D-Amphetamine-induced behavioral sensitization: effect of lesioning dopaminergic terminals in the medial prefrontal cortex, the amygdala and the entorhinal cortex

Bjijou, Y; Deurwaerdère, Philippe De; Spampinato, Umberto; Stinus, Luis; Cador, Martine

doi:10.1016/s0306-4522(01)00508-5

Cited by 53 publications

(34 citation statements)

References 51 publications

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“…The behavioral effects of prefrontal cortical DA depletion are in agreement with previous results obtained in rat (Pycock et al, 1980;Bjijou et al, 2002), but not with others (King et al, 1997). It is worth noting that selective DA depletion of pFC has been shown to increase the effects of systemic cocaine on DA outflow in the NAc as well as on locomotion, thus leading to sensitization-like effects in rats receiving acute psychostimulant challenge (Beyer and Steketee, 1999).…”

Section: Discussionsupporting

confidence: 90%

Dopamine in the Medial Prefrontal Cortex Controls Genotype-Dependent Effects of Amphetamine on Mesoaccumbens Dopamine Release and Locomotion

Ventura

Alcaro

Cabib

et al. 2003

Neuropsychopharmacol

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Mice of background DBA/2J are hyporesponsive to the behavioral effects of D-amphetamine in comparison with the widely exploited murine background C57BL/6J. In view of the important role of dopamine (DA) release in the nucleus accumbens (NAc) regarding the behavioral effects of psychostimulants, we tested the hypothesis of an inverse relationship between mesocortical and mesoaccumbens DA functioning in the two backgrounds. Systemic D-amphetamine induces a sustained increase in DA release in the medial prefrontal cortex (mpFC) accompanied by a poor increase in the NAc in mice of the low-responsive DBA/2J background, as shown by intracerebral microdialysis in freely moving animals. The opposite occurs in C57BL/6J mice, which show low prefrontal cortical DA outflow accompanied by high accumbal extracellular DA. Moreover, the DBA/2J background showed lower locomotor activity than C57BL/6J mice following D-amphetamine challenge. Selective DA depletion in the mpFC of DBA/2J mice produced a clear-cut increase in D-amphetamine-induced DA outflow in the NAc as well as locomotor activity that reached levels similar to those observed in C57BL/6J mice. Finally, local infusion of D-amphetamine by reverse microdialysis produced a similar increase in extracellular DA in both the mpFC and the NAc of DBA/2J mice. This finding points to similar transporter-related mechanisms in the two brain areas and supports the hypothesis that low accumbal DA release induced by systemic D-amphetamine in the DBA/2J background is determined by the inhibitory action of prefrontal cortical DA. The present results indicate that genotype-dependent susceptibility to addictive properties of D-amphetamine involves unbalanced DA transmission in the mesocorticolimbic system.

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Section: Discussionsupporting

confidence: 90%

Dopamine in the Medial Prefrontal Cortex Controls Genotype-Dependent Effects of Amphetamine on Mesoaccumbens Dopamine Release and Locomotion

Ventura

Alcaro

Cabib

et al. 2003

Neuropsychopharmacol

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“…As 6-hydroxydopamine lesions of the prefrontal cortex prevent development of amphetamine-induced behavioral sensitization (Bjijou et al, 2002), the retarded behavioral sensitization to METH seen here could result from a deficiency in prefrontal dopamine. Typically, perturbations to the prefrontal cortex, such as produced by chemical lesions, are only mildly detrimental to the acquisition and expression of CPP (eg Zavala et al, 2003), but have particularly strong effects on relapse behavior.…”

Section: Role Of Endogenous N/ofq In Behavioral Sensitizationmentioning

confidence: 69%

Endogenous Nociceptin (Orphanin FQ) Suppresses Basal Hedonic State and Acute Reward Responses to Methamphetamine and Ethanol, but Facilitates Chronic Responses

