Neuronal activity in the nucleus accumbens is necessary for performance-related increases in cortical acetylcholine release

Neigh, Gretchen N.; Arnold, H. Moore; Rabenstein, Rebecca L.; Sarter, Martin; Bruno, John P.

doi:10.1016/j.neuroscience.2003.10.006

Cited by 36 publications

(25 citation statements)

References 55 publications

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“…Specifically, it appears that DA receptor activation in the NAc modulates NBM cholinergic neuron activity and the release of ACh in the cortex (Moore et al 1999;Neigh et al 2004). The findings of the present experiments, together with those of Neigh et al (2004) and Moore et al (1999), suggest that the BLA influences memory consolidation, at least in part, by regulating the release of DA in the NAc, which, in turn, influences NBM activity and subsequent release of ACh in the cortex.…”

Section: Discussionsupporting

confidence: 64%

Modulation of memory consolidation by the basolateral amygdala or nucleus accumbens shell requires concurrent dopamine receptor activation in both brain regions

LaLumiere¹,

Nawar²,

McGaugh³

2005

Learn. Mem.

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Previous findings indicate that the basolateral amygdala (BLA) and the nucleus accumbens (NAc) interact in influencing memory consolidation. The current study investigated whether this interaction requires concurrent dopamine (DA) receptor activation in both brain regions. Unilateral, right-side cannulae were implanted into the BLA and the ipsilateral NAc shell or core in male Sprague-Dawley rats (∼300 g). One week later, the rats were trained on an inhibitory avoidance (IA) task and, 48 h later, they were tested for retention. Drugs were infused into the BLA and NAc shell or core immediately after training. Post-training intra-BLA infusions of DA enhanced retention, as assessed by latencies to enter the shock compartment on the retention test. Infusions of the general DA receptor antagonist cis-Flupenthixol (Flu) into the NAc shell (but not the core) blocked the memory enhancement induced by the BLA infusions of DA. In the reverse experiment, post-training intra-NAc shell infusions of DA enhanced retention and Flu infusions into the BLA blocked the enhancement. These findings indicate that BLA modulation of memory consolidation requires concurrent DA receptor activation in the NAc shell but not the core. Similarly, NAc shell modulation of memory consolidation requires concurrent DA receptor activation in the BLA. Together with previous findings, these results suggest that the dopaminergic innervation of the BLA and NAc shell is critically involved in the modulation of memory consolidation.

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Section: Discussionsupporting

confidence: 64%

Modulation of memory consolidation by the basolateral amygdala or nucleus accumbens shell requires concurrent dopamine receptor activation in both brain regions

LaLumiere¹,

Nawar²,

McGaugh³

2005

Learn. Mem.

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“…Therefore, the present results may not generalize to a test of the effects of the antipsychotic treatments in interaction with AMPH pretreatment and -challenges on other behavioral or cognitive operations that do not, or not to the same degree, depend on cortical cholinergic activity (see also Sarter et al, 2007). Furthermore, we hypothesized that the frozen cortical cholinergic input system in AMPH-pretreated and -challenged animals resulted from a disruption of limbictelencephalic circuitry (Goto and Grace, 2005;Homayoun and Moghaddam, 2006) involving, as a major final pathway, the projection from the nucleus accumbens to the cholinergic basal forebrain (Neigh et al, 2004;NeighMcCandless et al, 2002;Zmarowski et al, 2005Zmarowski et al, , 2007. Haloperdol and clozapine may restore a critical mechanism in the cortical-mesolimbic-basal forebrain interplay, therefore restoring the ability to recruit the basal forebrain cholinergic system for the mediation of attentional performance (see also Barak and Weiner, 2007).…”

Section: Discussionmentioning

confidence: 99%

Detection of the Moderately Beneficial Cognitive Effects of Low-Dose Treatment with Haloperidol or Clozapine in an Animal Model of the Attentional Impairments of Schizophrenia

