Sampling glutamate and GABA with microdialysis: suggestions on how to get the dialysis membrane closer to the synapse

Drew, Kelly L.; Pehek, Elizabeth A.; Rasley, Brian T.; Ma, Yilong; Green, T.K.

doi:10.1016/j.jneumeth.2004.04.039

Cited by 44 publications

(27 citation statements)

References 32 publications

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“…The small size and smooth edges of our MEA tips (333 ϫ 200 ϫ 125 m) cause less damage compared with a microdialysis probe (Clapp-Lilly et al, 1999;Borland et al, 2005;Rutherford et al, 2007). Furthermore, a faster sampling rate allows us to measure more synaptic Glu and subsequently the neuronal pool of Glu (Drew et al, 2004). The Glu that diffuses from the synapse to our MEA was able to be detected due to our enhanced temporal resolution.…”

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

confidence: 99%

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

100

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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 Postimplantationmentioning

confidence: 99%

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

100

123

View full text Add to dashboard Cite

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“…Nipecotic acid is not selective for neuronal or astrocytic transporters (Krogsgaard-Larsen et al, 2000), and the cellular location of the transporters in rat PnO remains unknown. As reviewed elsewhere, the source of basal GABA levels measured with microdialysis is likely to include extrasynaptic and/or non-neuronal pools, and GABA can be released into the extracellular space by astrocytes (Timmerman and Westerink, 1997, Araque et al, 1999, Del Arco et al, 2003, Drew et al, 2004, Watson et al, 2006a. Glial cells surrounding synapses are very efficient at taking up neuronally released GABA and may act as buffers between the microdialysis probe and the synapses.…”

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confidence: 99%

Sleep and GABA levels in the oral part of rat pontine reticular formation are decreased by local and systemic administration of morphine

2007

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Morphine, a μ-opioid receptor agonist, is a commonly prescribed treatment for pain. Although highly efficacious, morphine has many unwanted side effects including disruption of sleep and obtundation of wakefulness. One mechanism by which morphine alters sleep and wakefulness may be by modulating GABAergic signaling in brain regions regulating arousal, including the oral pontine reticular formation (PnO). This study used in vivo microdialysis in unanesthetized Sprague-Dawley rat to test the hypothesis that μ-opioid receptors modulate PnO GABA levels. Validation of the high performance liquid chromatographic technique used to quantify GABA was obtained by dialyzing the PnO (n=4 rats) with the GABA reuptake inhibitor nipecotic acid (500 μM). Nipecotic acid caused a 185±20% increase in PnO GABA levels, confirming chromatographic detection of GABA and demonstrating the existence of functional GABA transporters in rat PnO. Morphine caused a concentration-dependent decrease in PnO GABA levels (n=25 rats). Coadministration of morphine (100 μM) with naloxone (1 μM), a μ-opioid receptor antagonist, blocked the morphine-induced decrease in PnO GABA levels (n=5 rats). These results show for the first time that μ-opioid receptors in rat PnO modulate GABA levels. A second group of rats (n=6) was used to test the hypothesis that systemically administered morphine also decreases PnO GABA levels. Intravenous morphine caused a significant (p<0.05) decrease (19%) in PnO GABA levels relative to control intravenous infusions of saline. Finally, microinjections followed by 2 h recordings of electroencephalogram and electromyogram tested the hypothesis that PnO morphine administration disrupts sleep (n=8 rats). Morphine significantly (p<0.05) increased the percent of time spent in wakefulness (65%) and significantly (p<0.05) decreased the percent of rapid eye movement (REM) sleep (-53%) and non-REM sleep (-69%). The neurochemical and behavioral data suggest that morphine may disrupt sleep, at least in part, by decreasing GABAergic transmission in the PnO. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2009 August 20. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptOpioids such as morphine, that exert their effects primarily via the μ-opioid receptor, are the most efficacious and widely prescribed treatments for pain (Yaksh, 1997, Nicholson, 2003. Unfortunately, opioids have numerous side effects including sleep disruption (Kay et al., 1969, Kay, 1975. In healthy human voluntee...

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“…Despite its extrasynaptic placement, microdialysis is well suited to approximate minute to minute changes in "volume neurotransmission" of monoaminergic neurotransmitters that escape the synapse (Drew et al, 2004;Fillenz, 2005). However, amino acid neurotransmitters such as GABA and glutamate are effectively cleared by synaptic uptake systems, thus extrasynaptic GABA and glutamate levels are mostly independent of neuronal activity (Korte et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Transient fear-induced alterations in evoked release of norepinephrine and GABA in amygdala slices

2007

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Presentation of a tonal cue that previously had been associated with a fearful experience (footshock) produces alterations in arousal and sleep that occur after the fearful cue is no longer presented. To begin investigating neurochemical mechanisms that may underlie the effects of fearful cue presentation, we measured release of Depolarization-evoked release of [ 3 H]-NE from amygdalar slices of mice, which were trained to recognize a tone as a fearful cue, was suppressed at 2-3hrs after exposure of animals to the fearful cue, but recovered after 4-5 hrs. Interestingly, depolarization-evoked release of [ 14 C]-GABA was significantly increased in the amygdala, and also showed a tendency for enhancement in the hippocampus, NPO, and DRN at 2-3 hrs after cue presentation. The changes in [ 14 C]-GABA release were also transient; 4-5 hrs after cue presentation no significant differences were detected between samples derived from experimental groups which experienced fearful or neutral cues. The similar time course of fearful cue-induced changes in neurotransmitter release and changes in arousal and REM sleep suggests that alterations in amygdalar neurotransmission may be involved changes in arousal and sleep that occur after fear.

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Sampling glutamate and GABA with microdialysis: suggestions on how to get the dialysis membrane closer to the synapse

Cited by 44 publications

References 32 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

Sleep and GABA levels in the oral part of rat pontine reticular formation are decreased by local and systemic administration of morphine

Transient fear-induced alterations in evoked release of norepinephrine and GABA in amygdala slices

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