CRF/NPY interactions: A potential role in sleep dysregulation in depression and anxiety

Ehlers, Cindy L.; Somes, Christine; Seifritz, Erich; Rivier, J.

doi:10.1002/(sici)1520-6394(1997)6:1<1::aid-da1>3.0.co;2-j

Cited by 76 publications

(11 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…While CRF has been shown to be a potent anxiogenic agent (Dunn and File, 1987; Sutton et al, 1982; Thatcher-Britton et al, 1986), NPY given intracerebrally has anxiolytic effects (Heilig et al, 1993; Wahlestedt et al, 1993). The interplay and/or balance between the opposing actions of these neuropeptides have been suggested to play an important role in the regulation of stress, anxiety, sleep and depression (Ehlers et al, 1997; Heilig et al, 1994; Yamada et al, 1996). These findings suggest a potential role for these neuropeptides on protracted symptoms associated with ethanol withdrawal.…”

Section: Introductionmentioning

confidence: 99%

Prolonged chronic ethanol exposure alters neuropeptide Y and corticotropin-releasing factor levels in the brain of adult Wistar rats

Criado

Liu

Ehlers

et al. 2011

Pharmacology Biochemistry and Behavior

View full text Add to dashboard Cite

There is evidence to suggest that alterations in neuropeptide Y (NPY) and corticotropin-releasing factor (CRF) contribute to the escalated voluntary ethanol intake seen following long term chronic ethanol exposure. The present study assessed whether the duration of chronic ethanol exposure and abstinence alters brain levels of NPY and CRF in adult Wistar rats. NPY-like immunoreactivity (NPY-LI) and CRF-LI were determined in the amygdala (AMYG), frontal cortex (FCTX), hippocampus (HPC) and parietal cortex (PCTX) of adult Wistar rats after chronic ethanol exposure, and 24-hr and 2-wk following withdrawal (WD). Chronic ethanol exposure consisted of either a 2-wk or an 8-wk ethanol vapor regimen. No change in brain levels of NPY-LI, CRF-LI and the NPY-LI/CRF-LI ratio were observed 2-wk following ethanol exposure, whereas, 8-wk of ethanol exposure produced a significant effect on NPY-LI expression in the AMYG and FCTX. Moreover, an 8-wk ethanol vapor regimen significantly increased CRF-LI levels in the HPC and PCTX. Findings from the present study suggest that a longer duration of ethanol vapor, similar to what is required to enhance voluntary drinking, is required to produce changes in NPY-LI and CRF-LI expression in the adult rat brain.

show abstract

Section: Introductionmentioning

confidence: 99%

Prolonged chronic ethanol exposure alters neuropeptide Y and corticotropin-releasing factor levels in the brain of adult Wistar rats

Criado

Liu

Ehlers

et al. 2011

Pharmacology Biochemistry and Behavior

View full text Add to dashboard Cite

show abstract

“…This results in the compromise of many functions, and may constitute the cause for the formation of symptomatology. This could be true both at the level of specific brain regions and at the level of coordination between different brain structures, and it can be state or syndrome dependent [8-10]. …”

Section: Introductionmentioning

confidence: 99%

Disruption of biological rhythms as a core problem and therapeutic target in mood disorders: the emerging concept of 'rhythm regulators'

Fountoulakis

2010

Ann Gen Psychiatry

View full text Add to dashboard Cite

Biological rhythms have always been considered to be disrupted in depression, with the predominant theory being that of hyperarousal. However, recent data suggest that it might be more appropriate to suggest that depressed patients are incapable of achieving and maintaining the particular level of internal homeostasis which permits them to function smoothly, to lower the level of arousal during sleep sufficiently so that quality of sleep is good, and to increase this level enough during the day so the person can function properly. Therefore, the transition from one state to another is somewhat problematic, delayed, incomplete and desynchronised. Thus, agents with a 'rhythm stabilising' effect could be beneficial in the treatment of mood disorders. Such an agent should have a beneficial effect on restoring and stabilising the rhythm of a physiological function while not pushing it towards a specific pole, or inducing the opposite pole; it should also allow response to internal and environmental stimuli and zeitgebers, and restore synchronisation of the various body rhythms while not inducing or worsening desynchronisation. Agomelatine could represent the first of a new class of 'rhythm stabilising antidepressants', but further research is necessary to support this theory.

show abstract

“…In this conceptualization, NPY acting at Y 1 receptors has anxiolytic properties that counteract pro-stress effects of CRF. In agreement with this idea, NPY acts as a functional antagonist of CRF effects on arousal and sleep (Ehlers et al, 1997), and stress and anxiety (Sajdyk et al., 2006, Britton et al, 2000), and opposes ethanol-stimulated, CRF-dependent GABA release in the CeA (Nie et al, 2004, Gilpin et al, 2011). NPY also inhibits CRF neurons in the BNST via Y 1 receptors (Pleil et al, 2015), and CRF and NPY produce opposing regulation of GABAergic transmission in this region (Kash and Winder, 2006).…”

Section: Resultsmentioning

confidence: 59%

The Corticotropin Releasing Factor Receptor 1 in Alcohol Use Disorder: Still a Valid Drug Target?

Pomrenze

Fetterly

Winder

et al. 2017

Alcoholism Clin & Exp Res

View full text Add to dashboard Cite

Corticotropin releasing factor (CRF) is a neuropeptide that plays a key role in behavioral and physiological responses to stress. A large body of animal literature implicates CRF acting at type 1 CRF receptors (CRFR1) in consumption by alcohol dependent subjects, stress-induced reinstatement of alcohol seeking, and possibly binge alcohol consumption. These studies have encouraged recent pilot studies of CRFR1 antagonists in humans with alcohol use disorder (AUD). It was a great disappointment to many in the field that these studies failed to show an effect of these compounds on stress-induced alcohol craving. Here, we examine these studies to explore potential limitations, and discuss preclinical and human literature to ask whether CRFR1 is still a valid drug target to pursue for the treatment of alcohol use disorder.

show abstract

CRF/NPY interactions: A potential role in sleep dysregulation in depression and anxiety

Cited by 76 publications

References 54 publications

Prolonged chronic ethanol exposure alters neuropeptide Y and corticotropin-releasing factor levels in the brain of adult Wistar rats

Prolonged chronic ethanol exposure alters neuropeptide Y and corticotropin-releasing factor levels in the brain of adult Wistar rats

Disruption of biological rhythms as a core problem and therapeutic target in mood disorders: the emerging concept of 'rhythm regulators'

The Corticotropin Releasing Factor Receptor 1 in Alcohol Use Disorder: Still a Valid Drug Target?

Contact Info

Product

Resources

About