Corticotropin-releasing factor projections from limbic forebrain and paraventricular nucleus of the hypothalamus to the region of the ventral tegmental area

Rodaros, Demetra; Caruana, Douglas A.; Amir, Shimon; Stewart, Jane

doi:10.1016/j.neuroscience.2007.09.043

Cited by 182 publications

(166 citation statements)

References 25 publications

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“…Adrenergic receptor-regulated GABAergic inputs to the ventral tegmental area (VTA) have been characterized (Dumont and Williams, 2004). Alternatively, ␤-adrenergic receptors may regulate efferents from the BNST that release CRF into the VTA (Rodaros et al, 2007). We and others have reported that delivery of CRF into the VTA can reinstate cocaine seeking in rats and VTA CRF receptor activation is necessary for stressinduced reinstatement (Wang et al, 2005;Blacktop et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

β-Adrenergic Receptor Mediation of Stress-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Roles for β₁ and β₂ Adrenergic Receptors

Vranjkovic¹,

Hang²,

Baker³

et al. 2012

J Pharmacol Exp Ther

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Stress can trigger the relapse of drug use in recovering cocaine addicts and reinstatement in rodent models through mechanisms that may involve norepinephrine release and ␤-adrenergic receptor activation. The present study examined the role of ␤-adrenergic receptor subtypes in the stressor-induced reinstatement of extinguished cocaine-induced (15 mg/kg i.p.) conditioned place preference in mice. Forced swim (6 min at 22°C) stress or activation of central noradrenergic neurotransmission by administration of the selective ␣ 2 adrenergic receptor antagonist 2-[(4,5-dihydro-1H-imidazol-2-yl)methyl]-2,3-dihydro-1-methyl-1H-isoindole (BRL-44,408) (10 mg/kg i.p.) induced reinstatement in wild-type, but not ␤-adrenergic receptor-deficient Adrb1/Adrb2 double-knockout, mice. In contrast, cocaine administration (15 mg/kg i.p.) resulted in reinstatement in both wild-type and ␤-adrenergic receptor knockout mice. Stress-induced reinstatement probably involved ␤ 2 adrenergic receptors. The ␤ 2 adrenergic receptor antagonist -(isopropylamino)-1-[(7-methyl-4-indanyl)oxy]butan-2-ol (ICI-118,551) (1 or 2 mg/kg i.p.) blocked reinstatement by forced swim or BRL-44,408, whereas administration of the nonselective ␤-adrenergic receptor agonist isoproterenol (2 or 4 mg/kg i.p.) or the ␤ 2 adrenergic receptor-selective agonist clenbuterol (2 or 4 mg/kg i.p.) induced reinstatement. Forced swim-induced, but not BRL-44,408-induced, reinstatement was also blocked by a high (20 mg/kg) but not low (10 mg/kg) dose of the ␤ 1 adrenergic receptor antagonist betaxolol, and isoproterenol-induced reinstatement was blocked by pretreatment with either ICI-118,551 or betaxolol, suggesting a potential cooperative role for ␤ 1 and ␤ 2 adrenergic receptors in stress-induced reinstatement. Overall, these findings suggest that targeting ␤-adrenergic receptors may represent a promising pharmacotherapeutic strategy for preventing drug relapse, particularly in cocaine addicts whose drug use is stress related.

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Section: Discussionmentioning

confidence: 99%

β-Adrenergic Receptor Mediation of Stress-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Roles for β₁ and β₂ Adrenergic Receptors

Vranjkovic¹,

Hang²,

Baker³

et al. 2012

J Pharmacol Exp Ther

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“…Although the brain circuits mediating withdrawal and sensitization are often considered independently, a number of established anatomical and physiological mechanisms could underlie interactions between them. For example, corticotropin-releasing factor (CRF) systems in the extended amygdala are prominently activated during withdrawal (Koob and Volkow, 2010), and these same CRF systems project to the ventral tegmental area (Rodaros et al, 2007), where CRF is released during stress (Wang et al, 2005). Release of CRF in the ventral tegmental area during acute withdrawal could facilitate NMDA receptor-dependent forms of plasticity that promote the development of sensitization (Borgland et al, 2009;Covington et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Episodic Withdrawal Promotes Psychomotor Sensitization to Morphine

