4.6 Article

Taurine activates GABAergic networks in the neocortex of immature mice

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FRONTIERS MEDIA SA
DOI: 10.3389/fncel.2014.00026

关键词

GABA(A) receptor; glycine receptor; development; neocortex; GABAergic excitation; interneuron; cortical plate; subplate

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  1. Deutsche Forschungsgemeinschaft [DFG For 1341, KI 835/2]
  2. China Scholarship Council (CSC)

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Although it has been suggested that taurine s the main endogenous neurotransmitter acting on glycine receptors, the implications of glycine receptor mediated taurine actions on immature neocortical networks have not been addressed yet. To investigate the influence of taurine on the excitability of neuronal networks in the immature neocortex, we performed whole-cell patch-clamp recordings from visually identified pyramidal neurons and interneurons in coronal slices from C57B116 and GAD67-green fluorescent protein (GFP) transgenic mice (postnatal days 2-4). In 46% of the pyramidal neurons bath application of taurine at concentrations >= 300 mu M significantly enhanced the frequency of postsynaptic currents (PSCs) by 744.3 +/- 93.8% (n = 120 cells). This taurine-induced increase of PSC frequency was abolished by 0.2 uM tetrodotoxin (TTX), 1 RNA strychnine or 3 itM gabazine, but was unaffected by the glutamatergic antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and (1) R() 3 (2 carboxypiperazine-4-y1)propy1-1-phosphonic acid (CPR), suggesting that taurine specifically activates GABAergic network activity projecting to pyramidal neurons. Cell-attached recordings revealed that taurine enhanced the frequency of action potentials (Adis) in pyramidal neurons, indicating an excitatory action of the GABAergic PSCs. In order to identify the presynaptic targets of taurine we demonstrate that bath application of taurine induced in GAD67-GFP labeled interneurons an inward current that is mainly mediated by glycine receptors and can generate APs in these cells. We conclude from these results that taurine can enhance network excitability in the immature neocortex by selectively activating GABAergic interneurons via interact ons with glycine receptors.

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