Real time measurement of stimulated dopamine release in the conscious rat using fast cyclic voltammetry: dopamine release is not observed during intracranial self stimulation

Kruk, Zygmunt L.; Cheeta, Survjit; Milla, J Martinez; Muscat, Richard; Williams, Julian; Willner, Paul

doi:10.1016/s0165-0270(97)00156-8

Cited by 28 publications

(14 citation statements)

References 31 publications

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“…Although there is controversy as to whether BSR itself stimulates NAc DA release (Fiorino et al, 1993; Nakahara et al, 1992; Philips et al, 1989; Hernández and Shizgal, 2009; but see Miliaressis et al, 1991; Kruk et al, 1998), systemic administration of cocaine significantly elevates extracellular NAc DA by blocking DA reuptake (Giros et al, 1996; Carboni et al, 2001) and increasing DA release (Venton et al, 2006; Aragona et al, 2008). In the present study, we found that 2-PMPA itself produced a dose-dependent reduction in extracellular DA, while pretreatment with 2-PMPA also dose-dependently inhibited cocaine-enhanced NAc DA, suggesting that a DA-dependent mechanism may underlie 2-PMPA's action.…”

Section: Discussionmentioning

confidence: 99%

N-acetylaspartylglutamate (NAAG) inhibits intravenous cocaine self-administration and cocaine-enhanced brain-stimulation reward in rats

Kiyatkin

et al. 2010

Neuropharmacology

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Pharmacological activation of group II metabotropic glutamate (mGlu2 and mGlu3) receptors inhibits reward-seeking behavior and/or rewarding efficacy induced by drugs (cocaine, nicotine) or natural rewards (food, sucrose). In the present study, we investigated whether elevation of brain Nacetylaspartatylglutamate (NAAG), an endogenous group II mGlu receptor agonist, by the NAAG peptidase inhibitor 2-PMPA attenuates cocaine's rewarding effects, as assessed by intravenous cocaine self-administration and intracranial electrical brain-stimulation reward (BSR) in rats. Systemic administration of 2-PMPA (10, 30, 100 mg/kg, i.p.) or intranasal administration of NAAG (100, 300 μg/10 μl/nostril) significantly inhibited intravenous cocaine self-administration under progressive-ratio (PR), but not under fixed-ratio 2 (FR2), reinforcement conditions. In addition, 2-PMPA (1, 10, 30 mg/kg, i.p) or NAAG (50, 100 μg/10 μl/nostril) significantly inhibited cocaineenhanced BSR, but not basal BSR. Pretreatment with LY341495 (1 mg/kg, i.p.), a selective mGlu2/3 receptor antagonist, prevented the inhibitory effects produced by 2-PMPA or NAAG in both the selfadministration and BSR paradigms. In vivo microdialysis demonstrated that 2-PMPA (10, 30, 100 mg/kg) dose-dependently attenuated cocaine-enhanced extracellular dopamine (DA) in the nucleus accumbens (NAc). 2-PMPA alone inhibited basal NAc DA release, an effect that was prevented by LY341495. These findings suggest that systemic administration of 2-PMPA or intranasal administration of NAAG inhibits cocaine's rewarding efficacy and cocaine-enhanced NAc DAlikely by activation of presynaptic mGlu2/3 receptors in the NAc. These data suggest a potential utility for 2-PMPA or NAAG in the treatment of cocaine addiction.

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Section: Discussionmentioning

confidence: 99%

N-acetylaspartylglutamate (NAAG) inhibits intravenous cocaine self-administration and cocaine-enhanced brain-stimulation reward in rats

Kiyatkin

et al. 2010

Neuropharmacology

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“…For example, ICSS promotes DA release in nucleus accumbens; it is enhanced by drugs that themselves increase extracellular DA levels in nucleus accumbens, and it is blocked by drugs that deplete DA or block DA receptors (Stellar and Stellar, 1985;Phillips et al, 1989;Fiorino et al, 1993;Wise, 1998;You et al, 2001;Cheer et al, 2005) [but see (Miliaressis et al, 1991;Kruk et al, 1998)]. Mesolimbic DA neurons constitute one subset of neurons that project through the MFB Veening et al, 1982), and optogenetic studies suggest that direct activation of these neurons is sufficient to maintain ICSS (You et al, 2001;Kim et al, 2012).…”

Section: A Definition Discovery and Neural Substratesmentioning

confidence: 99%

Intracranial Self-Stimulation to Evaluate Abuse Potential of Drugs

2014

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“…Given the heterogeneity of brain microenvironments, the ability to conduct FSCV measurements from the same terminal population over multiple days is an exciting prospect for studies of disease and behavioral learning. Indeed, others have attempted to develop such a sensor (77, 78), albeit with little success. The performance of the fused-silica electrode design is attributed to its size, which may be small enough to bypass the immune response.…”

Section: Microsensor Developmentsmentioning

confidence: 99%

Electrochemical Analysis of Neurotransmitters

Bucher¹,

Wightman

2015

Annual Rev. Anal. Chem.

251

229

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Chemical signaling through the release of neurotransmitters into the extracellular space is the primary means of communication between neurons. More than four decades ago, Ralph Adams and his colleagues realized the utility of electrochemical methods for the study of easily oxidizable neurotransmitters, such as dopamine, norepinephrine, and serotonin and their metabolites. Today, electrochemical techniques are frequently coupled to microelectrodes to enable spatially resolved recordings of rapid neurotransmitter dynamics in a variety of biological preparations spanning from single cells to the intact brain of behaving animals. In this review, we provide a basic overview of the principles underlying constant-potential amperometry and fast-scan cyclic voltammetry, the most commonly employed electrochemical techniques, and the general application of these methods to the study of neurotransmission. We thereafter discuss several recent developments in sensor design and experimental methodology that are challenging the current limitations defining the application of electrochemical methods to neurotransmitter measurements.

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Real time measurement of stimulated dopamine release in the conscious rat using fast cyclic voltammetry: dopamine release is not observed during intracranial self stimulation

Cited by 28 publications

References 31 publications

N-acetylaspartylglutamate (NAAG) inhibits intravenous cocaine self-administration and cocaine-enhanced brain-stimulation reward in rats

N-acetylaspartylglutamate (NAAG) inhibits intravenous cocaine self-administration and cocaine-enhanced brain-stimulation reward in rats

Intracranial Self-Stimulation to Evaluate Abuse Potential of Drugs

Electrochemical Analysis of Neurotransmitters

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