Electrophysiological evaluation of the time-course of dopamine uptake inhibition induced by intravenous cocaine at a reinforcing dose

Wakazono, Yoshihiko; Kiyatkin, Eugene A.

doi:10.1016/j.neuroscience.2007.11.034

Cited by 8 publications

(9 citation statements)

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“…However new insight into the neural correlates of how cocaine and juice rewards were compatibly encoded within VStr and DStr is provided via determination of a complex hierarchical classification scheme composed of trial-specific neuronal firing patterns for cocaine vs. juice rewards for the same behaviors . Such a scheme is consistent with several new proposals regarding 1) the basis for activation of neuronal firing related to drug seeking in rats, NHPs and humans (Vezina 2004, Rebec and Sun 2005, Risinger et al 2005, Hollander and Carelli 2007, Wakazono and Kiyatkin 2008) and 2) the encoding of reward value by the striatum (Zink et al 2004, Di Pietro et al 2006, Ding and Hikosaka 2006, Grace et al 2007, Lee et al 2006) and other brain regions (Takeda and Funahashi 2006, Simmons and Richmond 2008, Mogami et al 2007, Belova et al 2007). …”

Section: Discussionsupporting

confidence: 87%

The encoding of cocaine vs. natural rewards in the striatum of nonhuman primates: categories with different activations

2009

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The behavioral and motivational changes that result from use of abused substances depend upon activation of neuronal populations in the reward centers of the brain, located primarily in the corpus striatum in primates. To gain insight into the cellular mechanisms through which abused drugs reinforce behavior in the primate brain, changes in firing of neurons in the ventral (VStr, nucleus accumbens) and dorsal (DStr, caudate-putamen) striatum to "natural" (juice) vs. drug (intravenous (IV) cocaine) rewards were examined in four rhesus monkeys performing a visual Go-Nogo decision task. Task-related striatal neurons increased firing to one or more of the specific events that occurred within a trial represented by: 1) Target stimuli (Go trials) or 2) Nogotarget stimuli (Nogo trials), and 3) Reward delivery for correct performance. These three cell populations were further subdivided into categories that reflected firing exclusively on one or the other type of signaled reward (juice or cocaine) trial (20-30% of all cells), or, a second subpopulation that fired on both (cocaine and juice) types of rewarded trial (50%). Results show that neurons in the primate striatum encoded cocaine rewarded trials similar to juice rewarded trials, except for 1) increased firing on cocaine rewarded trials, 2) prolonged activation during delivery of IV cocaine infusion, 3) differential firing in ventral (VStr cells) vs. dorsal (DStr cells) striatum cocaine rewarded trials. Reciprocal activations of antithetic subpopulations of cells during different temporal intervals within the same trial suggest a functional interaction between processes that encode drug and natural rewards in the primate brain.

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Section: Discussionsupporting

confidence: 87%

The encoding of cocaine vs. natural rewards in the striatum of nonhuman primates: categories with different activations

2009

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“…Since the effect of the prior cocaine reward was to significantly suppress PFC neuron firing and performance only on immediately succeeding juice trials (Fig. 7), it was likely that the residual pharmacological actions of cocaine reward delivery did not extend beyond 2 min (Wakazono and Kiyatkin 2008) and therefore did not affect responding on other juice trials in the same session.…”

Section: Discussionmentioning

confidence: 99%

Effects of cocaine rewards on neural representations of cognitive demand in nonhuman primates

et al. 2010

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Rationale Investigations of the neural consequences of the effects of cocaine on cognition have centered on specific brain circuits including prefrontal cortex, medial temporal lobe and striatum and their roles in controlling drug dependent behavior and addiction. These regions are critical to many aspects of drug abuse; however recent investigations in addicted individuals have reported possible cognitive deficits that impact recovery and other therapeutic interventions. Objectives Therefore a direct assessment of the effects of cocaine as a reward for cognitive function provides a means of determining how brain systems involved such as prefrontal cortex are affected under normal vs. conditions of acute drug exposure as a precursor to the final impaired function in the addicted state. Methods Nonhuman primates (NHPs) were tested in a delayed-match-to-sample decision making task to determine effects of high vs. low cognitive load trials on single neuron activity and fluorodeoxyglucose-positron emission tomography (FDG-PET) determined metabolic activation of prefrontal cortex when juice vs. intravenous cocaine were employed as rewards for successful performance. Results Cognitive processing in prefrontal cortex was altered primarily on high load trials in which cocaine was randomly presented as the signaled and delivered reward on particular trials. The detrimental actions of cocaine rewards were also shown to persist and impair task performance on subsequent juice rewarded trials. Conclusions The findings indicate that one of the ways in which cocaine use may disrupt performance of a cognitive task is to alter neural processing in prefrontal cortex when involved in discriminating circumstances on the basis of low vs. high cognitive demand.

