Loss of excitatory amino acid transporter restraint following chronic intermittent hypoxia contributes to synaptic alterations in nucleus tractus solitarii | Zendy

Diana Martínez | Zendy; Richard C. Rogers | Zendy; Eileen M. Hasser | Zendy; Gerlinda E. Hermann | Zendy; David D. Kline | Zendy

Open Access

Loss of excitatory amino acid transporter restraint following chronic intermittent hypoxia contributes to synaptic alterations in nucleus tractus solitarii

Author(s) -

Diana Martínez,

Richard C. Rogers,

Eileen M. Hasser,

Gerlinda E. Hermann,

David D. Kline

Publication year - 2020

Publication title -

journal of neurophysiology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.302

H-Index - 245

eISSN - 1522-1598

pISSN - 0022-3077

DOI - 10.1152/jn.00766.2019

Subject(s) - excitatory postsynaptic potential , glutamatergic , postsynaptic current , neuroscience , neurotransmission , inhibitory postsynaptic potential , postsynaptic potential , chemistry , excitatory amino acid transporter , hypoxia (environmental) , transporter , glutamate receptor , biology , receptor , biochemistry , organic chemistry , oxygen , gene

Removal of excitatory amino acid transporter (EAAT) restraint increases spontaneous synaptic activity yet decreases afferent [tractus solitarii (TS)]-driven excitatory postsynaptic current (EPSC) amplitude. In the chronic intermittent hypoxia model of obstructive sleep apnea, this restraint is lost due to reduction in EAAT expression and function. Thus EAATs are important in controlling elevated glutamatergic signaling, and loss of such control results in maladaptive synaptic signaling.

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