@ARTICLE{Wang2010-ab,
  title    = "Blocking early {GABA} depolarization with bumetanide results in
              permanent alterations in cortical circuits and sensorimotor
              gating deficits",
  author   = "Wang, Doris D and Kriegstein, Arnold R",
  abstract = "A high incidence of seizures occurs during the neonatal period
              when immature networks are hyperexcitable and susceptible to
              hypersyncrhonous activity. During development,
              $\gamma$-aminobutyric acid (GABA), the primary inhibitory
              neurotransmitter in adults, typically excites neurons due to high
              expression of the Na(+)-K(+)-2Cl(-) cotransporter (NKCC1). NKCC1
              facilitates seizures because it renders GABA activity excitatory
              through intracellular Cl(-) accumulation, while blocking NKCC1
              with bumetanide suppresses seizures. Bumetanide is currently
              being tested in clinical trials for treatment of neonatal
              seizures. By blocking NKCC1 with bumetanide during cortical
              development, we found a critical period for the development of
              $\alpha$-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate
              synapses. Disruption of GABA signaling during this window
              resulted in permanent decreases in excitatory synaptic
              transmission and sensorimotor gating deficits, a common feature
              in schizophrenia. Our study identifies an essential role for
              GABA-mediated depolarization in regulating the balance between
              cortical excitation and inhibition during a critical period and
              suggests a cautionary approach for using bumetanide in treating
              neonatal seizures.",
  journal  = "Cereb Cortex",
  volume   =  21,
  number   =  3,
  pages    = "574--587",
  month    =  jul,
  year     =  2010,
  language = "en"
}

{"_id":"5thJ7mwhN3CPWeJdd","bibbaseid":"wang-kriegstein-blockingearlygabadepolarizationwithbumetanideresultsinpermanentalterationsincorticalcircuitsandsensorimotorgatingdeficits-2010","author_short":["Wang, D. D","Kriegstein, A. R"],"bibdata":{"bibtype":"article","type":"article","title":"Blocking early GABA depolarization with bumetanide results in permanent alterations in cortical circuits and sensorimotor gating deficits","author":[{"propositions":[],"lastnames":["Wang"],"firstnames":["Doris","D"],"suffixes":[]},{"propositions":[],"lastnames":["Kriegstein"],"firstnames":["Arnold","R"],"suffixes":[]}],"abstract":"A high incidence of seizures occurs during the neonatal period when immature networks are hyperexcitable and susceptible to hypersyncrhonous activity. During development, $γ$-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in adults, typically excites neurons due to high expression of the Na(+)-K(+)-2Cl(-) cotransporter (NKCC1). NKCC1 facilitates seizures because it renders GABA activity excitatory through intracellular Cl(-) accumulation, while blocking NKCC1 with bumetanide suppresses seizures. Bumetanide is currently being tested in clinical trials for treatment of neonatal seizures. By blocking NKCC1 with bumetanide during cortical development, we found a critical period for the development of $α$-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate synapses. Disruption of GABA signaling during this window resulted in permanent decreases in excitatory synaptic transmission and sensorimotor gating deficits, a common feature in schizophrenia. Our study identifies an essential role for GABA-mediated depolarization in regulating the balance between cortical excitation and inhibition during a critical period and suggests a cautionary approach for using bumetanide in treating neonatal seizures.","journal":"Cereb Cortex","volume":"21","number":"3","pages":"574–587","month":"July","year":"2010","language":"en","bibtex":"@ARTICLE{Wang2010-ab,\n title = \"Blocking early {GABA} depolarization with bumetanide results in\n permanent alterations in cortical circuits and sensorimotor\n gating deficits\",\n author = \"Wang, Doris D and Kriegstein, Arnold R\",\n abstract = \"A high incidence of seizures occurs during the neonatal period\n when immature networks are hyperexcitable and susceptible to\n hypersyncrhonous activity. During development,\n $\\gamma$-aminobutyric acid (GABA), the primary inhibitory\n neurotransmitter in adults, typically excites neurons due to high\n expression of the Na(+)-K(+)-2Cl(-) cotransporter (NKCC1). NKCC1\n facilitates seizures because it renders GABA activity excitatory\n through intracellular Cl(-) accumulation, while blocking NKCC1\n with bumetanide suppresses seizures. Bumetanide is currently\n being tested in clinical trials for treatment of neonatal\n seizures. By blocking NKCC1 with bumetanide during cortical\n development, we found a critical period for the development of\n $\\alpha$-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate\n synapses. Disruption of GABA signaling during this window\n resulted in permanent decreases in excitatory synaptic\n transmission and sensorimotor gating deficits, a common feature\n in schizophrenia. Our study identifies an essential role for\n GABA-mediated depolarization in regulating the balance between\n cortical excitation and inhibition during a critical period and\n suggests a cautionary approach for using bumetanide in treating\n neonatal seizures.\",\n journal = \"Cereb Cortex\",\n volume = 21,\n number = 3,\n pages = \"574--587\",\n month = jul,\n year = 2010,\n language = \"en\"\n}\n\n","author_short":["Wang, D. D","Kriegstein, A. R"],"key":"Wang2010-ab","id":"Wang2010-ab","bibbaseid":"wang-kriegstein-blockingearlygabadepolarizationwithbumetanideresultsinpermanentalterationsincorticalcircuitsandsensorimotorgatingdeficits-2010","role":"author","urls":{},"metadata":{"authorlinks":{}}},"bibtype":"article","biburl":"https://bibbase.org/f/EJMp3HRuxirjxpcXh/references.bib","dataSources":["sAFYeB74DpbdXM9NN","4zx9n2tbeLTix3Wxr","k3cdWrThyTh5o59Rm","hq9pebjzmsTuyxGGx","h8Atv2SAy4PmShg5j"],"keywords":[],"search_terms":["blocking","early","gaba","depolarization","bumetanide","results","permanent","alterations","cortical","circuits","sensorimotor","gating","deficits","wang","kriegstein"],"title":"Blocking early GABA depolarization with bumetanide results in permanent alterations in cortical circuits and sensorimotor gating deficits","year":2010}