Stress-Induced Cocaine Seeking Requires a Beta-2 Adrenergic Receptor-Regulated Pathway from the Ventral Bed Nucleus of the Stria Terminalis That Regulates CRF Actions in the Ventral Tegmental Area

Vranjkovic, Oliver; Gasser, P.; Gerndt, Clayton H.; Baker, David L.; Mantsch, John R.

doi:10.1523/jneurosci.0680-14.2014

Cited by 70 publications

(72 citation statements)

References 72 publications

(10 reference statements)

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“…All of the experiments and analyses were performed by experimenters who were blind to the treatments, and the animals’ order of treatment was randomized. No statistical methods were used to predetermine sample sizes, but our sample sizes are similar to those reported in previous publications 13,25,37,39 . Different numbers of animals between groups and between the beginning and end of the study are a result of the loss of data due to improper cannula placement, improper brain perfusion, damaged brain samples, or computer failure during testing.…”

Section: Methodsmentioning

confidence: 61%

VTA CRF neurons mediate the aversive effects of nicotine withdrawal and promote intake escalation

et al. 2014

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SUMMARY Dopaminergic neurons in the ventral tegmental area (VTA) are well known for their role in mediating the positive reinforcing effects of drugs of abuse. Here, we identify in rodents and humans a population of VTA dopamine neurons co-expressing corticotropin releasing factor (CRF). We provide further evidence in rodents that chronic nicotine exposure upregulates CRF mRNA in dopaminergic neurons of the posterior VTA, activates local CRF1 receptors, and blocks nicotine-induced activation of transient GABAergic input to dopaminergic neurons. Local downregulation of CRF mRNA and specific pharmacological blockade of CRF1 receptors in the VTA reversed the effect of nicotine on GABAergic input to dopaminergic neurons, prevented the aversive effects of nicotine withdrawal, and limited the escalation of nicotine intake. These results link the brain reward and stress systems within the same brain region in signaling the negative motivational effects of nicotine withdrawal.

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Section: Methodsmentioning

confidence: 61%

VTA CRF neurons mediate the aversive effects of nicotine withdrawal and promote intake escalation

et al. 2014

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“…Moreover, during acute opiate withdrawal, norepinephrine can act through β-receptors to increase GABA A inhibition of VTAprojecting BNST neurons (Dumont and Williams, 2004), leading to increased inhibition of the VTA. Activation of β 2 -adrenergic receptors in the vBNST drives stress-induced reinstatement by releasing CRF in the VTA (Vranjkovic et al, 2014). Although increased VTA CRF can potentiate activity (Ungless et al, 2003), CRF receptor antagonism in the VTA blocks the decrease in NAc dopamine transients caused by aversive quinine infusions (Twining et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Reciprocal Catecholamine Changes during Opiate Exposure and Withdrawal

Fox

Rodeberg

Wightman

2016

Neuropsychopharmacol

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Dysregulated catecholamine signaling has long been implicated in drug abuse. Although much is known about adaptations following chronic drug administration, little work has investigated how a single drug exposure paired with withdrawal influences catecholamine signaling in vivo. We used fast-scan cyclic voltammetry in freely moving rats to measure real-time catecholamine overflow during acute morphine exposure and naloxone-precipitated withdrawal in two regions associated with the addiction cycle: the dopamine-dense nucleus accumbens (NAc) and norepinephrine-rich ventral bed nucleus of the stria terminalis (vBNST). We compared dopamine transients in the NAc with norepinephrine concentration changes in the vBNST, and correlated release with specific withdrawal-related behaviors. Morphine increased dopamine transients in the NAc, but did not elicit norepinephrine responses in the vBNST. Conversely, dopamine output was decreased during withdrawal, while norepinephrine was released in the vBNST during specific withdrawal symptoms. Both norepinephrine and withdrawal symptoms could be elicited in the absence of morphine by administering naloxone with an α 2 antagonist. The data support reciprocal roles for dopamine and norepinephrine signaling during drug exposure and withdrawal. The data also support the allostasis model and show that negative-reinforcement may begin working after a single exposure/withdrawal episode.

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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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Stress-Induced Cocaine Seeking Requires a Beta-2 Adrenergic Receptor-Regulated Pathway from the Ventral Bed Nucleus of the Stria Terminalis That Regulates CRF Actions in the Ventral Tegmental Area

Cited by 70 publications

References 72 publications

VTA CRF neurons mediate the aversive effects of nicotine withdrawal and promote intake escalation

VTA CRF neurons mediate the aversive effects of nicotine withdrawal and promote intake escalation

Reciprocal Catecholamine Changes during Opiate Exposure and Withdrawal

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

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