Impulse-dependent extracellular resting dopamine concentration in rat striatum in vivo

Zuo, Panli; Yao, Wei; Sun, Liang; Kuo, Shu-Ting; Li, Qing; Wang, Shirong; Dou, Hongwei; Xu, Hua‐Dong; Zhang, Claire Xi; Kang, Xinjiang; Zhou, Zhuan; Zhang, Bo

doi:10.1016/j.neuint.2012.11.006

Cited by 4 publications

(8 citation statements)

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“…This kinetic calibration was applied to in vivo measurements of electrically stimulated and spontaneous (transient) dopamine release in the nucleus accumbens of the mouse brain (Figure ). As shown in Figure A-B, FSCV measurement of a stimulated release event recorded a concentration change lasting ∼5 s with a maximal concentration of 900 nM using a flow-injection calibration (of 10 nA/μM). , However, the kinetic calibration indicates that the maximal concentration of dopamine released was 1.76 μM and the extracellular concentration was back to baseline in ∼1 s. Interestingly, the concentration undershoot following the peak in the kinetically calibrated data is only found in traces resulting from electrically evoked dopamine and may provide insight complexities in dopamine metabolism which have been shown previously …”

Section: Results and Discussionmentioning

confidence: 95%

“…17,27 However, the kinetic calibration indicates that the maximal concentration of dopamine released was 1.76 μM and the extracellular concentration was back to baseline in ∼1 s. Interestingly, the concentration undershoot following the peak in the kinetically calibrated data is only found in traces resulting from electrically evoked dopamine and may provide insight complexities in dopamine metabolism which have been shown previously. 28 The kinetic calibration presented here is also suitable for quantification of the transient release of dopamine. A combination of GBR-12909 (dopamine uptake inhibitor) and raclopride (D 2 antagonist) were used to slow clearance of dopamine following tonic firing, increasing the amplitude of tonic release events in anesthetized animals, which improves detectability.…”

Section: ■ Results and Discussionmentioning

confidence: 98%

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Improved Calibration of Voltammetric Sensors for Studying Pharmacological Effects on Dopamine Transporter Kinetics in Vivo

Atcherley

Laude

Monroe

et al. 2014

ACS Chem. Neurosci.

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The distribution and density of neurons within the brain poses many challenges when making quantitative measurements of neurotransmission in the extracellular space. A volume neurotransmitter is released into the synapse during chemical communication and must diffuse through the extracellular space to an implanted sensor for real-time in situ detection. Fast-scan cyclic voltammetry is an excellent technique for measuring biologically relevant concentration changes in vivo; however, the sensitivity is limited by mass-transport-limited adsorption. Due to the resistance to mass transfer in the brain, the response time of voltammetric sensors is increased, which decreases the sensitivity and the temporal fidelity of the measurement. Here, experimental results reveal how the tortuosity of the extracellular space affects the response of the electrode. Additionally, a model of mass-transport-limited adsorption is utilized to account for both the strength of adsorption and the magnitude of the diffusion coefficient to calculate the response time of the electrode. The response time is then used to determine the concentration of dopamine released in response to salient stimuli. We present the method of kinetic calibration of in vivo voltammetric data and apply the method to discern changes in the KM for the murine dopamine transporter. The KM increased from 0.32 ± 0.08 μM (n = 3 animals) prior to drug administration to 2.72 ± 0.37 μM (n = 3 animals) after treatment with GBR-12909.

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Section: Results and Discussionmentioning

confidence: 95%

Section: ■ Results and Discussionmentioning

confidence: 98%

Improved Calibration of Voltammetric Sensors for Studying Pharmacological Effects on Dopamine Transporter Kinetics in Vivo

Atcherley

Laude

Monroe

et al. 2014

ACS Chem. Neurosci.

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“…Tonic and burst firing neurons release Dopamine (DA) that can then diffuse and act predominantly at remote extra-synaptic receptors before reuptake by DA transporters. As a result, target neurons are tonically exposed to DA; e.g., approximately tens of nM in the striatum and prefrontal cortex (Owesson-White et al, 2012; Nirogi et al, 2013; Zuo et al, 2013), and superimposed upon this baseline are periodic fluctuations in DA that can transiently rise to ~µM levels near the release sites of bursting DA neurons (Park et al, 2011; Rice et al, 2011; Owesson-White et al, 2012). …”

Section: Introductionmentioning

confidence: 99%

Dopaminergic tone persistently regulates voltage-gated ion current densities through the D1R-PKA axis, RNA polymerase II transcription, RNAi, mTORC1, and translation

Krenz¹,

Parker²,

Rodgers³

et al. 2014

Front. Cell. Neurosci.

