Dopamine antagonist modulation of amphetamine response as detected using pharmacological MRI

Dixon, Aisling L.; Prior, M. J. W.; Morris, Peter; Shah, Yasmene B.; Joseph, Michael H.; Young, Andrew M. J.

doi:10.1016/j.neuropharm.2004.10.006

Cited by 73 publications

(59 citation statements)

References 39 publications

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“…Several phMRI studies have provided compelling evidence that the striatal hemodynamic response produced by amphetamine reflects primarily the dopaminergic effects (reviewed in Knutson and Gibbs, 2007). For example, amphetamine has been shown to elicit BOLD or rCBV increases in DA-rich ventrostriatal areas that are linearly correlated to synaptic DA concentrations (Dixon et al, 2005;Ren et al, 2009;Choi et al, 2006;Schwarz et al, 2007b;Preece et al, 2007). Moreover, amphetamine-induced rCBV responses are abolished in the DA denervated areas (Chen et al, 1997(Chen et al, , 1999, an effect that can be later restored after fetal or stem cell transplantation (Bjorklund et al, 2002;Chen et al, 1999).…”

Section: Altered Brain Function After Cocaine Self-administrationmentioning

confidence: 99%

Neuroimaging Evidence of Altered Fronto-Cortical and Striatal Function after Prolonged Cocaine Self-Administration in the Rat

Gozzi

Tessari

Dacome

et al. 2011

Neuropsychopharmacol

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Cocaine addiction is often modeled in experimental paradigms where rodents learn to self-administer (SA) the drug. However, the extent to which these models replicate the functional alterations observed in clinical neuroimaging studies of cocaine addiction remains unknown. We used magnetic resonance imaging (MRI) to assess basal and evoked brain function in rats subjected to a prolonged, extended-access cocaine SA scheme. Specifically, we measured basal cerebral blood volume (bCBV), an established correlate of basal metabolism, and assessed the reactivity of the dopaminergic system by mapping the pharmacological MRI (phMRI) response evoked by the dopamine-releaser amphetamine. Cocaine-exposed subjects exhibited reduced bCBV in fronto-cortical areas, nucleus accumbens, ventral hippocampus, and thalamus. The cocaine group also showed an attenuated functional response to amphetamine in ventrostriatal areas, an effect that was significantly correlated with total cocaine intake. An inverse relationship between bCBV in the reticular thalamus and the frontal response elicited by amphetamine was found in control subjects but not in the cocaine group, suggesting that the inhibitory interplay within this attentional circuit may be compromised by the drug. Importantly, histopathological analysis did not reveal significant alterations of the microvascular bed in the brain of cocaine-exposed subjects, suggesting that the imaging findings cannot be merely ascribed to cocaine-induced vascular damage. These results document that chronic, extended-access cocaine SA in the rat produces focal fronto-cortical and striatal alterations that serve as plausible neurobiological substrate for the behavioral expression of compulsive drug intake in laboratory animals.

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Section: Altered Brain Function After Cocaine Self-administrationmentioning

confidence: 99%

Neuroimaging Evidence of Altered Fronto-Cortical and Striatal Function after Prolonged Cocaine Self-Administration in the Rat

Gozzi

Tessari

Dacome

et al. 2011

Neuropsychopharmacol

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“…A prominent advantage of fMRI is the ability to collect temporal data of a drug's effect in different brain regions in a single animal. BOLD-induced brain activation has been used to examine the effects of pharmacological agents, such as amphetamine (Dixon et al, 2005), cocaine (Febo et al, 2005), and citalopram (Steward et al, 2005).…”

mentioning

confidence: 99%

5-Hydroxytryptamine2C Receptor Contribution to m-Chlorophenylpiperazine and N-Methyl-β-carboline-3-carboxamide-Induced Anxiety-Like Behavior and Limbic Brain Activation

