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Articles 1 - 5 of 5
Full-Text Articles in Life Sciences
Lack Of Depolarization-Induced Suppression Of Inhibition (Dsi) In Layer 2/3 Interneurons That Receive Cannabinoid-Sensitive Inhibitory Inputs, Fouad Lemtiri-Chlieh, Eric S. Levine
Lack Of Depolarization-Induced Suppression Of Inhibition (Dsi) In Layer 2/3 Interneurons That Receive Cannabinoid-Sensitive Inhibitory Inputs, Fouad Lemtiri-Chlieh, Eric S. Levine
fouad Lemtiri-Chlieh
In layer 2/3 of neocortex, brief trains of action potentials in pyramidal neurons (PNs) induce the mobilization of endogenous cannabinoids (eCBs), resulting in a depression of GABA release from the terminals of inhibitory interneurons (INs). This depolarization-induced suppression of inhibition (DSI) is mediated by activation of the type 1 cannabinoid receptor (CB1) on presynaptic terminals of a subset of INs. However, it is not clear whether CB1 receptors are also expressed at synapses between INs, and whether INs can release eCBs in response to depolarization. In the present studies, brain slices containing somatosensory cortex were prepared from 14- to 21-day-old …
Phenylalanyl-Trna Synthetase Editing Defects Result In Efficient Mistranslation Of Phenylalanine Codons As Tyrosine, Jiqiang Ling, Srujana S. Yadavalli, Michael Ibba
Phenylalanyl-Trna Synthetase Editing Defects Result In Efficient Mistranslation Of Phenylalanine Codons As Tyrosine, Jiqiang Ling, Srujana S. Yadavalli, Michael Ibba
Biology, Chemistry, and Environmental Sciences Faculty Articles and Research
Translational quality control is monitored at several steps, including substrate selection by aminoacyl-tRNA synthetases (aaRSs), and discrimination of aminoacyl-tRNAs by elongation factor Tu (EF-Tu) and the ribosome. Phenylalanyl-tRNA synthetase (PheRS) misactivates Tyr but is able to correct the mistake using a proofreading activity named editing. Previously we found that overproduction of editing-defective PheRS resulted in Tyr incorporation at Phe-encoded positions in vivo , although the misreading efficiency could not be estimated. This raised the question as to whether or not EF-Tu and the ribosome provide further proofreading mechanisms to prevent mistranslation of Phe codons by Tyr. Here we show that, …
An Aminoacyl-Trna Synthetase: Elongation Factor Complex For Substrate Channeling In Archaeal Translation, Corinne D. Hausmann, Mette Praetorius-Ibba, Michael Ibba
An Aminoacyl-Trna Synthetase: Elongation Factor Complex For Substrate Channeling In Archaeal Translation, Corinne D. Hausmann, Mette Praetorius-Ibba, Michael Ibba
Biology, Chemistry, and Environmental Sciences Faculty Articles and Research
Translation requires the specific attachment of amino acids to tRNAs by aminoacyl-tRNA synthetases (aaRSs) and the subsequent delivery of aminoacyl-tRNAs to the ribosome by elongation factor 1 alpha (EF-1α). Interactions between EF-1α and various aaRSs have been described in eukaryotes, but the role of these complexes remains unclear. To investigate possible interactions between EF-1α and other cellular components, a yeast two-hybrid screen was performed for the archaeon Methanothermobacter thermautotrophicus. EF-1α was found to form a stable complex with leucyl-tRNA synthetase (LeuRS; KD = 0.7 μ M). Complex formation had little effect on EF-1α activity, but increased the kcat …
Inhibition Of Astroglial Kir4.1 Channels By Selective Serotonin Reuptake Inhibitors, Y. Ohno, H. Hibino, Christoph Lossin, A. Inanobe, Y. Kurachi
Inhibition Of Astroglial Kir4.1 Channels By Selective Serotonin Reuptake Inhibitors, Y. Ohno, H. Hibino, Christoph Lossin, A. Inanobe, Y. Kurachi
Christoph Lossin, Ph.D.
The inwardly rectifying K+ (Kir) channel Kir4.1 is responsible for astroglial K+ buffering. We recently found that tricyclic antidepressants (TCAs) inhibit Kir4.1 channel currents, which suggests that astroglial Kir currents might be involved in the pharmacological action of antidepressants. We therefore further examined the effects of the currently most popular antidepressants, selective serotonin reuptake inhibitors (SSRIs), and other related agents on Kir4.1 channels heterologously expressed in HEK293T cells. The whole-cell patch clamp technique was used. Fluoxetine, the typical SSRI, inhibited Kir4.1 channel currents in a concentration-dependent manner with an IC50 value of 15.2 microM. The inhibitory effect of fluoxetine was …
Inhibition Of Astroglial Inwardly Rectifying Kir4.1 Channels By A Tricyclic Antidepressant, Nortriptyline., S. Su, Y. Ohno, Christoph Lossin, A. Inanobe, Y. Kurachi
Inhibition Of Astroglial Inwardly Rectifying Kir4.1 Channels By A Tricyclic Antidepressant, Nortriptyline., S. Su, Y. Ohno, Christoph Lossin, A. Inanobe, Y. Kurachi
Christoph Lossin, Ph.D.
The inwardly rectifying K(+) (Kir) channel Kir4.1 is responsible for astroglial K(+) buffering. We examined the effects of nortriptyline, a tricyclic antidepressant (TCA), on Kir4.1 channel currents heterologously expressed in HEK293T cells, using a whole-cell patch-clamp technique. Nortriptyline (3-300 microM) reversibly inhibited Kir4.1 currents in a concentration-dependent manner, whereas it marginally affected neuronal Kir2.1 currents. The inhibition of Kir4.1 channels by nortriptyline depended on the voltage difference from the K(+) equilibrium potential (E(K)), with greater potency at more positive potentials. Blocking kinetics of the drug could be described by first-order kinetics, where dissociation of the drug slowed down and association …