In some brain regions such as the hippocampus, COX-2 remained increased several fold over control levels even though the physical signs of ethanol withdrawal had completely subsided. COX-2 is known to form prostaglandins and other bioactive agents that can modulate synaptic efficacy, e.g., can change the volume of neuronal communication. In addition, COX-2 can stimulate the production of oxidative radicals capable of causing cellular injury. These results suggest that minimal exposure to alcohol may cause important changes in brain functioning and possibly even damage the brain. Some of these changes may contribute to the progression to and maintenance of alcoholism in susceptible individuals.
Alcoholics often comment that they are never cured.
It is possible that genes such as COX-2 are increased in brain by binge drinking changing brain function permanently. Alexey Kampov-Polevoi, Manjiri Sethna, Richard Hanes, Christopher J. Braun, Fulton T. Crews, Jen Obernier. Crews, Knapp and Robert Switzer III have also used cupric silver stain, which accumulates in damaged cells, to assess alcohol-induced brain damage during binge drinking. While measurement of COX-2 reflects increases in enzyme levels within neurons, cupric silver staining is used to measure cellular death. This damage is consistent with the maladaptive emotional decision-making we see in alcoholism, which can be conceptualized as the emotional perseverance on a single entity, the addiction.