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“…cocaine (Wakazono and Kiyatkin, 2008). In these studies, the effects of cocaine on DA uptake were indirectly estimated by measuring the increase in magnitude of DA-induced inhibition of striatal cell firing, resulting from DAT inhibition by i.v.…”

Section: Discussionmentioning

confidence: 99%

“…cocaine on DA-induced striatal neuronal responses occur approximately 5 min after i.v. administration (Wakazono and Kiyatkin, 2008). …”

mentioning

confidence: 99%

Short-acting cocaine and long-acting GBR-12909 both elicit rapid dopamine uptake inhibition following intravenous delivery

2008

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The rewarding effects of cocaine have been reported to occur within seconds of administration. Extensive evidence suggests that these actions involve the ability of cocaine to inhibit the dopamine (DA) transporter. We recently showed that 1.5 mg/kg intravenous (i.v.) cocaine inhibits DA uptake within 5 sec. Despite this evidence there remains a lack of consensus regarding how quickly i.v. cocaine and other DA uptake inhibitors elicit DA uptake inhibition. The current studies sought to better characterize the onset of cocaine-induced DA uptake inhibition and to compare these effects to those obtained with the high-affinity, long-acting DA transporter inhibitor, 1-(2-bis(4-fluorphenyl)-methoxy)-ethyl)-4-(3-phenyl-propyl)piperazine (GBR-12909). Using in vivo fast scan cyclic voltammetry, we showed that i.v. cocaine (0.75, 1.5, and 3.0 mg/kg) significantly inhibited DA uptake in the nucleus accumbens of anesthetized rats within 5 sec. DA uptake inhibition peaked at 30 sec and returned to baseline levels in approximately one hour. The effects of cocaine were dosedependent, with the 3.0 mg/kg dose producing greater uptake inhibition at the early time points and exhibiting a longer latency to return to baseline. Further, the blood-brain barrier impermiant cocainemethiodide had no effect on DA uptake or peak height, indicating that the generalized peripheral effects of cocaine do not contribute to the CNS alterations measured here. Finally, we show that GBR-12909 (0.75, 1.5, and 3.0 mg/kg) also significantly inhibited DA uptake within 5 sec postinjection, although the peak effect and return to baseline were markedly delayed compared to cocaine, particularly at the highest dose. Combined, these observations indicate that the central effects of dopamine uptake inhibitors occur extremely rapidly following i.v. drug delivery.Keywords nucleus accumbens; onset; cocaine methiodide; fast scan cyclic voltammetry; ratThe subjective effects of cocaine have been reported to begin within seconds of administration (Seecof and Tennant 1986;Evans et al., 1996;Zernig et al., 2003). Although it is well established that cocaine increases extracellular dopamine (DA) via inhibitory actions on the DA transporter (DAT), it remains unclear whether there is a direct relationship between DAT blockade and the rapid subjective reinforcing affects of cocaine (Koob and Bloom, 1988;Kuhar et al., 1991;Wise et al., 1995;Volkow et al., 1997). Slow and long-acting DAT inhibition has been associated with poor reinforcing effects, while rapid and short-acting DAT inhibition has Correspondence: Sara R. Jones, Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, NC 27157, Office:336-716-8533, Fax: 336-716-8501, E-mail: srjones@wfubmc.edu. 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...

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Electrophysiological evaluation of the time-course of dopamine uptake inhibition induced by intravenous cocaine at a reinforcing dose

Cited by 8 publications

References 58 publications

The encoding of cocaine vs. natural rewards in the striatum of nonhuman primates: categories with different activations

The encoding of cocaine vs. natural rewards in the striatum of nonhuman primates: categories with different activations

Effects of cocaine rewards on neural representations of cognitive demand in nonhuman primates

Short-acting cocaine and long-acting GBR-12909 both elicit rapid dopamine uptake inhibition following intravenous delivery

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