A critical assessment of electrochemical procedures applied to the measurement of dopamine and its metabolites during drug-induced and species-typical behaviours

Blaha, C. D.; Phillips, A. G.

doi:10.1097/00008877-199611000-00014

Cited by 65 publications

(71 citation statements)

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“…Repetitive chronoamperometric measurements selective for DA (Blaha and Phillips, 1996, and references therein) of oxidation current using an electrometer (Echempro, Vancouver, British Columbia, C anada) were made by applying a potential pulse from Ϫ0.15 V to ϩ0.25 V versus Ag-AgC l to the recording electrode for 1 sec at 30 sec intervals and monitoring the oxidation current at the end of each 1 sec pulse. The timing of the potential pulse was set so that it would occur Ͼ300 msec after electrical stimulation of the BL A to ensure that the artifact produced by the pulse would not overlap with spikes evoked by BL A stimulation.…”

Section: Methodsmentioning

confidence: 99%

Dopamine D₁and NMDA Receptors Mediate Potentiation of Basolateral Amygdala-Evoked Firing of Nucleus Accumbens Neurons

et al. 2001

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Interactions between the basolateral amygdala (BLA) and the nucleus accumbens (NAc) mediate reward-related processes that are modulated by mesoaccumbens dopamine (DA) transmission. The present in vivo electrophysiological study assessed: (1) changes in the firing probability of submaximal BLA-evoked single neuronal firing activity in the NAc after tetanic stimulation of the BLA, and (2) the functional roles of DA and NMDA receptors in these processes. Tetanic stimulation of the BLA potentiated BLA-evoked firing activity of NAc neurons for a short duration (ϳ25 min). This short-term potentiation was associated with an increase in DA oxidation currents that was monitored with chronoamperometry. Systemic or iontophoretic application before BLA tetanus of the D 1 receptor antagonist SCH23390, but not the D 2 receptor antagonist sulpiride, abolished the potentiation of BLA-evoked NAc activity, whereas administration of SCH23390 3 min after tetanus had no effect. However, systemic administration of the NMDA antagonist 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), either before or after BLA tetanus, abolished the potentiation of BLA-evoked firing of NAc neurons. These data suggest that higher-frequency activity in BLA efferents can autoregulate their excitatory influence over neural activity of NAc neurons by facilitating the release of DA and activating both DA D 1 and NMDA receptors. This may represent a cellular mechanism that facilitates approach behaviors directed toward reward-related stimuli that are mediated by BLA-NAc circuitries. Key words: nucleus accumbens; basolateral amygdala; dopamine; NMDA; extracellular recording; chronoamperometryThe association of previously neutral stimuli with primary rewards to establish conditioned reinforcers is dependent on interactions between the basolateral amygdala (BLA) and the nucleus accumbens (NAc) (Cador et al., 1991;Everitt et al., 1991; Everitt, 1992a, 1996;Baldwin et al., 2000). In addition, mesoaccumbens dopamine (DA) transmission has been shown to exert a powerful modulatory effect on behaviors mediated by BLA-NAc circuits (Robbins and Everitt, 1992a,b;Burns et al., 1993;Wolterink et al., 1993;Smith-Roe and Kelley, 2000). Contemporary theory regarding the role of mesoaccumbens DA in the modulation of reward-related learning has posited that DA transmission can exert a "gain-amplifying" effect over approach behavior that is mediated by the BLA (Robbins and Everitt, 1992b;.Glutamatergic projections from the BLA to the NAc (Kelley et al., 1982;Robinson and Beart, 1988), synapse in close apposition to DA axons on medium spiny neurons of the NAc (Johnson et al., 1994). Recent neurochemical studies have shown that tetanic stimulation of the BLA evokes DA efflux in the NAc via glutamate receptor-dependent mechanisms localized within the NAc (Floresco et al., 1998). In addition, electrophysiological studies have shown that application of either exogenous DA or synaptically released DA by stimulation of the ventral tegmental area can modulate excitatory respo...

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Section: Methodsmentioning

confidence: 99%

Dopamine D₁and NMDA Receptors Mediate Potentiation of Basolateral Amygdala-Evoked Firing of Nucleus Accumbens Neurons

et al. 2001

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“…In some rats, stearate-modified graphite paste electrochemical recording electrodes that permit in vivo measurement of changes in DA efflux without interference from other oxidizable compounds in brain extracellular fluid (Blaha and Phillips, 1996; cf. their references) were implanted stereotaxically into the NAc, ipsilateral to both stimulating electrodes (AP ϩ1.5, ML Ϫ1.0 at 15°angle, DV Ϫ6.5 mm).…”