Sakoori

Murphy

2007

Neuropsychopharmacol

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The opioid peptide nociceptin (orphanin FQ) suppresses drug reward, drug self-administration, and impedes some of the processes believed to underlie the transition to addiction. As virtually all previous studies have used administration of nociceptin receptor agonists to evaluate the role of nociceptin on addiction-like behavior, the current study used a pharmacological (nociceptin receptor antagonist) and genetic (nociceptin receptor knockout mice) approach to elucidate the role of endogenous nociceptin. The nociceptin receptor antagonist UFP-101 induced a modest place preference, and enhanced the conditioned place preference induced by methamphetamine. In agreement with this, nociceptin receptor knockout mice had slightly enhanced methamphetamine and ethanol conditioned place preferences compared to wild-type mice. This effect did not appear to depend on differences in learning ability, as nociceptin receptor knockout mice had slightly weaker-conditioned place aversions to lithium chloride, the k-opioid receptor agonist, U50488H, and the general opiate antagonist, naloxone. The development of behavioral sensitization to methamphetamine was lower in nociceptin receptor knockout mice, and attenuated by UFP-101 administration to wild-type mice. Additionally, ethanol consumption and preference in a two-bottle choice test was lower in nociceptin receptor knockout mice, though ethanol-stimulated locomotion was stronger. Whereas the rewarding effect of methamphetamine and ethanol following chronic treatment, as measured by place conditioning, strengthened in wild-type mice, this effect was absent in nociceptin receptor knockout mice. These results suggest that endogenous N/OFQ suppresses basal and drug-stimulated increases in hedonic state, and plays either a permissive or facilitatory role in the development of addiction.

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“…Both dopaminergic and non-dopaminergic projections from the VTA to the amygdala have been identified in other species [43]. The dopaminergic projections in particular are of interest since they are important in behavioral sensitization processes [4] that likely play a role in pair bonding. The amygdala in turn can modulate glutamate release in both the PFC and NAcc, and modulate dopamine release in the NAcc via a glutamate-mediated mechanism within the PFC [5].…”

Section: Partner Preference Inductionmentioning

confidence: 99%

Ventral tegmental area involvement in pair bonding in male prairie voles

Curtis

Wang

2005

Physiology & Behavior

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Dopamine is known to play a critical role in social attachment in monogamous voles. However, little is known about the neurochemical regulation of central dopamine release during pair bond formation. Here we examine the effects on partner preference formation in male prairie voles of neurochemical manipulations in the ventral tegmental area (VTA), a major source of dopamine to brain regions implicated in pair bonding. Administration of NBQX, an AMPA receptor antagonist, or bicuculline, a GABA receptor antagonist, into the VTA induced partner preferences within 6 h in the absence of mating. We also found that, after unilateral administration of NBQX into the VTA, neuronal activation, as indicated by the expression of the immediate early gene c-fos, was decreased in the nucleus accumbens, prefrontal cortex, and medial amygdala, but was unchanged in the lateral septum and in a control region, the arcuate nucleus. These results confirm a role for the VTA in partner preference formation in monogamous voles and extend the list of neurochemicals important in pair bonding to include glutamate and GABA. D

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D-Amphetamine-induced behavioral sensitization: effect of lesioning dopaminergic terminals in the medial prefrontal cortex, the amygdala and the entorhinal cortex

Cited by 53 publications

References 51 publications

Dopamine in the Medial Prefrontal Cortex Controls Genotype-Dependent Effects of Amphetamine on Mesoaccumbens Dopamine Release and Locomotion

Dopamine in the Medial Prefrontal Cortex Controls Genotype-Dependent Effects of Amphetamine on Mesoaccumbens Dopamine Release and Locomotion

Endogenous Nociceptin (Orphanin FQ) Suppresses Basal Hedonic State and Acute Reward Responses to Methamphetamine and Ethanol, but Facilitates Chronic Responses

Ventral tegmental area involvement in pair bonding in male prairie voles

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