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Publication : The Glutamine Transporter Slc38a1 Regulates GABAergic Neurotransmission and Synaptic Plasticity.

First Author  Qureshi T Year  2019
Journal  Cereb Cortex Volume  29
Issue  12 Pages  5166-5179
PubMed ID  31050701 Mgi Jnum  J:287861
Mgi Id  MGI:6382567 Doi  10.1093/cercor/bhz055
Citation  Qureshi T, et al. (2019) The Glutamine Transporter Slc38a1 Regulates GABAergic Neurotransmission and Synaptic Plasticity. Cereb Cortex 29(12):5166-5179
abstractText  GABA signaling sustains fundamental brain functions, from nervous system development to the synchronization of population activity and synaptic plasticity. Despite these pivotal features, molecular determinants underscoring the rapid and cell-autonomous replenishment of the vesicular neurotransmitter GABA and its impact on synaptic plasticity remain elusive. Here, we show that genetic disruption of the glutamine transporter Slc38a1 in mice hampers GABA synthesis, modifies synaptic vesicle morphology in GABAergic presynapses and impairs critical period plasticity. We demonstrate that Slc38a1-mediated glutamine transport regulates vesicular GABA content, induces high-frequency membrane oscillations and shapes cortical processing and plasticity. Taken together, this work shows that Slc38a1 is not merely a transporter accumulating glutamine for metabolic purposes, but a key component regulating several neuronal functions.
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