@phdthesis{
 title = {Regulation of neuronal Cl - homeostasis and GABAergic inhibition by components of excitatory neurotransmission},
 type = {phdthesis},
 year = {2015},
 institution = {University of Toronto},
 id = {9673b035-d913-3b0b-9521-fd5d99ba9c3d},
 created = {2015-08-27T20:41:36.000Z},
 file_attached = {true},
 profile_id = {d9838a1c-b610-3898-bad6-d5c9bde015b5},
 last_modified = {2018-05-23T00:04:21.542Z},
 read = {true},
 starred = {false},
 authored = {true},
 confirmed = {true},
 hidden = {false},
 citation_key = {Mahadevan2015a},
 folder_uuids = {cbca7189-8a5d-4449-a8ec-c08891db2bd9},
 private_publication = {false},
 abstract = {KCC2 is the neuron-specific member of the K+-Cl- cotransporter family of proteins, which maintains a low intracellular Cl− essential for fast inhibitory synaptic transmission in the mature central nervous system (CNS). KCC2 is essential for survival, as KCC2 knock-out mice die at birth due to respiratory failure. Moreover several neurological disorders including neuropathic pain, epileptic seizures and autism spectrum disorders exhibit impaired synaptic inhibition due to decreased KCC2 expression and function. Despite the critical importance of this protein in maintaining fast synaptic inhibition, KCC2 was discovered to be abundantly expressed at the vicinity of excitatory synapses in 2001. Since this discovery, no study has systematically analyzed how components of synaptic excitation regulate KCC2 function and fast synaptic inhibition in the CNS. The principal novel discoveries from my thesis research are: (i) native-KCC2 exists in a multiprotein complex with key members of excitatory synapse namely, the kainate-type ionotropic glutamate receptor (iGluR) subunit GluK2, and its auxiliary subunit Neto2; (ii) these components of excitatory synapse could serve as auxiliary subunits of KCC2 – a concept which was previously non-existent for transporters in general, and in particularly for KCC2; (iii) Neto2 and GluK2 regulates several aspects of KCC2 cellular regulation including total and surface abundance, oligomerization and transporter efficacy in vitro and in vivo; (iv) finally, loss of Neto2 or GluK2 result in impaired KCC2 transporter function in hippocampal neurons. Hence, my discovery represent a novel regulation of KCC2 function and fast synaptic inhibition by components of excitatory transmission, significantly advancing our growing understanding of the tight interplay between excitation and inhibition.},
 bibtype = {phdthesis},
 author = {Mahadevan, Vivek}
}

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KCC2 is essential for survival, as KCC2 knock-out mice die at birth due to respiratory failure. Moreover several neurological disorders including neuropathic pain, epileptic seizures and autism spectrum disorders exhibit impaired synaptic inhibition due to decreased KCC2 expression and function. Despite the critical importance of this protein in maintaining fast synaptic inhibition, KCC2 was discovered to be abundantly expressed at the vicinity of excitatory synapses in 2001. Since this discovery, no study has systematically analyzed how components of synaptic excitation regulate KCC2 function and fast synaptic inhibition in the CNS. The principal novel discoveries from my thesis research are: (i) native-KCC2 exists in a multiprotein complex with key members of excitatory synapse namely, the kainate-type ionotropic glutamate receptor (iGluR) subunit GluK2, and its auxiliary subunit Neto2; (ii) these components of excitatory synapse could serve as auxiliary subunits of KCC2 – a concept which was previously non-existent for transporters in general, and in particularly for KCC2; (iii) Neto2 and GluK2 regulates several aspects of KCC2 cellular regulation including total and surface abundance, oligomerization and transporter efficacy in vitro and in vivo; (iv) finally, loss of Neto2 or GluK2 result in impaired KCC2 transporter function in hippocampal neurons. Hence, my discovery represent a novel regulation of KCC2 function and fast synaptic inhibition by components of excitatory transmission, significantly advancing our growing understanding of the tight interplay between excitation and inhibition.","bibtype":"phdthesis","author":"Mahadevan, Vivek","bibtex":"@phdthesis{\n title = {Regulation of neuronal Cl - homeostasis and GABAergic inhibition by components of excitatory neurotransmission},\n type = {phdthesis},\n year = {2015},\n institution = {University of Toronto},\n id = {9673b035-d913-3b0b-9521-fd5d99ba9c3d},\n created = {2015-08-27T20:41:36.000Z},\n file_attached = {true},\n profile_id = {d9838a1c-b610-3898-bad6-d5c9bde015b5},\n last_modified = {2018-05-23T00:04:21.542Z},\n read = {true},\n starred = {false},\n authored = {true},\n confirmed = {true},\n hidden = {false},\n citation_key = {Mahadevan2015a},\n folder_uuids = {cbca7189-8a5d-4449-a8ec-c08891db2bd9},\n private_publication = {false},\n abstract = {KCC2 is the neuron-specific member of the K+-Cl- cotransporter family of proteins, which maintains a low intracellular Cl− essential for fast inhibitory synaptic transmission in the mature central nervous system (CNS). KCC2 is essential for survival, as KCC2 knock-out mice die at birth due to respiratory failure. Moreover several neurological disorders including neuropathic pain, epileptic seizures and autism spectrum disorders exhibit impaired synaptic inhibition due to decreased KCC2 expression and function. Despite the critical importance of this protein in maintaining fast synaptic inhibition, KCC2 was discovered to be abundantly expressed at the vicinity of excitatory synapses in 2001. Since this discovery, no study has systematically analyzed how components of synaptic excitation regulate KCC2 function and fast synaptic inhibition in the CNS. The principal novel discoveries from my thesis research are: (i) native-KCC2 exists in a multiprotein complex with key members of excitatory synapse namely, the kainate-type ionotropic glutamate receptor (iGluR) subunit GluK2, and its auxiliary subunit Neto2; (ii) these components of excitatory synapse could serve as auxiliary subunits of KCC2 – a concept which was previously non-existent for transporters in general, and in particularly for KCC2; (iii) Neto2 and GluK2 regulates several aspects of KCC2 cellular regulation including total and surface abundance, oligomerization and transporter efficacy in vitro and in vivo; (iv) finally, loss of Neto2 or GluK2 result in impaired KCC2 transporter function in hippocampal neurons. Hence, my discovery represent a novel regulation of KCC2 function and fast synaptic inhibition by components of excitatory transmission, significantly advancing our growing understanding of the tight interplay between excitation and inhibition.},\n bibtype = {phdthesis},\n author = {Mahadevan, Vivek}\n}","author_short":["Mahadevan, V."],"urls":{"Paper":"https://bibbase.org/service/mendeley/d9838a1c-b610-3898-bad6-d5c9bde015b5/file/36c94082-3a81-0b41-5348-5978f360c28c/2015-Regulation_of_neuronal_Cl_-_homeostasis_and_GABAergic_inhibition_by_components_of_excitatory_neurotransmission.pdf.pdf"},"bibbaseid":"mahadevan-regulationofneuronalclhomeostasisandgabaergicinhibitionbycomponentsofexcitatoryneurotransmission-2015","role":"author","downloads":0,"html":""},"search_terms":["regulation","neuronal","homeostasis","gabaergic","inhibition","components","excitatory","neurotransmission","mahadevan"],"keywords":[],"authorIDs":["5b041d6776b7c0100000007b"]}