Voltammetric study of extracellular dopamine near microdialysis probes acutely implanted in the striatum of the anesthetized rat

Borland, Laura M.; Shi, Guoyue; Yang, Hua; Michael, Adrian C.

doi:10.1016/j.jneumeth.2005.02.002

Cited by 143 publications

(161 citation statements)

References 34 publications

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“…anesthetized animal studies, microdialysis shows evidence of tissue disruption of at least 220-250 mm away from the probe (Borland et al, 2005), whereas the MEA showed evidence of some neuroinflammation only 50-100 mm away in a chronic study following 8 weeks in vivo (Rutherford et al, 2007). The temporal resolution of our MEA is an order of magnitude faster than the most sophisticated microdialysis techniques designed for measurement of aminoacid neurotransmitters (Kennedy et al, 2002).…”

Section: Discussionmentioning

confidence: 85%

Decreased Dopamine D4 Receptor Expression Increases Extracellular Glutamate and Alters Its Regulation in Mouse Striatum

Thomas

Grandy

Gerhardt

et al. 2008

Neuropsychopharmacol

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To better understand the effect of the dopamine D4 receptor (DRD4) on glutamate (Glu) neurotransmission in the brain, we utilized transgenic mice with partial or complete removal of functional DRD4 plasma membrane expression (DRD4 + /À and DRD4À/À, respectively). We measured resting extracellular Glu levels, Glu clearance kinetics, and KCl-evoked release of Glu in the striatum and nucleus accumbens core of these mice using in vivo amperometry coupled to a novel microelectrode array configured for sub-second detection of Glu. Recordings from DRD4À/À and DRD4 + /À mice were compared with their wild-type littermates (DRD4 + / + ). Resting extracellular levels of Glu were increased in the striatum of DRD4À/À mice (po0.01). Glu clearance kinetics were significantly decreased in the dorsal striatum of DRD4À/À mice (po0.05). KCl-evoked overflow of Glu was reliably measured but unchanged in the striatum of the three groups. By contrast, no changes in resting Glu, Glu uptake kinetics, or KCl-evoked release of Glu were observed in the nucleus accumbens core among the three genotypes. These data indicate that the DRD4 receptor is involved in modulation of Glu neurotransmission, primarily in the striatum. A better understanding of Glu control by the DRD4 may improve our understanding of the physiological role of the DRD4 in disorders such as attention-deficit/hyperactivity disorder and schizophrenia.

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Section: Discussionmentioning

confidence: 85%

Decreased Dopamine D4 Receptor Expression Increases Extracellular Glutamate and Alters Its Regulation in Mouse Striatum

Thomas

Grandy

Gerhardt

et al. 2008

Neuropsychopharmacol

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“…The postsurgery recovery time was between 42 and 48 h. In the previous study (Karkhanis et al, 2014), the recovery time was 18-24 h, and DA levels did not significantly differ between SI and GH rats. A longer recovery time after the surgery has been associated with increased stability of baseline DA levels (Borland et al, 2005). All dialysate samples were collected with an interval of 20 min and were collected for 2 h prior (baseline) to ethanol administration and 100 min after.…”

Section: Microdialysismentioning

confidence: 99%

Early-Life Social Isolation Stress Increases Kappa Opioid Receptor Responsiveness and Downregulates the Dopamine System

