ABSTRACT
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 0.001 level) was observed in 72% of the 57 structures examined. Increases in glucose utilization of greater than or equal to 180% of control values were noted in structures associated with the motor system (columns in the frontal sensorimotor cortex, globus pallidus, dentate nucleus of the cerebellum and ovoid areas in the cerebellar vermis), thalamic nuclei (lateral and posterior), dorsal lateral geniculate, mammillary body, cingulate cortex, locus ceruleus, and cerebellar flocculus and paraflocculus. The structures showing the greatest increase in glucose utilization were cerebellar paraflocculus (257% of control), columns in the frontal sensorimotor cortex (247% of control) and ovoid areas in the cerebellar vermis (223% of control). Areas of the brain that have been described as cell body areas for serotonergic (raphe), noradrenergic (locus ceruleus), dopaminergic (substantia nigra, zona compacta) and GABAergic (globus pallidus) neurons also showed increases in glucose utilization. The pattern of cerebral glucose utilization accompanying the phenobarbital withdrawal syndrome in rats contrasts with that for morphine withdrawal and exhibits both similarities and differences with respect to ethanol withdrawal.
Subject(s)
Brain/metabolism , Glucose/metabolism , Phenobarbital , Substance Withdrawal Syndrome/metabolism , Animals , Behavior, Animal/drug effects , Brain/physiopathology , Deoxyglucose/metabolism , Female , Rats , Rats, Inbred StrainsABSTRACT
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. Postwithdrawal was associated with increased amounts of 2-deoxyglucose in comparison to controls in 80% of the gray areas evaluated. Postwithdrawal and control rats did not differ in some areas involved with motor function and some limbic structures, such as the mamillary body-anterior thalamus-cingulate cortex pathway. It is concluded that the ethanol-withdrawal syndrome results in alterations in cerebral physiology, some of which persist for at least 5 weeks postwithdrawal.
Subject(s)
Brain/metabolism , Ethanol/adverse effects , Glucose/metabolism , Substance Withdrawal Syndrome/metabolism , Animals , Deoxyglucose/metabolism , Limbic System/metabolism , Male , Motor Activity/physiology , Rats , Rats, Inbred Strains , Serotonin/metabolism , Time FactorsABSTRACT
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.
Subject(s)
Brain/radiation effects , Sodium/metabolism , Synaptosomes/radiation effects , Veratridine/pharmacology , Veratrine/analogs & derivatives , Animals , Brain/drug effects , Dose-Response Relationship, Drug , Dose-Response Relationship, Radiation , Ion Channels/drug effects , Ion Channels/radiation effects , Male , Rats , Rats, Inbred Strains , Synaptosomes/drug effectsSubject(s)
Acetates/pharmacology , Alcoholism/metabolism , Aminooxyacetic Acid/pharmacology , Brain Chemistry/drug effects , Ethanol/pharmacology , Synaptic Transmission/drug effects , gamma-Aminobutyric Acid/metabolism , Animals , Caudate Nucleus/metabolism , Cerebellum/metabolism , Cerebral Cortex/metabolism , Humans , Male , RatsABSTRACT
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. Concomitantly, high-affinity choline uptake, an index of cholinergic activity, is elevated at times when dopamine release is depressed. Changes in dopaminergic or cholinergic receptor activity do not induce or result from these effects. Neither has a role for GABA or substance P yet been implicated. The data suggest that interactions between at least two trasmitters in the caudate nucleus may occur after acute and chronic ethanol treatment.