Real-time characterization of dopamine overflow and uptake in the rat striatum

Wightman, R. Mark; Amatorh, C.; Engstrom, Royce C.; Hale, Paul D.; Kristensen, Eric W.; Kuhr, Werner G.; May, Leslie J.

doi:10.1016/0306-4522(88)90255-2

Cited by 396 publications

(371 citation statements)

References 30 publications

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“…This decrease in DA release was greater following 7 days compared to 1 day of deprivation (po0.05, Figure 3b). With regard to DA uptake, baseline data fit well to the kinetic model when the apparent K m was set at the literature value of 0.16 mM (Wightman et al, 1988). The value of V max for naive rats was 1.670.1 mM/s (n ¼ 6).…”

Section: Lack Of Cocaine Effect In the Nac Core And Shell Of Rats Folmentioning

confidence: 72%

“…To evaluate the effects of cocaine and quinpirole, evoked levels of extracellular DA were modeled as a balance between release and uptake (Wightman et al, 1988). The change in DA concentration with respect to time was estimated…”

Section: Cyclic Voltammetry In Brain Slicesmentioning

confidence: 99%

“…(c) Following cocaine binge SA, DA uptake was significantly increased (po0.05) compared to naïve animals. Uptake rates were measured following evoked release of endogenous DA and evaluated by the parameter V max (Wightman et al, 1988). Responses for naïve rats (n ¼ 6) are represented by the filled bar and for rats following cocaine SA with 1 (n ¼ 6) or 7 (n ¼ 7) days of deprivation by the dark and light gray bars, respectively (*po0.05, 1 or 7 days off vs control).…”

Section: Dopamine Terminals and Reinforcing Efficacy Of Cocaine Y Matmentioning

confidence: 99%

See 2 more Smart Citations

Reduced Dopamine Terminal Function and Insensitivity to Cocaine Following Cocaine Binge Self-Administration and Deprivation

Mateo

Läck

Morgan

et al. 2005

Neuropsychopharmacol

122

139

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Despite large numbers of studies describing neuroadaptations caused by chronic cocaine exposure, there remains considerable uncertainty as to whether alterations in dopamine (DA) neurotransmission are responsible for progression into an addicted state. Highintake, 24-h access cocaine self-administration (SA, 10 days) followed by an extended (7 days), but not 1 day deprivation period produces an increased motivation to SA cocaine as measured by a progressive ratio protocol. Following binge cocaine SA and deprivation, the status of DA terminals in the nucleus accumbens (NAc) was investigated using microdialysis in freely moving rats and voltammetry in brain slices. At 1 and 7 days following binge cocaine SA, baseline extracellular DA concentrations in the NAc core were decreased by 40 and 55% of control levels, in the 1 and 7 day deprivation groups, respectively. Acute cocaine (1.5 mg/kg, i.v.) administration increased extracellular DA (350%) in the NAc core of naïve animals but failed to significantly increase DA at 1 or 7 days following binge cocaine SA. The shell of the NAc showed a similar lack of effect of cocaine. Analysis of DA terminals in brain slices showed that cocaine was markedly less effective in inhibiting DA uptake at 1 and 7 days of cocaine deprivation (max. effect 40% of control). Electrically stimulated DA release was decreased at 1 day and further decreased at 7 days of deprivation (67 and 49% of control, respectively). The rate of DA uptake was increased (150% of control) following binge SA, irrespective of deprivation period. Finally, presynaptic autoreceptors were subsensitive at both time points, as measured by the ability of quinpirole, a D2-like DA receptor agonist, to inhibit DA release. Thus, the NAc was hypodopaminergic and DA terminals were less sensitive to cocaine following binge cocaine SA and deprivation.

