Methodology for rapid measures of glutamate release in rat brain slices using ceramic-based microelectrode arrays: Basic characterization and drug pharmacology

Quintero, Jorge E.; Pomerleau, François; Huettl, Peter; Johnson, Kirk W.; Offord, James; Gerhardt, Greg A.

doi:10.1016/j.brainres.2011.05.025

Cited by 33 publications

(24 citation statements)

References 47 publications

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“…S2 ceramic-based microelectrode arrays (MEA) were prepared for in vivo recordings as previously described (Burmeister et al, 2002; Quintero et al, 2011). Briefly, recording sites were coated with a glutamate oxidase (GluOx) enzyme solution (U.S.…”

Section: Methodsmentioning

confidence: 99%

Altered glutamate release in the dorsal striatum of the MitoPark mouse model of Parkinson's disease

et al. 2016

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Mitochondrial dysfunction has been implicated in the degeneration of dopamine (DA) neurons in Parkinson’s disease (PD). In addition, animal models of PD utilizing neurotoxins, such as 6-hydroxydopamine and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, have shown that these toxins disrupt mitochondrial respiration by targeting complex I of the electron transport chain, thereby impairing DA neurons in these models. A MitoPark mouse model was created to mimic the mitochondrial dysfunction observed in the DA system of PD patients. These mice display the same phenotypic characteristics as PD, including accelerated decline in motor function and DAergic systems with age. Previously, these mice have responded to L-Dopa treatment and develop L-Dopa induced dyskinesia (LID) as they age. A potential mechanism involved in the formation of LID is greater glutamate release into the dorsal striatum as a result of altered basal ganglia neurocircuitry due to reduced nigrostriatal DA neurotransmission. Therefore, the focus of this study was to assess various indicators of glutamate neurotransmission in the dorsal striatum of MitoPark mice at an age in which nigrostriatal DA has degenerated. At 28 weeks of age, MitoPark mice had, upon KCl stimulation, greater glutamate release in the dorsal striatum compared to control mice. In addition, uptake kinetics were slower in MitoPark mice. These findings were coupled with reduced expression of the glutamate re-uptake transporter, GLT-1, thus providing an environment suitable for glutamate excitotoxic events, leading to altered physiological function in these mice.

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Section: Methodsmentioning

confidence: 99%

Altered glutamate release in the dorsal striatum of the MitoPark mouse model of Parkinson's disease

et al. 2016

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“…S2 ceramic-based microelectrode arrays (MEA) were prepared for in vivo recordings (Burmeister et al, 2002; Quintero et al, 2011). Briefly, recording sites were coated with a glutamate oxidase (GluOx) enzyme solution (U.S.…”

Section: Methodsmentioning

confidence: 99%

Effects of aging on glutamate neurotransmission in the substantia nigra of Gdnf heterozygous mice

Farrand

Gregory

Scofield

et al. 2015

Neurobiology of Aging

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Glial cell line-derived neurotrophic factor (GDNF) helps protect dopaminergic neurons in the nigrostriatal tract. Although the cause of nigrostriatal degeneration is unknown, one theory is that excess glutamate from the subthalamic nucleus (STN) results in excitotoxic events in the substantia nigra (SN). Since dopaminergic degeneration is accompanied by a reduction in GDNF, we examined glutamate neurotransmission in the SN using a Gdnf heterozygous mouse model (Gdnf+/−) at 8 and 12 months of age. At 8 months, Gdnf+/− mice have greater glutamate release and higher basal glutamate levels, which precede the SN dopaminergic degeneration observed at 12 months of age. However, at 12 months, Gdnf+/− mice have lower basal levels of glutamate and less glutamate release than wildtype (WT) mice. Also at 8 months, Gdnf+/− mice have lower levels of GLT-1 and greater GFAP levels in the SN compared to WT mice, differences that increase with age. These data suggest that reduced levels of GDNF induce excess glutamate release and dysregulation of GLT-1, causing excitotoxicity in the SN that precedes dopaminergic degeneration.

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“…For second-by-second glutamate measurement, a +0.7V (50 ms) potential was applied to the MEA once per second and referenced to a Ag/AgCl reference electrode outside the dura. The oxidation of H 2 O 2 by the pulse results in a relaxation current proportional to free glutamate concentration at the electrode[ [13][14][15].…”

Section: B Neural Activity and Glutamate Recordingmentioning

confidence: 99%

Conformal ceramic electrodes that record glutamate release and corresponding neural activity in primate prefrontal cortex

Hampson

Fuqua

Huettl

et al. 2013

2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC)

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Conformal ceramic electrodes utilized in prior recordings of nonhuman primate prefrontal cortical layer 2/3 and layer 5 neurons were used in this study to record tonic glutamate concentration and transient release in layer 2/3 PFC. Tonic glutamate concentration increased in the Match (decision) phase of a visual delayed-match-to-sample (DMS) task, while increased transient glutamate release occurred in the Sample (encoding) phase of the task. Further, spatial vs. object-oriented DMS trials evoked differential changes in glutamate concentration. Thus the same conformal recording electrodes were capable of electrophysiological and electrochemical recording, and revealed similar evidence of neural processing in layers 2/3 and layer 5 during cognitive processing in a behavioral task.

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Methodology for rapid measures of glutamate release in rat brain slices using ceramic-based microelectrode arrays: Basic characterization and drug pharmacology

Cited by 33 publications

References 47 publications

Altered glutamate release in the dorsal striatum of the MitoPark mouse model of Parkinson's disease

Altered glutamate release in the dorsal striatum of the MitoPark mouse model of Parkinson's disease

Effects of aging on glutamate neurotransmission in the substantia nigra of Gdnf heterozygous mice

Conformal ceramic electrodes that record glutamate release and corresponding neural activity in primate prefrontal cortex

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