Rothwell

Gewirtz

Thomas

2010

Neuropsychopharmacol

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The relative intermittency or continuity of drug delivery is a major determinant of addictive liability, and also influences the impact of drug exposure on brain function and behavior. Events that occur during the offset of drug action (ie, acute withdrawal) may have an important role in the consequences of intermittent drug exposure. We assessed whether recurrent episodes of acute withdrawal contribute to the development of psychomotor sensitization in rodents during daily morphine exposure. The acoustic startle reflexFa measure of anxiety induced by opiate withdrawalFwas used to resolve and quantify discrete withdrawal episodes, and pharmacological interventions were used to manipulate withdrawal severity. Startle potentiation was observed during spontaneous withdrawal from a single morphine exposure, and individual differences in initial withdrawal severity positively predicted the subsequent development of sensitization. Manipulations that reduce or exacerbate withdrawal severity also produced parallel changes in the degree of sensitization. These results demonstrate that the episodic experience of withdrawal during daily drug exposure has a novel role in promoting the development of psychomotor sensitizationFa prominent model of drug-induced neurobehavioral plasticity. Episodic withdrawal may have a pervasive role in many effects of intermittent drug exposure and contribute to the development of addiction.

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“…CRF, originating from outside sources including the bed nucleus of the stria terminalis (Rodaros et al, 2007;Vranjkovic et al, 2014) or within the VTA itself (Grieder et al, 2014), acts in complex, often opposing ways and can increase or decrease excitatory and/or inhibitory transmission in the VTA through numerous mechanisms. In vitro studies have revealed that CRF 1 receptors act presynaptically on glutamatergic terminals to increase glutamatergic drive onto dopamine neurons (Williams et al, 2014), as well as exerting postsynaptic actions to increase EPSCs and firing rates of dopamine neurons (Wanat et al, 2008).…”

Section: Crf Actions In the Vta And Effort-related Decision-makingmentioning

confidence: 99%

Perturbations in Effort-Related Decision-Making Driven by Acute Stress and Corticotropin-Releasing Factor

Bryce

Floresco

2016

Neuropsychopharmacol

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Acute stress activates numerous systems in a coordinated effort to promote homeostasis, and can exert differential effects on mnemonic and cognitive functions depending on a myriad of factors. Stress can alter different forms of cost/benefit decision-making, yet the mechanisms that drive these effects remain unclear. In the present study, we probed how corticotropin-releasing factor (CRF) may contribute to stress-induced alterations in cost/benefit decision-making, using an task where well-trained rats chose between a low effort/ low reward lever (LR; two pellets) and a high effort/high reward lever (HR; four pellets), with the effort requirement increasing over a session (2, 5, 10, and 20 presses). One-hour restraint stress markedly reduced preference for the HR option, but this effect was attenuated by infusions of the CRF antagonist, alpha-helical CRF. Conversely, central CRF infusion mimicked the effect of stress on decision-making, as well as increased decision latencies and reduced response vigor. CRF infusions did not alter preference for larger vs smaller rewards, but did reduce responding for food delivered on a progressive ratio, suggesting that these treatments may amplify perceived effort costs that may be required to obtain rewards. CRF infusions into the ventral tegmental area recapitulated the effect of central CRF treatment and restraint on choice behavior, suggesting that these effects may be mediated by perturbations in dopamine transmission. These findings highlight the involvement of CRF in regulating effort-related decisions and suggest that increased CRF activity may contribute to motivational impairments and abnormal decision-making associated with stress-related psychiatric disorders such as depression.

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Corticotropin-releasing factor projections from limbic forebrain and paraventricular nucleus of the hypothalamus to the region of the ventral tegmental area

Cited by 182 publications

References 25 publications

β-Adrenergic Receptor Mediation of Stress-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Roles for β₁ and β₂ Adrenergic Receptors

β-Adrenergic Receptor Mediation of Stress-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Roles for β₁ and β₂ Adrenergic Receptors

Episodic Withdrawal Promotes Psychomotor Sensitization to Morphine

Perturbations in Effort-Related Decision-Making Driven by Acute Stress and Corticotropin-Releasing Factor

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Corticotropin-releasing factor projections from limbic forebrain and paraventricular nucleus of the hypothalamus to the region of the ventral tegmental area

Cited by 182 publications

References 25 publications

β-Adrenergic Receptor Mediation of Stress-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Roles for β1 and β2 Adrenergic Receptors

β-Adrenergic Receptor Mediation of Stress-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Roles for β1 and β2 Adrenergic Receptors

Episodic Withdrawal Promotes Psychomotor Sensitization to Morphine

Perturbations in Effort-Related Decision-Making Driven by Acute Stress and Corticotropin-Releasing Factor

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β-Adrenergic Receptor Mediation of Stress-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Roles for β₁ and β₂ Adrenergic Receptors

β-Adrenergic Receptor Mediation of Stress-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Roles for β₁ and β₂ Adrenergic Receptors