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Section: Lack Of Cocaine Effect In the Nac Core And Shell Of Rats Folmentioning

confidence: 72%

Section: Cyclic Voltammetry In Brain Slicesmentioning

confidence: 99%

Section: Dopamine Terminals and Reinforcing Efficacy Of Cocaine Y Matmentioning

confidence: 99%

See 1 more Smart Citation

Reduced Dopamine Terminal Function and Insensitivity to Cocaine Following Cocaine Binge Self-Administration and Deprivation

Mateo

Läck

Morgan

et al. 2005

Neuropsychopharmacol

122

139

View full text Add to dashboard Cite

show abstract

“…Overviews about enzyme labels suitable for amperometric, potentiometric and conductimetric [133][134][135] for the in vivo and in vitro determination of neurotransmitters. Nevertheless, microelectrodes exhibit several other attractive possibilities, including the exploration of microscopic domains, detection in microflow system, time-resolved probing of processes in single cells, the in vivo monitoring of neurochemical events (e.g.…”

Section: Amperometric Biosensorsmentioning

confidence: 99%

Electrochemical sensors: a powerful tool in analytical chemistry

Stradiotto¹,

Yamanaka²,

Zanoni³

2003

J. Braz. Chem. Soc.

318

154

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Sensores potenciométricos, amperométricos e condutométricos são sensores eletroquímicos com imensa aplicação nas áreas de meio ambiente, indústria e análises clínicas. O presente trabalho apresenta uma revisão generalizada dos aspectos fundamentais, os desenvolvimento e a contribuição destes sensores na área de química analítica, e reporta alguns aspectos relevantes dos avanços na área de sensores eletroquímicos no Brasil.Potentiometric, amperometric and conductometric electrochemical sensors have found a number of interesting applications in the areas of environmental, industrial, and clinical analyses. This review presents a general overview of the three main types of electrochemical sensors, describing fundamental aspects, developments and their contribution to the area of analytical chemistry, relating relevant aspects of the development of electrochemical sensors in Brazil.

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“…This value was then used to convert electrical current to DA concentration. Evoked levels of DA were modeled using Michaelis-Menten kinetics, as a balance between release and uptake (Wightman et al, 1988). Michaelis-Menten modeling provides parameters that describe the amount of DA released following stimulation (ie, the peak height of the signal) and the maximal rate of DA uptake (V max ).…”

Section: Fast-scan Cyclic Voltammetry (Fscv)mentioning

confidence: 99%

Selective Deletion of GRK2 Alters Psychostimulant-Induced Behaviors and Dopamine Neurotransmission

Daigle

Ferris

Gainetdinov

et al. 2014

Neuropsychopharmacol

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GRK2 is a G protein-coupled receptor kinase (GRK) that is broadly expressed and is known to regulate diverse types of receptors. GRK2 null animals exhibit embryonic lethality due to a severe developmental heart defect, which has precluded the study of this kinase in the adult brain. To elucidate the specific role of GRK2 in the brain dopamine (DA) system, we used a conditional gene knockout approach to selectively delete GRK2 in DA D1 receptor (D1R)-, DA D2 receptor (D2R)-, adenosine 2A receptor (A2AR)-, or DA transporter (DAT)-expressing neurons. Here we show that select GRK2-deficient mice display hyperactivity, hyposensitivity, or hypersensitivity to the psychomotor effects of cocaine, altered striatal signaling, and DA release and uptake. Mice with GRK2 deficiency in D2R-expressing neurons also exhibited increased D2 autoreceptor activity. These findings reveal a cell-type-specific role for GRK2 in the regulation of normal motor behavior, sensitivity to psychostimulants, dopamine neurotransmission, and D2 autoreceptor function.

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Real-time characterization of dopamine overflow and uptake in the rat striatum

Cited by 396 publications

References 30 publications

Reduced Dopamine Terminal Function and Insensitivity to Cocaine Following Cocaine Binge Self-Administration and Deprivation

Reduced Dopamine Terminal Function and Insensitivity to Cocaine Following Cocaine Binge Self-Administration and Deprivation

Electrochemical sensors: a powerful tool in analytical chemistry

Selective Deletion of GRK2 Alters Psychostimulant-Induced Behaviors and Dopamine Neurotransmission

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