Section: Animals and Surg Ical Preparationsmentioning

confidence: 99%

Modulation of Hippocampal and Amygdalar-Evoked Activity of Nucleus Accumbens Neurons by Dopamine: Cellular Mechanisms of Input Selection

et al. 2001

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Inputs from multiple sites in the telencephalon, including the hippocampus and basolateral amygdala (BLA), converge on neurons in the nucleus accumbens (NAc), and dopamine (DA) is believed to play an essential role in the amplification and gating of these different limbic inputs. The present study used extracellular single-unit recordings of NAc neurons in combination with chronoamperometric sampling of mesoaccumbens DA efflux to assess the importance of DA in the integration of different limbic inputs to the NAc. Tetanic stimulation of the fimbria potentiated hippocampal-evoked firing activity of NAc neurons and increased DA extracellular levels. Systemic administration of the D 1 receptor antagonist SCH23390 or the NMDA receptor antagonist CPP abolished the potentiation of hippocampal-evoked activity and produced a D 2 receptormediated suppression of evoked firing. In neurons that received converging input from the hippocampus and BLA, fimbria tetanus potentiated hippocampal-evoked firing activity and suppressed BLA-evoked activity in the same neurons. Both D 1 and NMDA receptors participated in the potentiation of fimbriaevoked activity, whereas the suppression of BLA-evoked activity was blocked by either D 1 receptor antagonism with SCH23390 or the adenosine A 1 antagonist 8-cyclopentyl-1,2-dimethylxanthine. Coincidental tetanus of both the fimbria and BLA resulted in potentiation of both inputs, indicating that DA and adenosine-mediated suppression of BLA-evoked firing was activity-dependent. These data suggest that increases in mesoaccumbens DA efflux by hippocampal afferents to the NAc play a critical role in an input selection mechanism, which can ensure preferential responding to the information conveyed from the hippocampus to the ventral striatum.

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“…50,51 The rationale is that the presence of carboxylate anions on the surface (at pH 7.4) should reject AA anions by electrostatic repulsion. We therefore replaced the zwitterionic PEA with STA (5 dips in 100 mg ml 21 chloroform) in the dip coating of the Pt prior to enzyme Table 1 Average ± s Glu and AA currents calculated from individual calibrations in PBS (pH 7.4) at + 0.7 V versus SCE, the corresponding selectivity coefficients (S AA , see eqn.…”

Section: Other Modifications Of the Sensormentioning

confidence: 99%

Biosensor for Neurotransmitter L-Glutamic Acid Designed for Efficient Use of L-Glutamate Oxidase and Effective Rejection of Interference

Ryan

Lowry²,

O’Neill³

1997

Analyst

124

179

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An amperometric biosensor for l-glutamic acid (Glu) was constructed by the adsorption and dip coating of l-glutamate oxidase (GluOx, 200 U ml 21 phosphate buffer, pH 7.4) onto 60-mm radius Teflon-coated Pt wire (1 mm exposed length). The enzyme was then trapped on the surface by electropolymerisation of o-phenylenediamine that also served to block electroactive interference. This procedure afforded electrodes with similar substrate sensitivity compared with the classical approach of immobilising enzyme from a solution of monomer, and represents an approximately 10 000-fold increase in the yield of biosensors from a batch of enzyme. A number of strategies were examined to enhance the sensitivity and selectivity of the Pt/PPD/GluOx sensors operating at 0.7 V versus SCE. Pre-coating the Pt with lipid and incorporation of the protein bovine serum albumin into the polymer matrix were found to improve the performance of the electrode. The sensors had a fast response time, high sensitivity to Glu, with an LOD of about 0.3 mmol l 21 , and possessed selectivity characteristics suggesting that monitoring Glu in biological tissues in vivo may be feasible.

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A critical assessment of electrochemical procedures applied to the measurement of dopamine and its metabolites during drug-induced and species-typical behaviours

Cited by 65 publications

References 0 publications

Dopamine D₁and NMDA Receptors Mediate Potentiation of Basolateral Amygdala-Evoked Firing of Nucleus Accumbens Neurons

Dopamine D₁and NMDA Receptors Mediate Potentiation of Basolateral Amygdala-Evoked Firing of Nucleus Accumbens Neurons

Modulation of Hippocampal and Amygdalar-Evoked Activity of Nucleus Accumbens Neurons by Dopamine: Cellular Mechanisms of Input Selection

Biosensor for Neurotransmitter L-Glutamic Acid Designed for Efficient Use of L-Glutamate Oxidase and Effective Rejection of Interference

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A critical assessment of electrochemical procedures applied to the measurement of dopamine and its metabolites during drug-induced and species-typical behaviours

Cited by 65 publications

References 0 publications

Dopamine D1and NMDA Receptors Mediate Potentiation of Basolateral Amygdala-Evoked Firing of Nucleus Accumbens Neurons

Dopamine D1and NMDA Receptors Mediate Potentiation of Basolateral Amygdala-Evoked Firing of Nucleus Accumbens Neurons

Modulation of Hippocampal and Amygdalar-Evoked Activity of Nucleus Accumbens Neurons by Dopamine: Cellular Mechanisms of Input Selection

Biosensor for Neurotransmitter L-Glutamic Acid Designed for Efficient Use of L-Glutamate Oxidase and Effective Rejection of Interference

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Dopamine D₁and NMDA Receptors Mediate Potentiation of Basolateral Amygdala-Evoked Firing of Nucleus Accumbens Neurons

Dopamine D₁and NMDA Receptors Mediate Potentiation of Basolateral Amygdala-Evoked Firing of Nucleus Accumbens Neurons