Intracerebroventricular d-Pen2, d-Pen5-enkephalin administration soon after stressor imposition influences behavioral responsivity to a subsequent stressor encounter in CD-1 mice

Hebb, Andrea L.O.; Drolet, Guy; Mendella, Paul D.; Roach, Sean P.; Gauthier, Michelle; Zacharko, Robert M.

doi:10.1016/j.pbb.2005.10.001

Cited by 8 publications

(5 citation statements)

References 119 publications

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“…These results are also consistent with the wellknown anxiolytic properties of the ENKergic neurotransmission. The ENK through the activation of m-OR and/or d-OR may attenuate stress-induced neuroendocrine, autonomic, and anxiety-like behavioral responses (König et al, 1996;Kang et al, 2000;Filliol et al, 2000;Ragnauth et al, 2001;Drolet et al, 2001;Hebb et al, 2004;Hebb et al, 2005a;Hebb et al, 2005b;Jutkiewicz, 2007;Noble et al, 2007). In addition, pharmacological studies reported that systemic administration of m-OR or d-OR agonists have anxiolytic and antidepressant properties in rodents (Broom et al, 2002;Saitoh et al, 2004;Perrine et al, 2006;Vergura et al, 2008;Rezayof et al, 2009).…”

Section: Decreased Blap Enk: a Molecular Signature Of Vulnerabilitymentioning

confidence: 99%

“…Among the neuropeptide systems, the endogenous opioid enkephalins (ENKs) are very interesting candidates to participate in the naturally occurring variations in coping styles and to determine the individual capacity for adaptation during chronic stress exposure. The most consistent finding among studies using different species and stressors is that the ENKergic neurotransmission, through mu-opioid receptors (m-ORs) and/or delta-OR (d-ORs), is critical in different aspects of affective states, basal hedonic state, and attenuation of stress-induced neuroendocrine, autonomic, and anxiety-like behavioral responses (König et al, 1996;Kang et al, 2000;Filliol et al, 2000;Ragnauth et al, 2001;Drolet et al, 2001;Hebb et al, 2004;Hebb et al, 2005a;Hebb et al, 2005b;Jutkiewicz, 2007;Noble et al, 2007). In the present study, we assessed whether changes in the expression of ENK in 23 nuclei of the basal forebrain are associated to resilience or vulnerability to chronic unpredictable stress (CUS).…”

Section: Introductionmentioning

confidence: 97%

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Enkephalin Knockdown in the Basolateral Amygdala Reproduces Vulnerable Anxiety-Like Responses to Chronic Unpredictable Stress

Bérubé

Poulin

Laforest

et al. 2013

Neuropsychopharmacol

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The endogenous enkephalins (ENKs) are potential candidates participating in the naturally occurring variations in coping styles and determining the individual capacities for adaptation during chronic stress exposure. Here we demonstrate that there is a large variance in individual behavioral, as well as in physiological outcomes, in a population of Sprague-Dawley rats subjected to 3 weeks of chronic unpredictable stress (CUS). Separation of resilient and vulnerable subpopulations reveals specific long-term neuroadaptation in the ENKergic brain circuits. ENK mRNA expression was greatly reduced in the posterior basolateral nucleus of amygdala (BLAp) in vulnerable individuals. In contrast, ENK mRNA levels were similar in resilient and control (unstressed) individuals. Another group of rats were used for lentiviral-mediated knockdown of ENK to assess whether a decrease of ENK expression in the BLAp reproduces the behavioral disturbances found in vulnerable individuals. ENK knockdown specifically located in the BLAp was sufficient to increase anxiety in the behavioral tests, such as social interaction and elevated plus maze when compared with control individuals. These results show that specific neuroadaptation mediated by the ENKergic neurotransmission in the BLAp is a key regulator of resilience, whereas a decrease of the ENK in the BLAp is a maladaptation mechanism, which mediates the behavioral dichotomy observed between vulnerable and resilient following 3 weeks of CUS.

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Section: Decreased Blap Enk: a Molecular Signature Of Vulnerabilitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Enkephalin Knockdown in the Basolateral Amygdala Reproduces Vulnerable Anxiety-Like Responses to Chronic Unpredictable Stress

Bérubé

Poulin

Laforest

et al. 2013

Neuropsychopharmacol

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“…The ␦-opioid receptor (DOR) plays a protective role in cerebral ischemia, hypoxia, cardiac dysfunction, skeletal muscle damage, peripheral organ survival, and vulnerability to stress (Borlongan et al, 2004;Hebb et al, 2005;Hong et al, 2005;Saitoh et al, 2005;Chao et al, 2007;Förster et al, 2007). Interestingly, CNS expression of DORs is often dynamically induced following physiological challenge (Commons, 2003;Hack et al, 2005;Cahill et al, 2007) and trafficking to the plasma membrane is regulated through a variety of mechanisms, which are dependent on stimulus type and duration (Cahill et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

δ-Opioid Receptor Expression in the Ventral Tegmental Area Protects Against Elevated Alcohol Consumption

