Input from the amygdala to the rat nucleus accumbens: Its relationship with tyrosine hydroxylase immunoreactivity and identified neurons

Johnson, Luke R.; Aylward, R.L.M.; Hussain, Zawar; Totterdell, Susan

doi:10.1016/0306-4522(94)90408-1

Cited by 153 publications

(116 citation statements)

References 36 publications

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“…Indeed, excitation of NAc neurons by DSs depends on the VTA; these excitations are also dependent on the BLA . Furthermore, the glutamatergic terminals of BLA neurons projecting to the NAc synapse in close apposition to VTA-derived dopaminergic varicosities (Brog et al, 1993;Johnson et al, 1994;Phillips et al, 2003). These synapses are a possible site where the BLA glutamatergic projection can act presynaptically to increase dopamine efflux in the NAc (Floresco et al, 1998).…”

Section: Inactivation Of the Blamentioning

confidence: 99%

Contributions of the amygdala and medial prefrontal cortex to incentive cue responding

et al. 2008

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Reward-seeking behavior is controlled by neuronal circuits that include the basolateral nucleus of amygdala (BLA), medial prefrontal cortex (mPFC), nucleus accumbens (NAc) and ventral tegmental area. Using a discriminative stimulus (DS) task in which an intermittently presented cue (DS) directs the animals to make an operant response for sucrose, we previously demonstrated that dopamine receptor antagonism in the NAc reduced reinforced cue responding, whereas general inactivation of the NAc increased behavioral responding in the absence of the cue. Because they send major glutamatergic projections to the NAc, the BLA and mPFC may also contribute to reward-seeking behaviors modulated by the NAc. In this study we compare the effects of BLA and mPFC inactivation on the performance of a DS task. BLA inactivation by combined GABA A and GABA B agonists impaired cue responding with minimal effects on operant behavior in the absence of cues. Dorsal mPFC (dmPFC) inactivation also inhibited cue-evoked reward-seeking. In contrast, ventral mPFC (vmPFC) inactivation disinhibited responding to unrewarded cues with less influence on reinforced cue responding. These findings demonstrate that the BLA and dmPFC facilitate cue-evoked rewardseeking, whereas, in the same task the vmPFC exerts inhibitory control over unrewarded behaviors.Keywords basolateral nucleus; infralimbic cortex; nucleus accumbens; prelimbic cortex; cingulate cortex; reward-seeking behavior Cue-evoked reward-seeking behaviors require recognition of learned cues that predict reward availability and selection of appropriate motor responses. Performance of reward-seeking behavior requires integrated functions of multiple brain areas including the basolateral nucleus of the amygdala (BLA), medial prefrontal cortex (mPFC), nucleus accumbens (NAc) and ventral tegmental area (VTA). The BLA and mPFC play crucial roles in reward-related © 2008 IBRO. Published by Elsevier Ltd. All rights reserved.Corresponding author: Akinori Ishikawa 1-1-1 Minamikogushi, Ube, Yamaguchi, 755-8505, Japan Phone: 81-836-22-2211 Fax: 81-836-22-2211.jp. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2010 July 9. Published in final edited form as:Neuroscience. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript behaviors and are major sources of glutamatergic afferents to the NAc (McGeorge and Faull, 1989;Brog et al., 1993;Zahm, 2000). The NAc, which receives excitatory inputs from the BLA and mPFC and projects via both direct and indir...

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Section: Inactivation Of the Blamentioning

confidence: 99%

Contributions of the amygdala and medial prefrontal cortex to incentive cue responding

et al. 2008

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“…Thus, it is important to know whether dopamine can change on this timescale as well. Dopaminergic terminals form synapses on the neck of spines and dendrites of the projection neurons in the nucleus accumbens, and are in close proximity to glutametergic synapses originating from neurons in the hippocampus, basolateral amygdala, and prefrontal cortex (Totterdell and Smith, 1989;Sesack and Pickel, 1990;Johnson et al, 1994). Thus, dopamine is in a prominent position to modulate these inputs (O'Donnell et al, 1999;Nicola et al, 2000) and exert control over the activity of microcircuits within the nucleus accumbens that ultimately control behavior (Pennartz et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Rapid Dopamine Signaling in the Nucleus Accumbens during Contingent and Noncontingent Cocaine Administration

