Origin of noradrenergic afferents to the shell subregion of the nucleus accumbens: anterograde and retrograde tract-tracing studies in the rat

Delfs, Jill M.; Zhu, Yan; Druhan, Jonathan P.; Aston‐Jones, Gary

doi:10.1016/s0006-8993(98)00672-6

Cited by 243 publications

(203 citation statements)

References 76 publications

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“…However, we did not detect norepinephrine release in the vBNST during morphine, although elevated norepinephrine in the BNST may develop following chronic drug exposure (Fuentealba et al, 2000). Alternatively, NTS norepinephrine may instead modulate drug-reward through its projections to the NAc (Delfs et al, 1998) where it can regulate dopamine efflux, and presumably the rewarding property of abused drugs through α 1 receptors (Mitrano et al, 2012). Norepinephrine signaling is traditionally implicated in the aversive aspects of opiatewithdrawal (Aston-Jones et al, 1999).…”

Section: Discussionmentioning

confidence: 66%

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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Section: Discussionmentioning

confidence: 66%

Reciprocal Catecholamine Changes during Opiate Exposure and Withdrawal

Fox

Rodeberg

Wightman

2016

Neuropsychopharmacol

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“…The PFC, a brain region implicated in responses to psychostimulants, also receives dense noradrenergic input from the LC (Swanson and Hartman, 1975;Morrison et al, 1981), which then sends excitatory glutamatergic projections to dopaminergic VTA neuronsFthough this connection may involve another glutamatergic relay nucleus (Carr and Sesack, 2000). Finally, the VNB projects directly to the NAc (Berridge et al, 1997;Delfs et al, 1998;Tong et al, 2006). These results form the basis of a functional connection between the noradrenergic and dopaminergic systems that is a likely component of central responses to drugs of abuse.…”

Section: Control Of Dopamine Neuron Firing and Dopamine Release By Nementioning

confidence: 95%

“…In addition, intra-NAc infusion of a broadspectrum DA antagonist has no effect on morphine CPP in drug-naïve animals (Laviolette et al, 2002). A possible anatomical substrate for these potential DA-independent effects is the direct NE projection of the VNB to the NAc (Berridge et al, 1997;Delfs et al, 1998;Tong et al, 2006), a hypothesis buttressed by the fact that 6-OHDA lesions of accumbal DA (NE content was unaffected in this particular study) selectively attenuate cocaine SA, but not heroin SA, in rats (Pettit et al, 1984), whereas kainic acid lesions of the same structure disrupt both cocaine and heroin SA (Zito et al, 1985). Together, these data suggest that other neurotransmitters in the NAc, such as NE, mediate the primary reinforcing effects of opiates.…”

Section: Some Effects Of Ne On Drug Responses May Be Independent Of Damentioning

confidence: 99%

There and Back Again: A Tale of Norepinephrine and Drug Addiction

Weinshenker

Schroeder

2006

Neuropsychopharmacol

323

277

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Fueled by anatomical, electrophysiological, and pharmacological analyses of endogenous brain reward systems, norepinephrine (NE) was identified as a key mediator of both natural and drug-induced reward in the late 1960s and early 1970s. However, reward experiments from the mid-1970s that could distinguish between the noradrenergic and dopaminergic systems resulted in the prevailing view that dopamine (DA) was the primary 'reward transmitter' (a belief holding some sway still today), thereby pushing NE into the background. Most damaging to the NE hypothesis of reward were studies demonstrating that NE receptor antagonists and NE reuptake inhibitors failed to impact drug self-administration. In recent years new tools, such as genetically engineered mice, and new experimental paradigms, such as reinstatement of drug seeking following withdrawal, have propelled NE back into the awareness of addiction researchers. Of particular interest is disulfiram, an inhibitor of the NE biosynthetic enzyme dopamine b-hydroxylase, which has demonstrated promising efficacy in the treatment of cocaine dependence in preliminary clinical trials. The purpose of this review is to synthesize the new data linking NE to critical aspects of DA signaling and drug addiction, with a focus on psychostimulants (eg, cocaine), opiates (eg, morphine), and alcohol.

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“…These NE axons also originate from A2 [48]. On the other hand, the rostral part of the NAc as well as the dorsal striatum have scattered NE innervations [46-48]. These data were recently confirmed by direct catecholamine assay, in situ voltammetry, stimulations of the median forebrain bundle and various pharmacological manipulations [49].…”

Section: Anatomical Connections Of Lc Ne Neurons (Fig 1)mentioning

confidence: 97%

“…These NE axons also originate from A2 [48]. On the other hand, the rostral part of the NAc as well as the dorsal striatum have scattered NE innervations [46-48].…”

Section: Anatomical Connections Of Lc Ne Neurons (Fig 1)mentioning

confidence: 99%

The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

Ferrucci

Giorgi

Bartalucci

et al. 2013

Current Neuropharmacology

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The activity of locus coeruleus (LC) neurons has been extensively investigated in a variety of behavioural states. In fact this norepinephrine (NE)-containing nucleus modulates many physiological and pathological conditions including the sleep-waking cycle, movement disorders, mood alterations, convulsive seizures, and the effects of drugs such as psychostimulants and opioids. This review focuses on the modulation exerted by central NE pathways on the behavioural and neurotoxic effects produced by the psychostimulant methamphetamine, essentially the modulation of the activity of mesencephalic dopamine (DA) neurons. In fact, although NE in itself mediates some behavioural effects induced by methamphetamine, NE modulation of DA release is pivotal for methamphetamine-induced behavioural states and neurotoxicity. These interactions are discussed on the basis of the state of the art of the functional neuroanatomy of central NE- and DA systems. Emphasis is given to those brain sites possessing a remarkable overlapping of both neurotransmitters.

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Origin of noradrenergic afferents to the shell subregion of the nucleus accumbens: anterograde and retrograde tract-tracing studies in the rat

Cited by 243 publications

References 76 publications

Reciprocal Catecholamine Changes during Opiate Exposure and Withdrawal

Reciprocal Catecholamine Changes during Opiate Exposure and Withdrawal

There and Back Again: A Tale of Norepinephrine and Drug Addiction

The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

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