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Long-term intrinsic and synaptic plasticity must be coordinated to ensure stability and flexibility in neuronal circuits. Coordination might be achieved through shared transduction components. Dopamine (DA) is a well-established participant in many forms of long-term synaptic plasticity. Recent work indicates that DA is also involved in both activity-dependent and -independent forms of long-term intrinsic plasticity. We previously examined DA-enabled long-term intrinsic plasticity in a single identified neuron. The lateral pyloric (LP) neuron is a component of the pyloric network in the crustacean stomatogastric nervous system (STNS). LP expresses type 1 DA receptors (D1Rs). A 1 h bath application of 5 nM DA followed by washout produced a significant increase in the maximal conductance (Gmax) of the LP transient potassium current (IA) that peaked ~4 h after the start of DA application; furthermore, if a change in neuronal activity accompanied the DA application, then a persistent increase in the LP hyperpolarization activated current (Ih) was also observed. Here, we repeated these experiments with pharmacological and peptide inhibitors to determine the cellular processes and signaling proteins involved. We discovered that the persistent, DA-induced activity-independent (IA) and activity-dependent (Ih) changes in ionic conductances depended upon many of the same elements that enable long-term synaptic plasticity, including: the D1R-protein kinase A (PKA) axis, RNA polymerase II transcription, RNA interference (RNAi), and mechanistic target of rapamycin (mTOR)-dependent translation. We interpret the data to mean that increasing the tonic DA concentration enhances expression of a microRNA(s) (miRs), resulting in increased cap-dependent translation of an unidentified protein(s).

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“…As for the extracellular dopamine concentration, baseline estimates from voltammetry vary from 20–30 nM to 73 nM to 95–220 nM . Extracellular dopamine concentration may also be spatially heterogeneous, with some patches having concentrations in the low micromolar range. , In the present FSCV measurements (Figure ), no information about quantitative basal dopamine levels was obtained because all data were background subtracted.…”

Section: Resultsmentioning

confidence: 82%

“…As for the extracellular dopamine concentration, baseline estimates from voltammetry vary from 20–30 nM 58 to 73 nM 59 to 95–220 nM. 60 Extracellular dopamine concentration may also be spatially heterogeneous, with some patches having concentrations in the low micromolar range.…”

Section: Resultsmentioning

confidence: 99%

Understanding the Role α7 Nicotinic Receptors Play in Dopamine Efflux in Nucleus Accumbens

Maex¹,

Grinevich

et al. 2014

ACS Chem. Neurosci.

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Neuronal nicotinic acetylcholine receptors (NNRs) of the α7 subtype have been shown to contribute to the release of dopamine in the nucleus accumbens. The site of action and the underlying mechanism, however, are unclear. Here we applied a circuit modeling approach, supported by electrochemical in vivo recordings, to clarify this issue. Modeling revealed two potential mechanisms for the drop in accumbal dopamine efflux evoked by the selective α7 partial agonist TC-7020. TC-7020 could desensitize α7 NNRs located predominantly on dopamine neurons or glutamatergic afferents to them or, alternatively, activate α7 NNRs located on the glutamatergic afferents to GABAergic interneurons in the ventral tegmental area. Only the model based on desensitization, however, was able to explain the neutralizing effect of coapplied PNU-120596, a positive allosteric modulator. According to our results, the most likely sites of action are the preterminal α7 NNRs controlling glutamate release from cortical afferents to the nucleus accumbens. These findings offer a rationale for the further investigation of α7 NNR agonists as therapy for diseases associated with enhanced mesolimbic dopaminergic tone, such as schizophrenia and addiction.

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Impulse-dependent extracellular resting dopamine concentration in rat striatum in vivo

Cited by 4 publications

References 50 publications

Improved Calibration of Voltammetric Sensors for Studying Pharmacological Effects on Dopamine Transporter Kinetics in Vivo

Improved Calibration of Voltammetric Sensors for Studying Pharmacological Effects on Dopamine Transporter Kinetics in Vivo

Dopaminergic tone persistently regulates voltage-gated ion current densities through the D1R-PKA axis, RNA polymerase II transcription, RNAi, mTORC1, and translation

Understanding the Role α7 Nicotinic Receptors Play in Dopamine Efflux in Nucleus Accumbens

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