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Abstract Ethanol administration in hamsters altered glucose metabolism in the brain, resulting in increased glucose content and decreased incorporation of labeled carbon from 14C-glucose into the amino acids derived via the citric acid cycle and into lactate. In general, amino acid content of the brain changed little after ethanol, but there was a significant decrease in aspartate and an increase in glutamine. These changes in glucose and amino acid metabolism are enhanced by increasing ethanol doses. However, they seem to be an indirect effect of ethanol, since they do not appear until 20–30 min after ethanol injection, despite high blood ethanol levels throughout this period.

In Mauseversuchen wurde gezeigt, dass nicht Serotonin, sondern zwei seiner Metaboliten (5-Hydroxytryptophol oder dessen Ausgangsstoff 5-Hydroxyindolacetaldehyd) die Hypothermie erzeugen.

The properties of neurotransmitter receptor-effector systems were determined in C57BL/6 mice treated with 7% (v/v) ethanol and in mice selectively bred for differences in sleep time after ethanol administration. Mice treated with ethanol for 7 days and then withdrawn for 24 hours showed a decreased hypothermic response to apomorphine. There was no change in basal or dopamine-stimulated adenylate cyclase activity or in the density or affinity of the receptor for 3H-spiroperidol. A small decrease in the density of β-adrenergic receptors was observed in the cerebral cortex of alcohol-treated and withdrawn mice. This decrease was entirely due to a decrease in the density of β2-adrenergic receptors. No change was observed in cyclic AMP accumulation due to either α- or β-adrenergic receptor stimulation. Ethanol administration did result in a rapidly reversible increase in the density of muscarinic cholinergic receptors in the hippocampus and cortex.

The papers in this symposium demonstrate that lipid molecules are ubiquitous messengers that participate in intracellular signaling, function in intercellular communication, and serve as neurotransmitters. This review examines the contribution of lipid messengers in regulating a specific physiological function, the transmission of noxious sensory information (pain) in the nervous system. Lipid molecules play major roles in the modulation of pain sensitivity. Six types of lipid molecules (prostanoids, phosphatidyl inositol bisphosphate, ceramide, lipoxygenase metabolites of arachidonic acid, fatty acyl dopamines, and acylethanolamides) have been shown to modulate systems important in the regulation of pain responses. These molecules exert their actions by interacting with varied receptor systems. Evidence for their participation in the regulation of pain responses comes from in vitro demonstrations of their interactions with signaling systems known to be important in the regulation of pain sensitivity and, in some cases, from demonstration of their ability to modulate pain sensitivity after in vivo administration. One of these classes of lipid mediators, the acylethanolamides, inhibits pain responses, while the others appear to enhance pain sensitivity. Given the rapid growth in our understanding of lipidomics, evident in the papers of this issue, it is virtually certain that additional lipid mediators will be identified as being central to the regulation of pain responses.

Abstract Acute (4g/kg i.p.) and chronic (Sustacal TM diet containing 10% ethanol for 20 days) administration of ethanol to male Sprague-Dawley rats produced no change in the content or enzyme activity of brain arylsulphatase A. In contrast to the lack of effect on arylsulphatase A, the acute and chronic administration of ethanol resulted in an increase in the activity of brain arylsulphatase B (15.8% and 18.4%, respectively). However, the enhancement of the activity of arylsulphatase B was observed only in the brain homogenates which were subjected to osmotic shock. No enhancement of the arylsulphatase B activity was found in the supernatant soluble fraction after the acute and chronic administration of ethanol. Furthermore, acute and chronic ethanol administration did not alter the activities of arylsulphatase A and B in microsomes which have been suggested as sites of the synthesis of lysosomal hydrolases. In addition, 80 mM ethanol, in vitro, did not affect the activity of arylsulphatase A and B. The results of the present study suggest that the acute or chronic administration of ethanol might enhance the activity of lysosomal membrane bound arylsulphatase B via altering the lipid metabolism of lysosomal membranes.

Animal studies have long been an important tool for basic research as they offer a degree of control often lacking in clinical studies. Of particular value is the use of nonhuman primates (NHPs) for neuroimaging studies. Currently, studies have been published using functional magnetic resonance imaging (fMRI) to understand the default-mode network in the NHP brain. Network science provides an alternative approach to neuroimaging allowing for evaluation of whole-brain connectivity. In this study, we used network science to build NHP brain networks from fMRI data to understand the basic functional organization of the NHP brain. We also explored how the brain network is affected following an acute ethanol (EtOH) pharmacological challenge.Baseline resting-state fMRI was acquired in an adult male rhesus macaque (n = 1) and a cohort of vervet monkeys (n = 10). A follow-up scan was conducted in the rhesus macaque to assess network variability and to assess the effects of an acute EtOH challenge on the brain network.The most connected regions in the resting-state networks were similar across species and matched regions identified as the default-mode network in previous NHP fMRI studies. Under an acute EtOH challenge, the functional organization of the brain was significantly impacted.Network science offers a great opportunity to understand the brain as a complex system and how pharmacological conditions can affect the system globally. These models are sensitive to changes in the brain and may prove to be a valuable tool in long-term studies on alcohol exposure.

