In vivo monitoring of extracellular glutamate in the brain with a microsensor

Oldenziel, Weite Hendrik; Dijkstra, Gerard; Cremers, Thomas; Westerink, Ben H.C.

doi:10.1016/j.brainres.2006.08.015

Cited by 76 publications

(60 citation statements)

References 50 publications

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“…This was an approximate 20% decrease in resting Glu levels in the Str compared with averaged values from Table 1. This observation contrasts several microdialysis studies that do not show TTX dependence in rats (Timmerman and Westerink, 1997) and further supports findings conducted in rats with microelectrodes (Kulagina et al, 1999;Day et al, 2006;Oldenziel et al, 2006). Unlike other TTX studies using Glu-selective microelectrodes in anesthetized rats, our freely moving mouse studies did not completely attenuate resting Glu levels for two possible reasons.…”

Section: Table 1 Resting Glu Measures On Days 3 To 7 Postimplantationsupporting

confidence: 79%

“…What was often observed was pressure or dilution artifact due to local application of control solutions (saline or citrate) from cannula placed in proximity (50 -100 m) of the working electrode. This has been observed by our laboratory (Burmeister and Gerhardt, 2001) and other laboratories using microelectrodes (Oldenziel et al, 2006). These changes were not from the solutions evoking Glu release, but rather they were from introduction of exogenous fluid into the extracellular space surrounding the MEA.…”

Section: Methodssupporting

confidence: 63%

“…Within the past decade, several groups have developed Gluselective microelectrodes to address fast glutamatergic physiology (Hu et al, 1994;Rahman et al, 2005), and some studies using these electrodes have shown that Glu is TTX-dependent (Kulagina et al, 1999;Day et al, 2006;Oldenziel et al, 2006). Our laboratory has developed an enzyme-based microelectrode array (MEA) that is capable of detecting low levels of Glu on a subsecond time scale (500 -800 ms) that is free from central nervous system interferents such as 3,4-dihydroxyphenylacetic acid (DOPAC) and ascorbic acid (AA) (Burmeister and Gerhardt, 2001;Burmeister et al, 2002).…”

mentioning

confidence: 99%

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Second-by-Second Measures of l-Glutamate in the Prefrontal Cortex and Striatum of Freely Moving Mice

Hascup

Hascup²,

Pomerleau³

et al. 2007

J Pharmacol Exp Ther

123

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L-Glutamate (Glu) is the main excitatory neurotransmitter in the mammalian central nervous system, and it is involved in most aspects of normal brain function, including cognition, memory and learning, plasticity, and motor movement. Although microdialysis techniques have been used to study Glu, the slow temporal resolution of the technique may be inadequate to properly examine tonic and phasic Glu. Thus, our laboratory has developed an enzyme-based microelectrode array (MEA) with fast response time and low detection limits for Glu. We have modified the MEA design to allow for reliable measures in the brain of awake, freely moving mice. In this study, we chronically implanted the MEA in prefrontal cortex (PFC) or striatum (Str) of awake, freely moving C57BL/6 mice. We successfully measured Glu levels 7 days postimplantation without loss of MEA sensitivity. In addition, we determined resting (tonic) Glu levels to be 3.3 M in the PFC and 5.0 M in the Str. Resting Glu levels were subjected to pharmacological manipulation with tetrodotoxin (TTX) and DL-threo-␤-hydroxyaspartate (THA). TTX significantly (p Ͻ 0.05) decreased resting Glu by 20%, whereas THA significantly (p Ͻ 0.05) increased resting Glu by 60%. Taken together, our data show that chronic recordings of tonic and phasic clearance of exogenously applied Glu can be carried out in awake mice for at least 7 days in vivo, allowing for longer term studies of Glu regulation.

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Section: Table 1 Resting Glu Measures On Days 3 To 7 Postimplantationsupporting

confidence: 79%

Section: Methodssupporting

confidence: 63%

mentioning

confidence: 99%

See 1 more Smart Citation

Second-by-Second Measures of l-Glutamate in the Prefrontal Cortex and Striatum of Freely Moving Mice

Hascup

Hascup²,

Pomerleau³

et al. 2007

J Pharmacol Exp Ther

123

View full text Add to dashboard Cite

show abstract

“…In contrast, ABT-089-evoked glutamate signal amplitudes recorded by the present method were reduced by 76.4 Ϯ 8.1% after TTX administration (80 pmol; t (5) ϭ 6.52, p ϭ 0.001) (Fig. 8c,d) (Day et al, 2006;Oldenziel et al, 2006).…”

Section: Glutamatergic Transients Evoked By Nicotine and Abt-089mentioning

confidence: 53%

Glutamatergic Contributions to Nicotinic Acetylcholine Receptor Agonist-Evoked Cholinergic Transients in the Prefrontal Cortex

Parikh¹,

Man²,

Decker³

et al. 2008

J. Neurosci.

118

148

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“…In addition, evidence suggests that amphetamine-induced glutamate efflux may involve the formation of reactive oxygen species resulting from metabolic or oxidative stress independent of synaptic activity (Wolf et al, 2000). Future work in this area of investigation may incorporate microsensor technology, which may be more sensitive than microdialysis to neuronally-derived glutamate (Oldenziel et al, 2006). It is known that the NAcc and related neural pathways are involved in the psychostimulant effects of amphetamine (Wolf, 1998;Rockhold et al, 1998;Wolf et al, 2004;Kalivas and Volkow, 2005).…”

Section: Discussionmentioning

confidence: 99%

Environmental enrichment increases amphetamine-induced glutamate neurotransmission in the nucleus accumbens: A neurochemical study

Rahman

Bardo

2008

Brain Research

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In addition to dopamine (DA), evidence indicates that glutamatergic regulation of the mesolimbic reward pathway is involved in mediating the abuse-related effects of psychostimulants, including amphetamine. Since rats raised in an enrichment condition (EC) during development are more sensitive to the locomotor stimulant effects of acute amphetamine compared to rats raised in an impoverished condition (IC), the present study examined amphetamine-induced extracellullar glutamate and aspartate levels in the nucleus accumbens (NAcc) of EC and IC rats using in vivo microdialysis coupled with HPLC-electrochemical detection. Basal extracellular levels of glutamate or aspartate were not significantly different between EC and IC rats. Acute systemic amphetamine (0.5 or 2.0 mg/kg, sc) increased extracellular glutamate levels in NAcc of EC rats (137% or 305% of basal) and IC rats (120% or 187% of basal). Similarly, acute systemic amphetamine (0.5 or 2.0 mg/kg, sc) elevated aspartate levels in NAcc of EC rats (148% or 237% of basal) and IC rats (115% or 170% of basal). Glutamate levels were elevated by amphetamine to a greater extent in EC rats than in IC rats. Pretreatment with systemic MK-801 (0.25 mg/kg, ip), a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, prevented the acute amphetamine-induced increase in extracellular glutamate and aspartate levels in NAcc. Overall, these results suggest that alterations in glutamate in the NAcc may be involved in the environment-dependent effects of amphetamine.

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In vivo monitoring of extracellular glutamate in the brain with a microsensor

Cited by 76 publications

References 50 publications

Second-by-Second Measures of l-Glutamate in the Prefrontal Cortex and Striatum of Freely Moving Mice

Second-by-Second Measures of l-Glutamate in the Prefrontal Cortex and Striatum of Freely Moving Mice

Glutamatergic Contributions to Nicotinic Acetylcholine Receptor Agonist-Evoked Cholinergic Transients in the Prefrontal Cortex

Environmental enrichment increases amphetamine-induced glutamate neurotransmission in the nucleus accumbens: A neurochemical study

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