Cerebral glucose utilization in rat brain during phenobarbital withdrawal.

The phenobarbital withdrawal syndrome in rats is characterized by tremors, arched back, weight loss and hyperactivity. This syndrome is shown to be associated with both general and localized increases in cerebral glucose utilization. An increase in glucose utilization (significant at the P less than or equal to 0.

Cerebral 2-deoxyglucose uptake in rats during ethanol withdrawal and postwithdrawal.

The overt ethanol withdrawal syndrome is associated with a generalized increase in cerebral uptake of 2-deoxyglucose. Relatively high elevations of 2-deoxyglucose were observed in many structures associated with motor function, the mamillary body-anterior thalamus-cingulate cortex pathway, many thalamic nuclei, and the raphe. Overtly withdrawing rats had higher levels of 2-deoxyglucose than postwithdrawing animals that had been abstinent for 1-5 weeks in 96% of the gray areas evaluated.

Ionizing radiation decreases veratridine-stimulated uptake of sodium in rat brain synaptosomes.

Veratridine-stimulated uptake of sodium-22 in brain synaptosomes was significantly reduced by ionizing radiation over a dose range of 10 to 1000 rads. The response was dose-dependent and involved a decrease in the maximum effect of veratridine on uptake. The central nervous system may be more sensitive to ionizing radiation than generally thought, perhaps through a loss of the ability of the sodium channel to respond properly to stimulation.

Alterations in neurotransmitter activity after acute and chronic ethanol treatment: studies of transmitter interactions.

Acute and chronic ethanol treatment has multiple effects on the neurotransmitter systems in the nigrostriatal complex. A single dose of ethanol increases striatal dopamine release at low doses, but depresses it at high doses. In ethanol-dependent rats, dopamine release is accelerated during intoxication, but is reduced during a withdrawal syndrome.