However, our lab has found similar findings looking at macrostructural changes in adolescent hippocampal volumes. We found reduced hippocampal volumes and abnormal asymmetry in adolescent drinkers compared to controls, but did not observe volume or asymmetry abnormalities in teens reporting both alcohol and marijuana use [59]. It is possible that marijuana may have some neuroprotective properties in mitigating alcohol-related oxidative stress or excitoxic cell death as suggested in animal models of alcohol-induced neuronal death and cell regeneration [24,37,101,102]. Although research on the neuroprotective role of cannabinoids is not completely understood, studies have identified several potential neuroprotective molecular mechanisms. For example, activation of cannabinoid receptors may reduce inflammatory activity and excess glutamate neurotransmission that can lead to toxic cell death due to influx of intracellular calcium ion concentrations. Marijuana may also prevent toxicity through anti-oxidative benefits that prevent damage to cellular lipids and proteins, and which may not require cannabinoid-receptor mediated action [18,36,78]. Research on the role of cannabinoids in animal models of binge drinking has found evidence for cannabinoids as a neuroprotectant against binge alcohol toxicity in hippocampal regions when