Hackler¹,

Turner²,

Gresch³

et al. 2006

J Pharmacol Exp Ther

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Activation of 5-hydroxytryptamine2C (5-HT 2C ) receptors by the 5-HT 2 receptor agonist m-chlorophenylpiperazine (m-CPP) elicits anxiety in humans and anxiety-like behavior in animals. We compared the effects of m-CPP with the anxiogenic GABA A receptor inverse agonist N-methyl-␤-carboline-3-carboxamide (FG-7142) on both anxiety-like behavior and regional brain activation using functional magnetic resonance imaging (fMRI) in the rat. We also determined whether the selective 5-HT 2C receptor antagonist SB 242084 [6-chloro-2,3-dihydro-5-methyl-N-[6-[(2-methyl-3-pyridinyl)oxy]-3-pyridinyl]-1H-indole-1-carboxyamide dihydrochloride] would blunt m-CPP or FG-7142-induced neuronal activation. Both m-CPP (3 mg/kg i.p.) and FG-7142 (10 mg/kg i.p.) elicited anxiety-like behavior when measured in the social interaction test, and pretreatment with SB 242084 (1 mg/kg i.p.) completely blocked the behavioral effects of both anxiogenic drugs. Regional brain activation in vivo in response to anxiogenic drug challenge was determined by blood oxygen level-dependent (BOLD) fMRI using a powerful 9.4T magnet. Region of interest analyses revealed that m-CPP and FG-7142 significantly increased BOLD signals in brain regions that have been linked to anxiety, including the amygdala, dorsal hippocampus, and medial hypothalamus. These BOLD signal increases were blocked by pretreatment with SB 242084. In contrast, injection of m-CPP and FG-7142 resulted in BOLD signal decreases in the medial prefrontal cortex that were not blocked by SB 242084. In conclusion, the brain activation signals produced by anxiogenic doses of both m-CPP and FG-7142 are mediated at least partially by the 5-HT 2C receptor, indicating that this receptor is a key component in anxiogenic neural circuitry.The 5-hydroxytryptamine 2C (5-HT 2C ) receptor has been implicated in mood and anxiety disorders and is a target for development of novel anxiolytic drugs (Wood, 2003). Selective and nonselective 5-HT 2C receptor antagonists reduce anxiety-like behavior in several animal models of anxiety (Stutzmann et al., 1991;Kennett et al., 1995;Griebel et al., 1997). (Charney et al., 1987;Lowy and Meltzer, 1988;Kahn and Wetzler, 1991;Gatch, 2003;de Mello Cruz et al., 2005). For example, m-CPP administration to mice resulted in less time spent on the open arms of an elevated plus maze (Benjamin et al., 1990), and in rats, anxiety-like behavior has been reported in the This study was supported by National Institutes of Health Grants T32 GM07628, RO1 MH34007, and R01 EB02326 and a predoctoral fellowship from the PhRMA foundation (to E.A.H.).Article, publication date, and citation information can be found at http://jpet.aspetjournals.org. doi:10.1124/jpet.106.113357. 2C , 5-hydroxytryptamine2C; m-CPP, m-chlorophenylpiperazine; FG-7142, N-methyl-␤-carboline-3-carboxamide; SB 242084, 6-chloro-2,3-dihydro-5-methyl-N-[6-[(2-methyl-3-pyridinyl)oxy]-3-pyridinyl]-1H-indole-1-carboxyamide dihydrochloride; fMRI, functional magnetic resonance imaging; BOLD, blood oxygen level-dependent;...

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“…Moreover, administering amphetamine or cocaine to the basolateral region of amygdala failed to induce conditioned place preference/aversion in animals, while administering amphetamine into the central region of amygdala induced a strong conditioned place preference in rats (Vollm, 2004). Additionally, administering agonists and antagonists of dopamine, as well as GABAergic and cholinergic drugs into different regions of the amygdala yielded no effects (Dixon and Prior, 2005). Hsu et al (2002) demonstrated that administering bupivacaine (a topical anesthetic agent) into the basolateral region of amygdala suppresses the conditioned place preference caused by amphetamine.…”

Section: Discussionmentioning

confidence: 95%

Effect of amygdaloid complex inhibition on nicotine-induced conditioned place preference in rats

2017

J App Pharma Sci

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Nicotine dependence is the major cause of cigarette smoking. The dependence occurred in the brain mesolimbic system and the amygdala has an important role in its initiation. Nicotine can activate dopaminergic neurons within the amygdaloid complex However, there is no evidence about complete inhibition of amygdala on nicotine dependence, thus in the present study we used conditioned-place preference (CPP) method to study the effect of transient inhibition of left and/or right side of the amygdala by lidocain e on nicotine reward properties in male Wistar rats. One week after two side cannulation and recovery the rats were conditioned to nicotine. Lidocaine hydrochloride (2%) was injected in amygdaloid complex, five min before each nicotine intraperitoneal (IP) injection for transient inhibition. On the test day, the animals were placed in the apparatus and their behaviors were recorded by a camera for 600 seconds. Then the records were analysis off line for sniffing, rearing, locomotion and compartment crossing. Three-way analysis of variance (ANOVA) was performed for statistical analysis. Our results showed that intra-peritoneal injection of nicotine (1 and 1.5 mg/kg) induced place preference. Transient inhibition of left or /and right side of the amygdaloid co mplex reduces nicotine place conditioning. In addition, rearing and compartment crossing also were reduced. However, when left side of the nucleus was inhibited, sniffing was increased, but when the right side was inhibited the sniffing was decreased. In conclusion, these results confirmed the involvement of both left and right sides of the amygdaloid complex in nicotine place conditioning.

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Dopamine antagonist modulation of amphetamine response as detected using pharmacological MRI

Cited by 73 publications

References 39 publications

Neuroimaging Evidence of Altered Fronto-Cortical and Striatal Function after Prolonged Cocaine Self-Administration in the Rat

Neuroimaging Evidence of Altered Fronto-Cortical and Striatal Function after Prolonged Cocaine Self-Administration in the Rat

5-Hydroxytryptamine2C Receptor Contribution to m-Chlorophenylpiperazine and N-Methyl-β-carboline-3-carboxamide-Induced Anxiety-Like Behavior and Limbic Brain Activation

Effect of amygdaloid complex inhibition on nicotine-induced conditioned place preference in rats

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