Martı́nez

Sarter

2007

Neuropsychopharmacol

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The absence of effective cognition enhancers for the treatment of patients with schizophrenia limits the validation of animal models and behavioral tests used for drug finding and characterization. However, low doses of haloperidol and clozapine were documented to produce moderately beneficial effects in patients. Therefore, this experiment was designed to determine the attentional effects of such treatments in a repeated-amphetamine (AMPH) animal model. Animals were trained in an operant-sustained attention task and underwent a 40-day pretreatment period with saline or increasing doses (1-10 mg per kg) of AMPH. After regaining baseline performance following 10 days of saline treatment, animals were treated with haloperidol (0.025 mg per kg), clozapine (2.5 mg per kg), or vehicle for 10 days. Furthermore, the effects of AMPH challenges (1.0 mg per kg) were assessed. In AMPH-pretreated animals, the administration of AMPH challenges resulted in the disruption of attentional performance. Treatment with haloperidol and clozapine attenuated the detrimental performance effects of these challenges, with clozapine exhibiting more robust attenuation. Furthermore, clozapine, but not haloperidol, impaired the performance of control animals. In contrast, the performance of AMPH-pretreated animals remained unaffected by clozapine. As this animal model detects the moderately beneficial cognitive effects of haloperidol and clozapine, it may be useful for preclinical research designed to detect and characterize treatments for the cognitive symptoms of schizophrenia.

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“…These data indicate that, as a result of prior psychostimulant exposure, a fundamental re-regulation of the target neuronal system and associated circuitry radically alters the effects of subsequent psychostimulant exposure, and that it requires performance-induced activation of the target system and associated circuits to reveal such re-regulation. Repeated psychostimulant exposure may have modified the regulation of cortical ACh release via altered prefrontal regulation of circuits linking mesolimbic with basal forebrain cholinergic neurons (Neigh-McCandless et al, 2002;Neigh et al, 2001Neigh et al, , 2004. Importantly, the functional impact of this dysregulation is only revealed in interaction with the activation of distributed circuits by task performance (see also Sarter and Bruno, 2000).…”

Section: Neurotransmitter Dysregulation In Recruited Circuits: the Simentioning

confidence: 99%

Abnormal Neurotransmitter Release Underlying Behavioral and Cognitive Disorders: Toward Concepts of Dynamic and Function-Specific Dysregulation

Sarter

Bruno

Parikh

2006

Neuropsychopharmacol

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Abnormalities in the regulation of neurotransmitter release and/or abnormal levels of extracellular neurotransmitter concentrations have remained core components of hypotheses on the neuronal foundations of behavioral and cognitive disorders and the symptoms of neuropsychiatric and neurodegenerative disorders. Furthermore, therapeutic drugs for the treatment of these disorders have been developed and categorized largely on the basis of their effects on neurotransmitter release and resulting receptor stimulation. This perspective stresses the theoretical and practical implications of hypotheses that address the dynamic nature of neurotransmitter dysregulation, including the multiple feedback mechanisms regulating synaptic processes, phasic and tonic components of neurotransmission, compartmentalized release, differentiation between dysregulation of basal vs activated release, and abnormal release from neuronal systems recruited by behavioral and cognitive activity. Several examples illustrate that the nature of the neurotransmitter dysregulation in animal models, including the direction of drug effects on neurotransmitter release, depends fundamentally on the state of activity of the neurotransmitter system of interest and on the behavioral and cognitive functions recruiting these systems. Evidence from evolving techniques for the measurement of neurotransmitter release at high spatial and temporal resolution is likely to advance hypotheses describing the pivotal role of neurotransmitter dysfunction in the development of essential symptoms of major neuropsychiatric disorders, and also to refine neuropharmacological mechanisms to serve as targets for new treatment approaches. The significance and usefulness of hypotheses concerning the abnormal regulation of the release of extracellular concentrations of primary messengers depend on the effective integration of emerging concepts describing the dynamic, compartmentalized, and activitydependent characteristics of dysregulated neurotransmitter systems.

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Neuronal activity in the nucleus accumbens is necessary for performance-related increases in cortical acetylcholine release

Cited by 36 publications

References 55 publications

Modulation of memory consolidation by the basolateral amygdala or nucleus accumbens shell requires concurrent dopamine receptor activation in both brain regions

Modulation of memory consolidation by the basolateral amygdala or nucleus accumbens shell requires concurrent dopamine receptor activation in both brain regions

Detection of the Moderately Beneficial Cognitive Effects of Low-Dose Treatment with Haloperidol or Clozapine in an Animal Model of the Attentional Impairments of Schizophrenia

Abnormal Neurotransmitter Release Underlying Behavioral and Cognitive Disorders: Toward Concepts of Dynamic and Function-Specific Dysregulation

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