CRF1R antagonism may be mediated via enhanced CRF2R activation. These observations provide the first direct behavioral pharmacological evidence that CRF receptor activity in the mPFC modulates binge-like ethanol consumption.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Corticotropin Releasing Factor Type 1 and 2 Receptor Signaling in the Medial Prefrontal Cortex Modulates Binge-Like Ethanol Consumption in C57BL/6J Mice

2019

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“…In mammals, including humans, the brain norepinephrine (NE) and dopamine (DA) systems, originating from the locus coeruleus (LC) and the ventral tegmental area (VTA) respectively, produce spread brain networks with cortical and subcortical projections ( 3 ). Both NE and DA brainstem neurons are targeted by stress hormones of the hypothalamus-pituitary axis (HPA) ( 4 , 5 ). NE-LC and DA-VTA neurons are readily activated by stressful events involving neural processes related to perception, cognitive evaluation, appraisal, and stress-dependent hormonal factors.…”

Section: Introductionmentioning

confidence: 99%

“…Noteworthy, stress is likely to affect catecholamine metabolism and neuroplasticity in a way which is reminiscent of the effects produced by abused substances ( 7 , 46 – 48 ). In fact, stressful events are often reported to cause neuropsychiatric disorders going from depression to substance abuse, up to neurodegenerative insults where brain catecholamine-containing neurons and/or their projections are involved ( 4 , 5 ). Chronic or heavy stress, similar to substance abuse, produces catecholamine-driven behavioral effects ranging from depression to addiction, and schizophrenia-like phenotypes.…”

Section: Introductionmentioning

confidence: 99%

Autophagy-Based Hypothesis on the Role of Brain Catecholamine Response During Stress

et al. 2020

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Stressful events, similar to abused drugs, significantly affect the homeostatic balance of the catecholamine brain systems while activating compensation mechanisms to restore balance. In detail, norepinephrine (NE)-and dopamine (DA)-containing neurons within the locus coeruleus (LC) and ventral tegmental area (VTA), are readily and similarly activated by psychostimulants and stressful events involving neural processes related to perception, reward, cognitive evaluation, appraisal, and stress-dependent hormonal factors. Brain catecholamine response to stress results in time-dependent regulatory processes involving mesocorticolimbic circuits and networks, where LC-NE neurons respond more readily than VTA-DA neurons. LC-NE projections are dominant in controlling the forebrain DA-targeted areas, such as the nucleus accumbens (NAc) and medial pre-frontal cortex (mPFC). Heavy and persistent coping demand could lead to sustained LC-NE and VTA-DA neuronal activity, that, when persisting chronically, is supposed to alter LC-VTA synaptic connections. Increasing evidence has been provided indicating a role of autophagy in modulating DA neurotransmission and synaptic plasticity. This alters behavior, and emotional/cognitive experience in response to drug abuse and occasionally, to psychological stress. Thus, relevant information to address the role of stress and autophagy can be drawn from psychostimulants research. In the present minireview we discuss the role of autophagy in brain catecholamine response to stress and its dysregulation. The findings here discussed suggest a crucial role of regulated autophagy in the response and adaptation of LC-NE and VTA-DA systems to stress.

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“…1 The behavioral effects of stress are mediated in part through CRF signaling within the mesocorticolimbic system. 2,3 For example, CRF receptor activation within the ventral tegmental area (VTA) is required for the stress-induced reduction in the motivation to work for food rewards. 4 Acute stress also decreases the preference for high effort/large reward options in decision-making tasks using food rewards.…”

Section: Introductionmentioning

confidence: 99%

Cocaine experience abolishes the motivation suppressing effect of CRF in the ventral midbrain

et al. 2019

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Stress affects dopamine-dependent behaviors in part through the actions of corticotropin releasing factor (CRF) in the ventral tegmental area (VTA). For example, acute stress engages CRF signaling in the VTA to suppress the motivation to work for food rewards. In contrast, acute stress promotes drug-seeking behavior through the actions of CRF in the VTA. These diverging behavioral effects in food-and drugbased tasks could indicate that CRF modulates goal-directed actions in a reinforcerspecific manner. Alternatively, prior drug experience could functionally alter how CRF in the VTA regulates dopamine-dependent behavior. To address these possibilities, we examined how intra-VTA injections of CRF influenced cocaine intake and whether prior drug experience alters how CRF modulates the motivation for food rewards. Our results demonstrate that intra-VTA injections of CRF had no effect on drug intake when self-administering cocaine under a progressive ratio reinforcement schedule. We also found that a prior history of either contingent or noncontingent cocaine infusions abolished the capacity for CRF to reduce the motivation for food rewards. Furthermore, voltammetry recordings in the nucleus accumbens illustrate that CRF in the VTA had no effect on cocaine-evoked dopamine release. These results collectively illustrate that exposure to abused substances functionally alters how neuropeptides act within the VTA to influence motivated behavior.

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Corticotropin-Releasing Factor (CRF) circuit modulation of cognition and motivation

Cited by 69 publications

References 151 publications

Corticotropin Releasing Factor Type 1 and 2 Receptor Signaling in the Medial Prefrontal Cortex Modulates Binge-Like Ethanol Consumption in C57BL/6J Mice

Corticotropin Releasing Factor Type 1 and 2 Receptor Signaling in the Medial Prefrontal Cortex Modulates Binge-Like Ethanol Consumption in C57BL/6J Mice

Autophagy-Based Hypothesis on the Role of Brain Catecholamine Response During Stress

Cocaine experience abolishes the motivation suppressing effect of CRF in the ventral midbrain

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