Alcohol dependence treating agent, acamprosate, prevents traumatic brain injury-induced neuron death through vesicular zinc depletion.

Alcohol dependence treating agent, acamprosate, prevents traumatic brain injury-induced neuron death through vesicular zinc depletion. Transl Res. 2019 Jan 17;: Authors: Choi BY, Lee SH, Choi HC, Lee SK, Yoon HS, Park JB, Chung WS, Suh SW Abstract Acamprosate, also known as N-acetyl homotaurine, is an N-methyl-d-aspartate receptor antagonist that is used for treating alcohol dependence. Although the exact mechanism of acamprosate has not been clearly established, it appears to work by promoting a balance between the excitatory and inhibitory neurotransmitters, glutamate, and gamma-aminobutyric acid, respectively. Several studies have demonstrated that acamprosate provides neuroprotection against ischemia-induced brain injury. However, no studies have been performed evaluating the effect of acamprosate on traumatic brain injury (TBI). In the present study, we sought to evaluate the therapeutic potential of acamprosate to protect against neuronal death following TBI. Rats were given oral acamprosate (200 mg/kg/d for 2 weeks) and then subjected to a controlled cortical impact injury localized over the parietal cortex. Histologic analysis was performed at 3 hours, 24 hours, and 7 days after TBI. We found that acamprosate treatment reduced the concentration of vesicular glutamate and zinc in the hippocampus. Consequently, this reduced vesicular glutamate and zinc level resulted in a reduction of reactive oxygen species production after TB...
Source: Translational Research : the journal of laboratory and clinical medicine - Category: Laboratory Medicine Authors: Tags: Transl Res Source Type: research