Margolis¹,

Fields²,

Hjelmstad³

et al. 2008

J. Neurosci.

106

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Alcoholism is a complex and debilitating syndrome affecting ϳ140 million people worldwide. However, not everyone who consumes ethanol develops abuse, raising the possibility that some individuals have a protective mechanism that inhibits elevated alcohol consumption. We tested the hypothesis that the ␦-opioid receptor (DOR) plays such a protective role. Here we show that DOR activity in the ventral tegmental area (VTA) robustly decreases ethanol consumption in rats and that these effects depend on baseline ethanol consumption. Intra-VTA microinjection of the DOR agonist DPDPE decreases drinking, particularly in low-drinking animals. Furthermore, VTA microinjection of the DOR selective antagonist TIPP-⌿ increases drinking in low, but not high, drinkers and this increase is blocked by comicroinjection of the GABA A antagonist bicuculline. Using electrophysiological techniques we found that in VTA brain slices from drinking rats DPDPE presynaptically inhibits GABA A receptor mediated IPSCs in low drinkers, but not in high drinkers or naive animals, most likely through activation of DORs on GABA terminals. This DOR-mediated inhibition of IPSCs also correlates inversely with behavioral correlates of anxiety measured in the elevated plus maze. In contrast, presynaptic inhibition of VTA GABA A IPSCs by theopioid receptor agonist DAMGO is significantly reduced in both high-and low-drinking rats (Ͻ30%) compared with age-matched nondrinking controls (Ͼ70%). Together, our findings demonstrate the protective nature of VTA DORs and identify an important new target for therapeutic intervention for alcoholism.

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“… ‡ [1] (Cahill et al 2001b), [2] (Morinville et al 2003), [3] (Ma et al 2006), [4] (Bie et al 2009b), [5] (Chieng and Christie 2009), [6] (Lucido et al 2005), [7] (Morinville et al 2004a), [8] (Hack et al 2005), [9] (Lesscher et al 2003), [10] (Hyytia et al 1999), [11] (Khotib et al 2004), [12] (Bie et al 2010), [13] (Zhang and Pan 2010), [14] (Cahill et al 2003), [15] (Codd et al 2009), [16] (Morinville et al 2004b), [17] (Gendron et al 2007b), [18] (Gendron et al 2007a), [19] (Pol et al 1994), [20] (Shook et al 1989), [21] (Wade et al), [22] (Hurley and Hammond 2000), [23] (van Rijn et al 2010), [24] (van Rijn et al 2012b), [25] (Margolis et al 2008), [26] (Bie et al 2009a), [27] (Nielsen et al 2012), [28] (Charness et al 1986), [29] (Mendez et al 2004), [30] (Margolis et al 2011), [31] (Commons 2003), [32] (Hebb et al 2005), [33] (Pohorecky et al 1999), [34] (Krajnik et al 2010), [35] (Madar et al 2007), [36] (Schreiber et al 1998), [37] (Evans et al 2001), [38] (Kamei et al 1997), [39] (Kamei et al 1994a), [40] (Zhang et al 2006a), [41] (Ma et al 2005), [42] (Kabli and Cahill 2007), [43] (Salemi et al 2007), [44] (Madar et al 1997), [45] (Bolte et al 2009) …”

Section: Figurementioning

confidence: 99%

“…During stress the body does not only release stress hormones such as corticotropin releasing hormone, but it also releases endogenous opioids/enkephalins (Amir et al 1980; Kalivas and Abhold 1987), suggesting that DORs may be part of a negative feedback system. Indeed, in already stressed mice, DPDPE drastically reduces the response to future stress (Hebb et al 2005). In rats, foot-shock stress specifically enhances postsynaptic DOR activity in dopaminergic neurons of the ventral tegmental area (Margolis et al 2011).…”

Section: Introductionmentioning

confidence: 99%

Pharmacological traits of delta opioid receptors: pitfalls or opportunities?

2013

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Delta opioid receptors (DORs) have been considered as a potential target to relieve pain as well as treat depression and anxiety disorders, and are known to modulate other physiological responses, including ethanol and food consumption. A small number of DOR selective drugs are in clinical trials, but no DOR selective drugs have been approved by the Federal Drug Administration and some candidates have failed in phase II clinical trials, highlighting current difficulties producing effective delta opioid based therapies. Recent studies have provided new insights into the pharmacology of the DOR, which is often complex and at times paradoxical. This review will discuss the existing literature focusing on four aspects: 1) Two DOR subtypes have been postulated based on differences in pharmacological effects of existing DOR-selective ligands 2) DORs are expressed ubiquitously throughout the body and central nervous system and are, thus, positioned to play a role in a multitude of diseases. 3) DOR expression is often dynamic, with many reports of increased expression during exposure to chronic stimuli, such as stress, inflammation, neuropathy, morphine, or changes in endogenous opioid tone. 4) A large structural variety in DOR ligands implies potential different mechanisms of activating the receptor. These combined features of DOR pharmacology illustrate the potential benefit of designing tailored or biased DOR ligands.

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Intracerebroventricular d-Pen2, d-Pen5-enkephalin administration soon after stressor imposition influences behavioral responsivity to a subsequent stressor encounter in CD-1 mice

Cited by 8 publications

References 119 publications

Enkephalin Knockdown in the Basolateral Amygdala Reproduces Vulnerable Anxiety-Like Responses to Chronic Unpredictable Stress

Enkephalin Knockdown in the Basolateral Amygdala Reproduces Vulnerable Anxiety-Like Responses to Chronic Unpredictable Stress

δ-Opioid Receptor Expression in the Ventral Tegmental Area Protects Against Elevated Alcohol Consumption

Pharmacological traits of delta opioid receptors: pitfalls or opportunities?

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