Dopamine enhances recovery after traumatic brain injury through ubiquitylation and autophagic degradation of RIPK1.

ABSTRACT:

Background

Although the neurotransmitter dopamine (DA) plays a crucial pathophysiologic role after traumatic brain injury (TBI), its function and specific underlying mechanisms of action remain unclear.

Methods

Adult male mice underwent controlled cortical impact (CCI). We administered DA intraperitoneally to mice for 14 consecutive days, starting 8 h before CCI. On day 3 after brain injury, cortical lesion volume and brain water content were measured. On days 7-13, behavioral tests were performed.

Results

Herein we report that DA inhibits neural death after injury, which is mediated via the dopamine D1 receptor (DRD1). Our results also showed that DRD1 signaling promotes RIPK1 ubiquitination via the E3 ubiquitin ligase Chip and then degradation through autophagy. Imp

SUBMITTER: Luo H 

PROVIDER: S-EPMC10875858 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature