It has been postulated that excess ammonia and neuroinflammation resulting from liver failure induces astrocytic swelling which can lead to increased BBB permeability and neuronal dysfunction. The impacts of high levels of blood ammonia on the brain energy metabolism is not clear. The objective of current study is to evaluate the neurotransmitter metabolism in CCl4 induced liver injury mouse model using using 1H-[13C]-NMR spectroscopy together with [1,6-13C2]glucose infusion. Our findings indicate reduction in the activity of glutamatergic and GABAergic neurons in the chronic liver damage condition.
How to access this content:
For one year after publication, abstracts and videos are only open to registrants of this annual meeting. Registrants should use their existing login information. Non-registrant access can be purchased via the ISMRM E-Library.
After one year, current ISMRM & ISMRT members get free access to both the abstracts and videos. Non-members and non-registrants must purchase access via the ISMRM E-Library.
After two years, the meeting proceedings (abstracts) are opened to the public and require no login information. Videos remain behind password for access by members, registrants and E-Library customers.
Keywords