Brain neurotransmitter turnover rates during rat intravenous cocaine self-administration

Smith, James E.; Koves, Timothy R.; Co, C.

doi:10.1016/s0306-4522(02)00819-9

Cited by 45 publications

(48 citation statements)

References 63 publications

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“…These functional adaptations to noncontingently administered cocaine in the present study may occur without an alteration in glutamatergic inputs. Supporting this possibility, Smith et al (2003) revealed that rats yoked to animals self-administering cocaine do not show changes in VP glutamate turnover (even though increases were seen in the selfadministering rats).…”

Section: Morphine Cross-sensitization To Cocaine and Ventral Pallidummentioning

confidence: 93%

Cross-Sensitization to Morphine in Cocaine-Sensitized Rats: Behavioral Assessments Correlate with Enhanced Responding of Ventral Pallidal Neurons to Morphine and Glutamate, with Diminished Effects of GABA

McDaid

Dallimore

Mackie³

et al. 2005

J Pharmacol Exp Ther

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Common neurobiological substrates contribute to the progressively increased behavioral effects (i.e., sensitization) that occur with repeated intermittent treatments of cocaine and morphine. Consequently, repeated exposure to cocaine can augment responding to morphine (termed cross-sensitization). Drug-induced sensitization in rats may model aspects of the dysfunction in motivation that are imposed by addiction. The ventral pallidum (VP) is involved in motivated behaviors and its function is altered by acute administration of cocaine and morphine, but the effects of repeated drug exposure remain unknown. Targeting this paucity, the present study evaluated electrophysiological changes in the VP of rats exposed to five once-daily cocaine treatments (15 mg/kg i.p.). This regimen also induced behavioral-sensitization that was expressed 3 days later when the rats received either an acute injection of cocaine (15 mg/kg i.p.) or morphine (10 mg/kg i.p.). VP neurons recorded in vivo 3 days after the repeated cocaine treatment regimen demonstrated increased excitatory responding to microiontophoretic applications of morphine and glutamate. The maximal effect (E max ) was increased without altering potency, suggesting a change in the functional efficacy of the respective receptor systems. This did not represent a potentiation in transmission in general, for the effects of GABA were diminished. The results provide the first evidence for cellular adaptation in the VP after a sensitizing drug treatment paradigm and reveal that crosssensitization of drug-induced behaviors temporally correlates with changes in VP neuronal responding. These findings advance an emerging theme that alterations in the VP may contribute to the increased motivation for drug seeking that occurs in drug-withdrawn addicts.

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Section: Morphine Cross-sensitization To Cocaine and Ventral Pallidummentioning

confidence: 93%

Cross-Sensitization to Morphine in Cocaine-Sensitized Rats: Behavioral Assessments Correlate with Enhanced Responding of Ventral Pallidal Neurons to Morphine and Glutamate, with Diminished Effects of GABA

McDaid

Dallimore

Mackie³

et al. 2005

J Pharmacol Exp Ther

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“…Rats given access to nicotine SA were compared with rats that received the same history of nicotine infusion patterns using a response-independent yoked administration (YA) design (Hemby et al, 1997;Smith et al, 1982Smith et al, , 2003. To provide a temporal correlation between drug exposure and changes in brain eCB levels, we employed in vivo microdialysis to sample interstitial lipids in the VTA, a region critically involved in the mediation of nicotine reward and addiction (Markou, 2008).…”

Section: Introductionmentioning

confidence: 99%

The Volitional Nature of Nicotine Exposure Alters Anandamide and Oleoylethanolamide Levels in the Ventral Tegmental Area

Buczynski

Polis

Parsons

2012

Neuropsychopharmacol

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Cannabinoid-1 receptors (CB 1 ) have an important role in nicotine reward and their function is disrupted by chronic nicotine exposure, suggesting nicotine-induced alterations in endocannabinoid (eCB) signaling. However, the effects of nicotine on brain eCB levels have not been rigorously evaluated. Volitional intake of nicotine produces physiological and behavioral effects distinct from forced drug administration, although the mechanisms underlying these effects are not known. This study compared the effects of volitional nicotine self-administration (SA) and forced nicotine exposure (yoked administration (YA)) on levels of eCBs and related neuroactive lipids in the ventral tegmental area (VTA) and other brain regions. Brain lipid levels were indexed both by in vivo microdialysis in the VTA and lipid extractions from brain tissues. Nicotine SA, but not YA, reduced baseline VTA dialysate oleoylethanolamide (OEA) levels relative to nicotine-naïve controls, and increased anandamide (AEA) release during nicotine intake. In contrast, all nicotine exposure paradigms increased VTA dialysate 2-arachidonoyl glycerol (2-AG) levels. Thus, nicotine differentially modulates brain lipid (2-AG, AEA, and OEA) signaling, and these modulations are influenced by the volitional nature of the drug exposure. Corresponding bulk tissue analysis failed to identify these lipid changes. Nicotine exposure had no effect on fatty acid amide hydrolase activity in the VTA, suggesting that changes in AEA and OEA signaling result from alterations in their nicotine-induced biosynthesis. Both CB 1 (by AEA and 2-AG) and non-CB 1 (by OEA) targets can alter the excitability and activity of the dopaminergic neurons in the VTA. Collectively, these findings implicate disrupted lipid signaling in the motivational effects of nicotine.

