Acute manganese exposure impairs glutamatergic function in a young mouse model of Alzheimer's disease.

ABSTRACT: Manganese (Mn) is an essential metal that serves as a cofactor for metalloenzymes important in moderating oxidative stress and the glutamate/glutamine cycle. Mn is typically obtained through the diet, but toxic overexposure can occur through other environmental or occupational exposure routes such as inhalation. Mn is known to accumulate in the brain following exposure and may contribute to the etiology of neurodegenerative disorders such as Alzheimer's disease (AD) even in the absence of acute neurotoxicity. In the present study, we used in vitro primary cell culture, ex vivo slice electrophysiology and in vivo behavioral approaches to determine if Mn-induced changes in glutamatergic signaling may be altered by genetic risk factors for AD neuropathology. Primary cortical astrocytes incuba

SUBMITTER: Spitznagel BD 

PROVIDER: S-EPMC9998360 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature