Alcohol binge drinking decreases brain glucose metabolism and functional connectivity in adolescent rats.

Alcohol misuse represents a serious health concern, especially during adolescence, with approximately 18% of high school students engaging in binge drinking. Despite widespread misuse of alcohol, its effects on how the brain functions is not fully understood. This study utilized a binge drinking model in adolescent rats to examine effects on brain function as measured by brain glucose metabolism (BGluM). Following an injection of [18 FDG] fluro-2-deoxy-D-glucose, rats had voluntary access to either water or various concentrations of ethanol to obtain the following targeted doses: water (no ethanol), low dose ethanol (0.29 ± 0.03 g/kg), moderate dose ethanol (0.98 ± 0.05), and high dose ethanol (2.19 ± 0.23 g/kg). Rats were subsequently scanned using positron emission tomography. All three doses of ethanol were found to decrease BGluM in the restrosplenial cortex, visual cortex, jaw region of the somatosensory cortex, and cerebellum. For both the LD and MD ethanol dose, decreased BGluM was seen in the superior colliculi. The MD ethanol dose also decreased BGluM in the subiculum, frontal association area, as well as the primary motor cortex. Lastly, the HD ethanol dose decreased BGluM in the hippocampus, thalamus, raphe nucleus, inferior colliculus, and the primary motor cortex. Similar decreases in the hippocampus were also seen in the LD group. Taken together, these results highlight the negative consequences of acute binge drinking on BGluM in many regions of the brain involved in sensory, motor, and cognitive processes. Future studies are needed to assess the long-term effects of alcohol binge drinking on brain function as well as its cessation.

The long-term interaction of diet and dopamine D2 gene expression on brain microglial activation.

Dopamine D2 receptors are expressed on microglial in the central nervous system and promote anti-inflammatory responses. Little work has been done on the interaction between the dopamine D2 receptors and diet on activated microglial expression in the brain. To assess this, the current study uses in vitro autoradiography to look at microglial activation in the brain as a marker for neuroinflammation. Mice with different levels of expression of the DA D2 gene were given a chronic diet of either normal diet chow or high fat diet chow for 30 weeks. Mice were then euthanized and their brains were processed for [3H]PK11195 autoradiography. Mice with reductions or lack of the D2 gene showed higher [3H]PK11195 binding in a diet-specific manner within somatosensory and striatal regions, as well as the piriform, frontal, insular, and entorhinal regions compared to mice with normal D2 gene levels. These brain regions are important for sensory processing, habit formation, as well as cognitive function tasks related to learning, motivation, and memory. These results suggest that decreased D2R levels may increase vulnerability to specific inflammatory markers. Future studies will need to examine the implications of these inflammatory changes on brain function and behavior.