The effect of dietary ethanol on metabolic fates of glucose and ethanol, and activities of lipoprotein lipase and hormone‐sensitive lipase in several tissues of miniature pigs were determined in vitro. Ethanol and glucose were used at similar rates for fatty acid synthesis in liver and brain and CO2 production in liver. Ethanol was preferred over glucose for fatty acid and CO2 production in ileal mucosal cells. Glucose was the preferred substrate for lipogenesis and oxidation to CO2 in adipose tissue and skeletal muscle, and for oxidation to CO2 in brain. Dietary ethanol decreased glucose and ethanol conversion to fatty acids in ileal mucosa and brain, respectively. Dietary ethanol had no effect on the capacity of liver, adipose tissue, and skeletal muscle to convert either glucose or ethanol to long‐chain fatty acids. The capacity to oxidize ethanol, but not glucose, to CO2 in liver was increased by dietary ethanol. No dietary ethanol effect was observed in other tissues. The capacity for removal of plasma triglycerides (based on lipoprotein lipase activity) tended to increase in adipose tissue and skeletal muscle of pigs fed ethanol. Mobilization of long‐chain fatty acids from adipose tissue (based on hormone‐sensitive lipase activity), triglyceride concentration in plasma, and percentage of lipid in liver remained unchanged when ethanol was fed. Livers of ethanol‐fed pigs, however, were larger than livers of control pigs. Our results indicate that feeding miniature pigs 21–37% of total caloric intake as ethanol causes significant metabolic adaptations of lipid metabolism in liver and ileal mucosa, but not in adipose tissue, skeletal muscle, and brain. The ethanol feeding, however, did not cause fatty livers or hyperlipidemia.

Summary:We reviewed the case records of 249 adult patients with generalized convulsive status epilepticus (SE) examined at San Francisco General Hospital between 1977 and 1989 and identified 27 patients (10.8%) in whom alcohol abuse was the only identifiable precipitating cause of SE. In 12 patients (44% of the study group), SE was the first presentation of alcohol‐related seizures. Seizures with focal features were observed in 11 patients (40.1%), but there was little correlation with localized computed tomography (CT) or EEG abnormalities. SE was controlled with phenytoin (PHT), with or without a benzodiazepine (BZD), in 18 patients (66.7%). Twentytwo patients (81.5%) were discharged with no new neurologic deficits, but time to recovery of baseline mental status was prolonged (>12 h) in 24 patients. With regard to alcohol abuse history, study patients did not differ from a comparison group with isolated alcohol withdrawal seizures. The results indicate that alcohol abuse is a common cause of SE and that SE may be the first presentation of alcohol‐related seizures. Furthermore, the outcome of patients with alcohol‐related SE compares favorably with that of patients with SE due to other causes, but recovery of these patients may be complicated by a prolonged postictal state.

Alcoholic patients who have undergone multiple detoxifications/relapses show altered processing of emotional signals. We performed functional magnetic resonance imaging during performance of implicit and explicit versions of a task in which subjects were presented with morphs of fearful facial emotional expressions. Participants were abstaining, multiply detoxified (MDTx; n=12) or singly detoxified patients (SDTx; n=17), and social drinker controls (n=31). Alcoholic patients were less able than controls to recognize fearful expressions, and showed lower activation in prefrontal areas, including orbitofrontal cortex and insula, which mediate emotional processing. The decrease in activation was greater in MDTx patients who also showed decreased connectivity between insula and prefrontal areas, and between amygdala and globus pallidus. In the explicit condition, the strength of connectivity between insula and areas involved in regulation of emotion (inferior frontal cortex and frontal pole) was negatively correlated with both the number of detoxifications and dependency (measured by the severity of alcohol dependency (SADQ) and control over drinking score (Impaired Control questionnaire, ICQ)). In contrast, increased connectivity was found between insula and the colliculus neuronal cluster, and between amygdala and stria terminalis bed nucleus. In the implicit condition, number of detoxifications and ICQ score correlated positively with connectivity between amygdala and prefrontal cortical areas involved in attentional and executive processes. Repeated episodes of detoxification from alcohol are associated with altered function both in fear perception pathways and in cortical modulation of emotions. Such changes may confer increased sensitivity to emotional stress and impaired social competence, contributing to relapse.