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Purpose: Heavy ion and proton brain irradiations occur during space travel and in Hadron therapy for cancer. Heavy ions produce distinct patterns of energy deposition in neuron cells and brain tissues compared to X-rays leading to large uncertainties in risk estimates. We make a critical review of findings from research studies over the last 25 years for understanding risks at low dose. Conclusions: A large number of mouse and rat cognitive testing measures have been reported for a variety of particle species and energies for acute doses. However, tissue reactions occur above dose thresholds and very few studies were performed at the heavy ion doses to be encountered on space missions (<0.04 Gy/y) or considered dose-rate effects, such that threshold doses are not known in rodent models. Investigations of possible mechanisms for cognitive changes have been limited by experimental design with largely group specific and not subject specific findings reported. Persistent oxidative stress and activated microglia cells are common mechanisms studied, while impairment of neurogenesis, detriments in neuron morphology, and changes to gene and protein expression were each found to be important in specific studies. Future research should focus on estimating threshold doses carried out with experimental designs aimed at understating causative mechanisms, which will be essential for extrapolating rodent findings to humans and chronic radiation scenarios, while establishing if mitigation are needed.

Relatively few investigators have made use of the golden hamster as an experimental animal for ethanol studies. This is somewhat surprising insofar as hamsters show a marked preference for ethanol solutions in free-choice experiments. Given a choice of water or a 10% ethanol solution, hamsters will drink 88% of their total fluid as ethanol solution (Arvola and Forsander, 1961). Furthermore, the most preferred concentration of ethanol for the male hamster is 15% (Arvola and Forsander, 1963) in contrast to the rat that shows a preference only for much lower ethanol concentrations.

Human genetic variation in the nicotinic receptor gene cluster CHRNA5/A3/B4, in particular the non-synonymous and frequent CHRNA5 variant rs16969968 (α5SNP), has an important consequence on smoking behavior in humans. A number of genetic association studies have additionally implicated the CHRNA5 gene in addictions to other drugs, and also body mass index (BMI). Here, we model the α5SNP, in a transgenic rat line, and establish its role in alcohol dependence, and feeding behavior. Rats expressing the α5SNP consume more alcohol, and exhibit increased relapse to alcohol seeking after abstinence. This high-relapsing phenotype is reflected in altered activity in the insula, linked to interoception, as established using c-Fos immunostaining. Similarly, relapse to food seeking is increased in the transgenic group, while a nicotine treatment reduces relapse in both transgenic and control rats. These findings point to a general role of this human polymorphism in reward processing, and multiple addictions other than smoking. This could pave the way for the use of medication targeting the nicotinic receptor in the treatment of alcohol use and eating disorders, and comorbid conditions in smokers.

Ethanol was administered to Sprague-Dawley rats for 4–6 weeks following which these animals thrived in a manner comparable to a naive control group. Over 6 months after an ethanol-free interval, the alcohol-exposed animals responded to a test dose of ethanol with a greater disturbance in REM sleep than noted in the naive group.

Despite general reports of fires in the operating room, those during neurosurgical procedures are rare. The most significant contributor to perioperative fires is excess oxygenation. The consideration of novel gel-based surgical preparation solutions as potential fuel sources should be included in the literature. Given the significant patient risk and legal ramifications of surgical fires, education regarding operating room fires and the potential for prevention and treatment is requisite. The authors describe the case of an 18-month-old girl who, while undergoing a resection of a right retroauricular scalp mass, suffered partial thickness bums as a result of the ignition of surgical preparation solution following the use of monopolar electrocautery.

To address whether defective melanocortin activation is one element of leptin resistance with age, we infused centrally the melanocortin agonist, MTII and antagonist, SHU9119 in young and old rats. Food intake, energy expenditure, adiposity, BAT UCP1, and leptin expression in white fat as well as hypothalamic expressions of MC3R, MC4R, POMC, AgRP and NPY were assessed. The MTII-evoked anorexia was transient whereas the SHU9119-induced hyperphagia was sustained in young and old. MTII elevated oxygen consumption in both ages. The oxygen consumption waned gradually in young but increased continuously in aged following MTII infusion. The MTII-mediated induction in BAT UCP1 was similarly robust in both ages as was the SHU9119-mediated suppression in UCP1. POMC and MC3/4 receptor expressions were unaltered with age. These findings demonstrate the effectiveness of MTII to bypass leptin resistance in aged-obese rats. The equally strong orexigenic response to SHU9119 coupled with unaltered POMC expression and food intake in the young versus old suggest that melanocortin tone is unchanged with age despite impaired melanocortin activation by leptin.

Abstract : The activation of phospholipase D (PLD) is a common response to mitogenic stimuli in various cell types. As PLD‐mediated signaling is known to be disrupted in the presence of ethanol, we tested whether PLD is involved in the ethanol‐induced inhibition of cell proliferation in rat cortical primary astrocytes. Readdition of fetal calf serum (FCS) to serum‐deprived astroglial cultures caused a rapid, threefold increase of PLD activity and a strong mitogenic response ; both effects were dependent on tyrosine kinases but not on protein kinase C. Ethanol (0.1‐2%) suppressed the FCS‐induced, PLD‐mediated formation of phosphatidic acid (PA) as well as astroglial cell proliferation in a concentration‐dependent manner. Moreover, exogenous bacterial PLD increased astroglial proliferation in an ethanol‐sensitive manner, whereas exogenous PA or lysophosphatidic acid was less effective. Formation of PA and astroglial proliferation were strongly inhibited by 1‐butanol (0.1‐1%), a substrate of PLD, but were unaffected by t‐butanol, a nonsubstrate ; 2‐butanol had intermediate effects. Platelet‐derived growth factor and endothelin‐1 mimicked the mitogenic effect of FCS ; their effects were also inhibited by the butanols in the potency order 1‐butanol > 2‐butanol > tert‐butanol. Our results, in particular, the differential effects of 1‐, 2‐, and tert‐butanol with respect to PA formation and astroglial proliferation, strongly suggest that the antiproliferative effects of ethanol in glial cells are due to the disruption of the PLD signaling pathway. This mechanism may also contribute to the inhibition of astroglial growth and brain development observed in alcoholic embryopathy.

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.