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The Brain Can Reveal Drinking Status Even After Death

Scientists who use postmortem brain tissue to study alcohol’s effects on brain structure and function will find this research interesting. Phosphatidylethanol (PEth) is an alcohol metabolite and its concentration in whole blood samples is a biomarker of drinking habits. For this study, scientists examined PEth levels in postmortem brains of individuals known to have had alcohol use disorders (AUDs).

Researchers divided 30 postmortem brains into three groups: 10 with AUDs that had positive serum alcohol levels present at the time of autopsy; 10 with AUDs that did not show positive serum alcohol levels at the time of autopsy; and 10 normal brains. PEth levels were measured in the cerebellum and orbital frontal cortex (OFC) regions.

Results showed that PEth was present in the cerebellum and OFC of all brains in all three groups of subjects, including the controls. The AUD group with detectable serum alcohol levels at the time of autopsy had much higher levels of PEth in both brain areas than either the control group or the AUD group whose subjects did not have detectable serum ethanol at autopsy. Thus, the ability to measure PEth levels in postmortem human brains can be helpful in classifying drinking status in individuals with AUDs at the time of death.

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One of the best ways to get people to do something is to make it fun. A marketing campaign called ‘The Fun Theory’ found that when stairs next to an escalator were turned into giant, functional piano keys, the amount of people who took the stairs increased 66%, and when a trash can had sound effects that made it seem infinitely deep, people started picking up and throwing away litter just to hear it. Source

(Image caption: The empty stomach releases the hormone called ghrelin. By receiving ghrelin, the hypothalamus in the brain senses hunger and produces “hunger signaling” through the action of neuropeptide Y (NPY). The hunger signaling activates neurons in the reticular formation of the medulla oblongata, which then inhibit sympathetic output to reduce metabolic heat production and simultaneously provide masticatory motor rhythm to facilitate feeding. Credit: © 2017 Yoshiko Nakamura)

New Insights into Brain Circuit for Hunger Responses during Starvation

The human body responds to starving conditions, such as famine, to promote the chance of survival. It reduces energy expenditure by stopping heat production and promotes feeding behavior. These “hunger responses” are activated by the feeling of hunger in the stomach and are controlled by neuropeptide Y (NPY) signals released by neurons in the hypothalamus. However, how NPY signaling in the hypothalamus elicits the hunger responses has remained unknown.

Sympathetic motor neurons in the medulla oblongata are responsible for heat production by brown adipose tissue (BAT). Researchers centered at Nagoya University have now tested whether the heat-producing neurons respond to the same hypothalamic NPY signals that control hunger responses. They injected NPY into the hypothalamus of rats and tested the effect on heat production. Under normal conditions, blocking inhibitory GABAergic receptors or stimulating excitatory glutamatergic receptors in the sympathetic motor neurons induced heat production in BAT. After NPY injection, stimulating glutamatergic receptors did not produce heat, but inhibiting GABAergic receptors did. The study was reported in Cell Metabolism.

“This indicated that hypothalamic NPY signals prevent BAT thermogenesis by using inhibitory GABAergic inputs to sympathetic motor neurons,” study lead author Yoshiko Nakamura says.

Retrograde and anterograde tracing with fluorescent dyes revealed which brain region provided the inhibitory GABAergic inputs to heat-producing motor neurons.

“Tracing experiments showed that sympathetic motor neurons are directly innervated by GABAergic inputs from reticular nuclei in the medulla oblongata,” corresponding author Kazuhiro Nakamura explains, “selective activation of these GABAergic reticular neurons inhibits BAT thermogenesis.”

The researchers’ further findings showed that GABAergic inputs from medullary reticular neurons are involved in hypothalamic NPY-mediated inhibition of heat production in BAT. This hunger response circuit probably explains why anorexic individuals suffer from hypothermia.

Interestingly, stimulation of these medullary reticular neurons prompted rats to begin chewing and feeding. This effect was similar to injecting NPY into the hypothalamus, suggesting that hypothalamic NPY signaling activates reticular neurons in the medulla oblongata to promote feeding and mastication during the hunger response.

Abnormal activation of these neurons under non-starved conditions may contribute to obesity. Understanding these mechanisms could lead to development of more effective treatments for obesity.

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