Literature DB >> 2066777

The lateral nucleus of the amygdala mediates expression of the amphetamine-produced conditioned place preference.

N Hiroi1, N M White.   

Abstract

We investigated the involvement of the hippocampal formation and the amygdala in the acquisition and expression of the amphetamine-produced conditioned place preference (CPP). Animals were conditioned in four sessions that included two pairings of d-amphetamine (2.0 mg/kg, s.c.) with one of two distinct compartments and two pairings of vehicle with the other compartment in a counterbalanced manner. Animals' preferences for the compartments were then tested in the absence of amphetamine. The CPP was attenuated by preconditioning electrolytic or excitotoxic lesions of the lateral nucleus of amygdala, but not by electrolytic lesions of the central or basolateral nucleus of amygdala, endopiriform nucleus, or ventral hippocampus or by radio-frequency lesions of the fornix-fimbria. When the lateral nucleus of amygdala was damaged by electrolytic or excitotoxic lesions after conditioning, animals failed to express an amphetamine-produced CPP. These results demonstrate that expression of the amphetamine-produced CPP is mediated by intrinsic neurons of the lateral nucleus of the amygdala, and that neither acquisition nor expression of the CPP is mediated by the central or basolateral amygdaloid nucleus or the hippocampus-accumbens projection. Combined with our previous finding that the expression of the amphetamine-produced CPP is also mediated by dopamine receptor activation in the nucleus accumbens (Hiroi and White, 1989, 1990), it could be suggested that the lateral nucleus of the amygdala and dopamine terminals in the nucleus accumbens are parts of the neural circuitry that mediates the expression of the amphetamine-produced CPP.

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Year:  1991        PMID: 2066777      PMCID: PMC6575472     

Source DB:  PubMed          Journal:  J Neurosci        ISSN: 0270-6474            Impact factor:   6.167


  45 in total

1.  Control of response selection by reinforcer value requires interaction of amygdala and orbital prefrontal cortex.

Authors:  M G Baxter; A Parker; C C Lindner; A D Izquierdo; E A Murray
Journal:  J Neurosci       Date:  2000-06-01       Impact factor: 6.167

2.  Excitotoxic lesions of the amygdala fail to produce impairment in visual learning for auditory secondary reinforcement but interfere with reinforcer devaluation effects in rhesus monkeys.

Authors:  L Málková; D Gaffan; E A Murray
Journal:  J Neurosci       Date:  1997-08-01       Impact factor: 6.167

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Review 5.  Neurobiologic processes in drug reward and addiction.

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6.  Incidental information acquired by the amygdala during acquisition of a stimulus-response habit task.

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7.  Selective, retrieval-independent disruption of methamphetamine-associated memory by actin depolymerization.

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8.  Extinction of drug- and withdrawal-paired cues in animal models: relevance to the treatment of addiction.

Authors:  Karyn M Myers; William A Carlezon
Journal:  Neurosci Biobehav Rev       Date:  2010-01-28       Impact factor: 8.989

Review 9.  Dopamine reward circuitry: two projection systems from the ventral midbrain to the nucleus accumbens-olfactory tubercle complex.

Authors:  Satoshi Ikemoto
Journal:  Brain Res Rev       Date:  2007-05-17

10.  The effects of infusions of CART 55-102 into the basolateral amygdala on amphetamine-induced conditioned place preference in rats.

Authors:  David J Rademacher; Elyse M Sullivan; David A Figge
Journal:  Psychopharmacology (Berl)       Date:  2009-12-16       Impact factor: 4.530

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