Enhanced recruitment of glutamate receptors underlies excitotoxicity of mitral cells in acute hyperammonemia.

ABSTRACT: Hepatic encephalopathy (HE)-a major complication of liver disease-has been found to increase the risk of olfactory dysfunction, which may be attributed to elevated levels of ammonia/ammonium in the blood and cerebrospinal fluid. However, the cellular mechanisms underlying hyperammonemia-induced olfactory dysfunction remain unclear. By performing patch-clamp recordings of mitral cells (MCs) in the mouse olfactory bulb (OB), we found that 3 mM ammonium (NH₄ ⁺) increased the spontaneous firing frequency and attenuated the amplitude, but synaptic blockers could prevent the changes, suggesting the important role of glutamate receptors in NH₄ ⁺-induced hyperexcitability of MCs. We also found NH₄ ⁺ reduced the currents of voltage-g

SUBMITTER: Li M 

PROVIDER: S-EPMC9651449 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature