Changes in the Effect of Isoflurane on N -methyl-d-aspartic Acid-gated Currents in Cultured Cerebral Cortical Neurons with Time in Culture

Zhang, Ming; Griffith, Benjamin L.; Breese, George R.; Mueller, Robert A.; Criswell, Hugh E.

doi:10.1097/00000542-200210000-00017

Cited by 24 publications

(16 citation statements)

References 27 publications

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“…The decreased efficacy of Con G on 19 DIV neurons is most likely caused by a developmental switch in the type of NR2 subunits that are expressed at the synapse. Faster deactivation kinetics and decreased sensitivity to ifenprodil and glycine are associated with increased NR2A expression in cortical and hippocampal neurons with time in culture (Kew et al 1998;Ming et al 2002;Thomas et al 2006;Williams et al 1993;Zhong et al 1994). Increased expression of NR1/NR2A and NR1/NR2A/NR2B receptors at mature synapses has also been reported (Armentia and Sah 2003;Rumbaugh and Vicini 1999;Stocca and Vicini 1998;Thomas et al 2006;Tovar and Westbrook 1999).…”

Section: Discussionmentioning

confidence: 99%

Effect of Conantokin G on NMDA Receptor–Mediated Spontaneous EPSCs in Cultured Cortical Neurons

Alex¹,

Baucum²,

Wilcox³

2006

Journal of Neurophysiology

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. Effect of Conantokin G on NMDA receptor-mediated spontaneous EPSCs in cultured cortical neurons. J Neurophysiol 96: 1084 -1092. First published June 7, 2006 doi:10.1152/jn.01325.2005. Conantokin G (Con G), derived from the venom of Conus geographus, is the most characterized natural peptide antagonist targeted to N-methyl-D-aspartate (NMDA) receptors. Although Con G is known to bind to the glutamate binding site on the NR2 subunit of the receptor, it is unclear whether it can allosterically modulate the function of the receptor through the glycine binding site on the NR1 subunit. This study was designed to evaluate the action of Con G on NMDA receptormediated spontaneous excitatory postsynaptic currents (sEPSCs) and its modulation by glycine in cultured cortical neurons (13-19 days in vitro) using the whole cell patch-clamp technique. Con G inhibited NMDA receptor-mediated sEPSCs in a concentration-dependent manner. Also, the potency of Con G decreased as a function of time in culture. The inhibition of EPSCs observed after application of Con G in the presence of high (10 M) and nominal (no added) concentrations of glycine was not different at 13 days in vitro (DIV). Furthermore, similar results were obtained with experiments on Con G-induced inhibition of NMDA-evoked whole cell currents. These results indicate that glycine concentrations do not have a direct effect on Con G-induced inhibition of NMDA currents. In addition, age dependency in the action of Con G on cortical neurons in vitro suggests that this model system would be useful in examining the effects of different agonists/antagonists on native synaptic NMDA receptors.

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Section: Discussionmentioning

confidence: 99%

Effect of Conantokin G on NMDA Receptor–Mediated Spontaneous EPSCs in Cultured Cortical Neurons

Alex¹,

Baucum²,

Wilcox³

2006

Journal of Neurophysiology

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“…In experiment two, OHSs were maintained in culture for 14 days after isoflurane/fresh gas exposure. These experiments were performed to determine whether the number of days in vitro affected the response to isoflurane to control for possible changes in GABA A and NMDA receptor subunit composition known to be a function of development in vivo (21).…”

Section: Experiments 1 and 2: Isoflurane Exposure And Ohssmentioning

confidence: 99%

Isoflurane-Induced Neuronal Degeneration: An Evaluation in Organotypic Hippocampal Slice Cultures

Wise‐Faberowski¹,

Zhang²,

Ing³

et al. 2005

Anesthesia & Analgesia

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Prolonged exposure of postnatal day (PND) 7 rat pups to anesthetics, which act via N-methyl-D-aspartate antagonism and/or gamma-amino butyric acid enhancement, causes neurodegeneration and persistent behavioral deficits. We studied these findings in vitro and determined whether the age of rat pups used for study or duration of anesthetic exposure modulates resultant neurodegeneration. Organotypic hippocampal slices (OHSs) were prepared from rat pups on PNDs 4, 7, and 14 and cultured 7 or 14 days in vitro. The slices were exposed to 1.5% isoflurane or fresh gas for durations of 1, 3, or 5 h. Hippocampal CA1, CA3, and dentate gyrus neuronal survival was assessed 3 days later. Neuronal cell death was greatest in OHSs prepared from PND 7 rat pups (P < 0.001) and was most evident after 5 h exposure to isoflurane (P < 0.001). By eliminating variables such as hemodynamics, nutrition, oxygenation, and carbon dioxide elimination, this in vitro investigation supports both an age- and duration-dependent relationship between 1.5% isoflurane exposure and perinatal neuronal death.

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“…Whereas it must be understood that neuronal development in vitro is not a faithful recapitulation of in vivo maturation (Chilton and Gordon-Weeks 2006), the ontological progress of neurons in both environments is driven by common stage-specific events. For example, changes in NMDAR subunit or CaBP expression follow similar in vitro and in vivo patterns that appear to be linked to specific stages of neuronal maturation (Zhong et al 1994;Tucker and Morton 1995;Zhong et al 1995;Cheng et al 1999;Hoffmann et al 2000;Ming et al 2002).…”

Section: Introductionmentioning

confidence: 99%

Effects of Disrupting Calcium Homeostasis on Neuronal Maturation: Early Inhibition and Later Recovery

et al. 2008

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It has become increasingly clear that agents that disrupt calcium homeostasis may also be toxic to developing neurons. Using isolated primary neurons, we sought to understand the neurotoxicity of agents such as MK801 (which blocks ligand-gated calcium entry), BAPTA (which chelates intracellular calcium), and thapsigargin (TG; which inhibits the endoplasmic reticulum Ca 2+ -ATPase pump). Thus, E18 at cotical neuons wee grown for 1 day in vitro (DIV) and then exposed to vehicle (0.1% DMSO), MK801 (0.01-20 μM), BAPTA (0.1-20 μM), or TG (0.001-1 μM) for 24 h. We found that all three agents could profoundly influence early neuronal maturation (growth cone expansion, neurite length, neurite complexity), with the order of potency being MK801 < BAPTA < TG. We next asked if cultures exposed to these agents were able to re-establish their developmental program once the agent was removed. When we examined network maturity at 4 and 7 DIV, the order of recovery was MK801 > BAPTA > TG. Thus, mechanistically distinct ways of disrupting calcium homeostasis differentially influenced both short-term and long-term neuronal maturation. These observations suggest that agents that act by altering intracellular calcium and are used in obstetrics or neonatology may be quite harmful to the still-developing human brain.

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Changes in the Effect of Isoflurane on N -methyl-d-aspartic Acid-gated Currents in Cultured Cerebral Cortical Neurons with Time in Culture

Cited by 24 publications

References 27 publications

Effect of Conantokin G on NMDA Receptor–Mediated Spontaneous EPSCs in Cultured Cortical Neurons

Effect of Conantokin G on NMDA Receptor–Mediated Spontaneous EPSCs in Cultured Cortical Neurons

Isoflurane-Induced Neuronal Degeneration: An Evaluation in Organotypic Hippocampal Slice Cultures

Effects of Disrupting Calcium Homeostasis on Neuronal Maturation: Early Inhibition and Later Recovery

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