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“…These have included in situ autoradiography to identify changes in receptor densities (Lodge and Lawrence 2003;BeadlesBohling and Wiren 2005;Short et al 2006), in situ hybridization (Chen et al 1998; Beadles-Bohling and Wiren 2005; Short et al 2006) and immunohistochemistry (Bachtell et al 2004) to identify densities of specific proteins, microdialysis (Doyon et al 2004) and in vivo voltametry (Budygin et al 2001;Jones et al 2006) to identify extracellular fluid levels of neurohumors, 2-deoxyglucose autoradiography to identify cell groups showing changes in glucose metabolism (Eckardt et al 1992;Porrino et al 1998), c-Fos expression to identify cell groups having immediate early gene activation (Ryabinin et al 2003;Wedzony et al 2003) and neurotransmitter TOR procedures to identify changes in the activity of discrete subsets of cell groups by measuring the dynamics of the functional pool of neurotransmitters (Milio and Hadfield 1992;Bailey et al 2000;Smith et al 2003). This latter technology was chosen for the present study.…”

mentioning

confidence: 99%

“…Neurotransmitter TOR measures were developed as a mechanism for investigating the role of the functional pool as an index of pre-synaptic neuronal activity. This has become even more challenging since recent data showing that the less labor intensive TOR measurement procedure using metabolite/neurotransmitter ratios appears to be inaccurate and apparently represents only changes in the concentration of the metabolites (Smith et al 2003). The experiment described here used radioactive pulse labeling techniques to measure the TORs of DA, NE, 5-HT, GABA, Glu, and Asp in small brain regions of rats drinking EtOH to assess the role of neurons releasing these neurotransmitters in the processes that underlie this behavior.…”

mentioning

confidence: 99%

Chronic binge‐like moderate ethanol drinking in rats results in widespread decreases in brain serotonin, dopamine, and norepinephrine turnover rates reversed by ethanol intake

Smith¹,

Co²,

McIntosh³

et al. 2008

Journal of Neurochemistry

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This research was initiated to assess the turnover rates (TORs) of dopamine (DA), norepinephrine (NA), serotonin (5-HT), aspartate, glutamate, and GABA in brain regions during rodent ethanol/sucrose (EtOH) and sucrose (SUC) drinking and in animals with a history of EtOH or SUC drinking to further characterize the neuronal systems that underlie compulsive consumption. Groups of five male rats were used, with two trained to drink EtOH solutions, two to drink SUC and one to serve as a non-drinking control. When stable drinking patterns were obtained, rats were pulse labeled intravenously and killed 60 or 90 min later and the TORs of DA, norepinephrine, 5-HT, aspartate, glutamate, and GABA determined in brain regions. Changes in the TOR of 5-HT, DA, and NA were detected specific to EtOH drinking, SUC drinking or a history of EtOH or SUC drinking. An acute EtOH deprivation effect was detected that was mostly reversed with EtOH drinking. These results suggest that binge-like drinking of moderate amounts of EtOH produces a deficit in neuronal function that could set the stage for the alleviation of anhedonic stimuli with further EtOH intake that strengthen EtOH seeking behaviors which may contribute to increased EtOH use in at risk individuals.

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Brain neurotransmitter turnover rates during rat intravenous cocaine self-administration

Cited by 45 publications

References 63 publications

Cross-Sensitization to Morphine in Cocaine-Sensitized Rats: Behavioral Assessments Correlate with Enhanced Responding of Ventral Pallidal Neurons to Morphine and Glutamate, with Diminished Effects of GABA

Cross-Sensitization to Morphine in Cocaine-Sensitized Rats: Behavioral Assessments Correlate with Enhanced Responding of Ventral Pallidal Neurons to Morphine and Glutamate, with Diminished Effects of GABA

The Volitional Nature of Nicotine Exposure Alters Anandamide and Oleoylethanolamide Levels in the Ventral Tegmental Area

Chronic binge‐like moderate ethanol drinking in rats results in widespread decreases in brain serotonin, dopamine, and norepinephrine turnover rates reversed by ethanol intake

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