NMDA induces protein kinase C translocation in hippocampal slices of immature rat brain

Etoh, Susumu; Baba, Akemichi; Iwata, Hisato

doi:10.1016/0304-3940(91)90533-y

Cited by 25 publications

(10 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…16 -18 With ketamine exposure, the NMDA receptor is not activated and does not initiate downstream signaling. Ketamine alters Ca 2ϩ , 16 cAMP, 19 protein kinase C, 20 and mitogen activated protein kinase 21 signaling.…”

Section: Discussionmentioning

confidence: 99%

The Correlation Between Ketamine and Posttraumatic Stress Disorder in Burned Service Members

McGhee

Maani²,

Garza³

et al. 2008

Journal of Trauma: Injury, Infection &Amp; Critical Care

147

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

The Correlation Between Ketamine and Posttraumatic Stress Disorder in Burned Service Members

McGhee

Maani²,

Garza³

et al. 2008

Journal of Trauma: Injury, Infection &Amp; Critical Care

147

View full text Add to dashboard Cite

“…Moreover, it has been proposed that phospholipase AZ must be phosphorylated to be activated by a receptor-mediated process (Xing and Mattera, 1992;Lin et al, 1993) and that calcium could contribute to the translocation of the enzyme from the cytosol to the membrane (Channon and Leslie, 1990) . Because carbachol strongly stimulates phospholipase C in striatal neurons (El-Etr et al ., 1989;Tencé et al, 1994), this could result in a subsequent activation of protein kinase C. Furthermore, NMDA also induces an activation of protein kinase C (Etch et al, 1991 ;Vaccarino et al ., 1991) . All these observations led us to investigate the role of calcium and protein kinase C activity on the synergistic effects of carbachol and NMDA on [ 3H]AA release .…”

Section: Discussionmentioning

confidence: 99%

Synergistic Effects of Acetylcholine and Glutamate on the Release of Arachidonic Acid from Cultured Striatal Neurons

Tencé

Murphy

Cordier

et al. 1995

Journal of Neurochemistry

View full text Add to dashboard Cite

The activation of muscarinic and NMDA receptors by carbachol and NMDA, respectively, stimulated the release of [3H]arachidonic acid ([3H]AA) from cultured striatal neurons. Striking synergistic effects were observed when both agonists were coapplied. This synergistic response was suppressed by atropine or (5R, 10S)‐(+)‐5‐methyl‐10,11‐dihydro‐5H‐dibenzo[a,d]cyclohepten‐5,10‐imine hydrogen maleate and inhibited by magnesium. It was markedly reduced in the absence of external calcium and suppressed by mepacrine. NMDA strongly elevated the intracellular calcium concentration ([Ca2+]i), but carbachol was ineffective. Ionomycin, α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate, or potassium depolarization, which increased [Ca2+]i but was ineffective on [3H]AA release, also potentiated the carbachol response. Sphingosine and Ro 31‐8220 suppressed the responses evoked by carbachol, NMDA, or both agonists. However, no synergistic responses could be observed when phorbol 12‐myristate 13‐acetate was associated with either carbachol or NMDA. Together, these results suggest that both the massive influx of calcium induced by NMDA and the coupling of muscarinic receptors with a putative phospholipase A2 are required for the strong synergistic effects of carbachol and NMDA on [3H]AA release. Synergistic effects were also observed with acetylcholine and glutamate in the presence of magnesium, further revealing the physiological relevance of this process.

show abstract

“…PKC may also participate in this cascade by phosphorylating specific Ca2' channel proteins or by regulating the NMDA-receptor operated Ca'+ channel (21). PKC potentiates the NMDA response by increasing the duration of Ca2' channel opening, producing a more sustained Ca2' influx (22)(23)(24). The sustained rise of intracellular Ca" may lead to cell injury and eventually death.…”

Section: Discussionmentioning

confidence: 99%

Cyanide induces protein kinase C translocation: Blockade by NMDA antagonists

Rathinavelu

Sun

Pavlaković

et al. 1994

J. Biochem. Toxicol.

View full text Add to dashboard Cite

Activation and translocation of protein kinase C (PKC) during KCN-induced histotoxic hypoxia was studied in rat brain slices prepared from cerebellum, hippocampus, and cortex. Treatment with 1-10 mM KCN produced a significant increase in PKC translocation and enzyme activity in the particulate fraction of cerebellar and hippocampal slices. In cortical slices, PKC activity was not affected by cyanide treatment. The membrane-associated PKC activity reached a maximum 30 minutes after incubation with KCN and remained elevated up to 60 minutes in both the hippocampus and cerebellum. Pretreatment with MK-801 and APV, specific NMDA receptor antagonists, blocked the cyanide-stimulated translocation in the hippocampus and cerebellum, whereas CNQX, an AMPA/kainate receptor antagonist, did not alter the response. These results demonstrate that cyanide stimulates PKC activation and translocation from the cytosol to membranes in select brain areas and NMDA receptor activation mediates this process.

show abstract

NMDA induces protein kinase C translocation in hippocampal slices of immature rat brain

Cited by 25 publications

References 13 publications

The Correlation Between Ketamine and Posttraumatic Stress Disorder in Burned Service Members

The Correlation Between Ketamine and Posttraumatic Stress Disorder in Burned Service Members

Synergistic Effects of Acetylcholine and Glutamate on the Release of Arachidonic Acid from Cultured Striatal Neurons

Cyanide induces protein kinase C translocation: Blockade by NMDA antagonists

Contact Info

Product

Resources

About