Karkhanis¹,

Rose

Weiner³

et al. 2016

Neuropsychopharmacol

106

107

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Chronic early-life stress increases vulnerability to alcoholism and anxiety disorders during adulthood. Similarly, rats reared in social isolation (SI) during adolescence exhibit augmented ethanol intake and anxiety-like behaviors compared with group housed (GH) rats. Prior studies suggest that disruption of dopamine (DA) signaling contributes to SI-associated behaviors, although the mechanisms underlying these alterations are not fully understood. Kappa opioid receptors (KORs) have an important role in regulating mesolimbic DA signaling, and other kinds of stressors have been shown to augment KOR function. Therefore, we tested the hypothesis that SI-induced increases in KOR function contribute to the dysregulation of NAc DA and the escalation in ethanol intake associated with SI. Our ex vivo voltammetry experiments showed that the inhibitory effects of the kappa agonist U50,488 on DA release were significantly enhanced in the NAc core and shell of SI rats. Dynorphin levels in NAc tissue were observed to be lower in SI rats. Microdialysis in freely moving rats revealed that SI was also associated with reduced baseline DA levels, and pretreatment with the KOR antagonist nor-binaltorphimine (nor-BNI) increased DA levels selectively in SI subjects. Acute ethanol elevated DA in SI and GH rats and nor-BNI pretreatment augmented this effect in SI subjects, while having no effect on ethanol-stimulated DA release in GH rats. Together, these data suggest that KORs may have increased responsiveness following SI, which could lead to hypodopaminergia and contribute to an increased drive to consume ethanol. Indeed, SI rats exhibited greater ethanol intake and preference and KOR blockade selectively attenuated ethanol intake in SI rats. Collectively, the findings that nor-BNI reversed SI-mediated hypodopaminergic state and escalated ethanol intake suggest that KOR antagonists may represent a promising therapeutic strategy for the treatment of alcohol use disorders, particularly in cases linked to chronic early-life stress.

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“…The discrepancy that MEAs detect neuronally derived glutamate, whereas microdialysis samples extracellular glutamate derived from non-neuronal origins, may be because of the inherent differences in the methodologies. The extensive damage to the local brain area during implantation of the microdialysis probe and the large area of tissue sampled (1-4 mm in length), restricts microdialysis measurements of glutamate to large regions far beyond synapses (Borland et al, 2005;Hillered et al, 2005;Jaquins-Gerstl and Michael, 2009;Obrenovitch, 1999, Obrenovitch et al, 2000Timmerman and Westerink 1997). Furthermore, the inadequate temporal resolution of microdialysis (*1-20 min) prevents microdialysis from detecting the rapid dynamic changes in extracellular glutamate that occur in the order of milliseconds to seconds (Diamond, 2005).…”

Section: Calcium Channel Dependent Neuronal Glutamate Release Contribmentioning

confidence: 99%

Disruptions in the Regulation of Extracellular Glutamate by Neurons and Glia in the Rat Striatum Two Days after Diffuse Brain Injury

Hinzman

Thomas

Quintero

et al. 2012

Journal of Neurotrauma

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Disrupted regulation of extracellular glutamate in the central nervous system contributes to and can exacerbate the acute pathophysiology of traumatic brain injury (TBI). Previously, we reported increased extracellular glutamate in the striatum of anesthetized rats 2 days after diffuse brain injury. To determine the mechanism(s) responsible for increased extracellular glutamate, we used enzyme-based microelectrode arrays (MEAs) coupled with specific pharmacological agents targeted at in vivo neuronal and glial regulation of extracellular glutamate. After TBI, extracellular glutamate was significantly increased in the striatum by (*90%) averaging 4.1 -0.6 lM compared with sham 2.2 -0.4 lM. Calcium-dependent neuronal glutamate release, investigated by local application of an N-type calcium channel blocker, was no longer a significant source of extracellular glutamate after TBI, compared with sham. In brain-injured animals, inhibition of glutamate uptake with local application of an excitatory amino acid transporter inhibitor produced significantly greater increase in glutamate spillover (* 65%) from the synapses compared with sham. Furthermore, glutamate clearance measured by locally applying glutamate into the extracellular space revealed significant reductions in glutamate clearance parameters in brain-injured animals compared with sham. Taken together, these data indicate that disruptions in calcium-mediated glutamate release and glial regulation of extracellular glutamate contribute to increased extracellular glutamate in the striatum 2 days after diffuse brain injury. Overall, these data suggest that therapeutic strategies used to regulate glutamate release and uptake may improve excitatory circuit function and, possibly, outcomes following TBI.

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Voltammetric study of extracellular dopamine near microdialysis probes acutely implanted in the striatum of the anesthetized rat

Cited by 143 publications

References 34 publications

Decreased Dopamine D4 Receptor Expression Increases Extracellular Glutamate and Alters Its Regulation in Mouse Striatum

Decreased Dopamine D4 Receptor Expression Increases Extracellular Glutamate and Alters Its Regulation in Mouse Striatum

Early-Life Social Isolation Stress Increases Kappa Opioid Receptor Responsiveness and Downregulates the Dopamine System

Disruptions in the Regulation of Extracellular Glutamate by Neurons and Glia in the Rat Striatum Two Days after Diffuse Brain Injury

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