ArticleAlcohol (Fayetteville, N.Y.)2011
Acute ethanol exposure prevents PMA-mediated augmentation of N-methyl-D-aspartate receptor function in primary cultured cerebellar granule cells.
Article in Alcohol (Fayetteville, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Ovariectomy Exacerbates Acute Ethanol-Induced Tachycardia: Role of Nitric Oxide and NMDA Receptors in the Rostral Ventrolateral Medulla.International journal of molecular sciences · 2023Article
- Role of Acetaldehyde in Ethanol Reversal of Tolerance to Morphine-Induced Respiratory Depression in Mice.Advances in drug and alcohol research · 2022Article
- Oxycodone-induced tolerance to respiratory depression: reversal by ethanol, pregabalin and protein kinase C inhibition.British journal of pharmacology · 2018Article
- Ethanol Reversal of Tolerance to the Respiratory Depressant Effects of Morphine.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Ethanol reversal of cellular tolerance to morphine in rat locus coeruleus neurons.Molecular pharmacology · 2013Article
- Phorbol ester reduces ethanol excitation of dopaminergic neurons of the ventral tegmental area: involvement of protein kinase C theta.Frontiers in integrative neuroscience · 2013Article
- Ethanol blocks the reversal of prolonged dopamine inhibition of dopaminergic neurons of the ventral tegmental area.Alcoholism, clinical and experimental research · 2012Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Many intracellular proteins and signaling cascades contribute to the ethanol sensitivity of native N-methyl-D-aspartate receptors (NMDARs). One putative protein is the serine/threonine kinase, protein kinase C (PKC). The purpose of this study was to assess if PKC modulates the ethanol sensitivity of native NMDARs expressed in primary cultured cerebellar granule cells (CGCs). With the whole-cell patch-clamp technique, we assessed if ethanol inhibition of NMDA-induced currents (I(NMDA)) (100 μM NMDA plus 10 μM glycine) were altered in CGCs in which the novel and classical PKC isoforms were activated by phorbol-12-myristate-13-acetate (PMA). Percent inhibition by 10, 50, or 100 mM ethanol of NMDA-induced steady-state current amplitudes (I(SS)) or peak current amplitudes (I(Pk)) of NMDARs expressed in CGCs in which PKC was activated by a 12.5 min, 100 nM PMA exposure at 37°C did not differ from currents obtained from receptors contained in control cells. However, PMA-mediated augmentation of I(Pk) in the absence of ethanol was abolished after brief applications of 10 or 1 mM ethanol coapplied with agonists, and this suppression of enhanced receptor function was observed for up to 8 min post-ethanol exposure. Because we had previously shown that PMA-mediated augmentation of I(NMDA) of NMDARs expressed in these cells is by activation of PKCα, we assessed the effect of ethanol (1, 10, 50, and 100 mM) on PKCα activity. Ethanol decreased PKCα activity by 18% for 1 mM ethanol and activity decreased with increasing ethanol concentrations with a 50% inhibition observed with 100 mM ethanol. The data suggest that ethanol disruption of PMA-mediated augmentation of I(NMDA) may be due to a decrease in PKCα activity by ethanol. However, given the incomplete blockade of PKCα activity and the low concentration of ethanol at which this phenomenon is observed, other ethanol-sensitive signaling cascades must also be involved.
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