Stuber

Roitman

Phillips

et al. 2004

Neuropsychopharmacol

204

231

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Cocaine acts as a reinforcer through its pharmacological effects on brain monoaminergic systems, which, through repeated pairings with environmental stimuli, lead to the development of conditioned effects of the drug. Both the pharmacological and conditioned aspects of cocaine are implicated in several facets of acquisition and maintenance of addiction, including drug craving. Here, we compare the effects of contingent (response dependent) and noncontingent (response independent) cocaine on rapid dopaminergic signaling in the core of the nucleus accumbens. Dopamine was monitored using fast-scan cyclic voltammetry. Noncontingent cocaine administered to both naïve and animals with a history of self-administration resulted in a profound increase in the frequency of transient dopamine release events that are not time-locked to any specific environmental stimuli. Pharmacological effects were detectable approximately 40 s after cocaine administration. In contrast, when animals where allowed to self-administer cocaine on an FR-1 schedule, dopamine transients (69712 nM) were consistently observed time-locked to each reinforced response (peaking approximately 1.5 s after response completion). Importantly, no pharmacological effect of cocaine was observed within the 10 s following noncontingent cocaine administration, indicating that dopamine signals time-locked to the reinforced response are a result of the pairing of the operant behavior, the drug-associated cues, and cocaine. These data demonstrate that this pharmacological action of cocaine occurs for an extended period following either contingent or noncontingent administration, but is distinct from those dopamine transients that are time-locked to each lever-press in self-administering animals.

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“…In particular, several studies have found the opioid receptor-rich basolateral amygdala (13) to be important for encoding the incentive value of the rewards that support the performance of goal-directed actions in rats (14)(15)(16)(17). Although it is possible that opioid-related processes form an integrated reward network (18), the neural processes mediating palatability, or liking, may be distinct from those that establish the desirability of the consequences of goal-directed actions (19,20).…”

mentioning

confidence: 99%

Distinct opioid circuits determine the palatability and the desirability of rewarding events

Wassum

Ostlund²,

Maidment³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

155

167

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It generally is assumed that a common neural substrate mediates both the palatability and the reward value of nutritive events. However, recent evidence suggests this assumption may not be true. Whereas opioid circuitry in both the nucleus accumbens and ventral pallidum has been reported to mediate taste-reactivity responses to palatable events, the assignment of reward or inventive value to goal-directed actions has been found to involve the basolateral amygdala. Here we found that, in rats, the neural processes mediating palatability and incentive value are indeed dissociable. Naloxone infused into either the ventral pallidum or nucleus accumbens shell blocked the increase in sucrose palatability induced by an increase in food deprivation without affecting the performance of sucrose-related actions. Conversely, naloxone infused into the basolateral amygdala blocked food deprivation-induced changes in sucrose-related actions without affecting sucrose palatability. This double dissociation of opioidmediated changes in palatability and incentive value suggests that the role of endogenous opioids in reward processing does not depend on a single neural circuit. Rather, changes in palatability and in the incentive value assigned to rewarding events seem to be mediated by distinct neural processes.incentive value ͉ taste reactivity ͉ instrumental conditioning ͉ opioid receptors ͉ basolateral amygdala

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Input from the amygdala to the rat nucleus accumbens: Its relationship with tyrosine hydroxylase immunoreactivity and identified neurons

Cited by 153 publications

References 36 publications

Contributions of the amygdala and medial prefrontal cortex to incentive cue responding

Contributions of the amygdala and medial prefrontal cortex to incentive cue responding

Rapid Dopamine Signaling in the Nucleus Accumbens during Contingent and Noncontingent Cocaine Administration

Distinct opioid circuits determine the palatability and the desirability of rewarding events

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