Publications by authors named "Linseman M"

Research in "stop-and-go" sports has demonstrated that carbohydrate ingestion improves performance and fatigue, and that dehydration of ∼1.5%-2% body mass (BM) loss results in decreased performance, increased fatigue, and increased core temperature. The purpose of this investigation was to assess the physiological, performance, and fatigue-related effects of maintaining hydration with a carbohydrate-electrolyte solution (CES) versus dehydrating by ∼2% BM (no fluid; NF) during a 70-min ice hockey scrimmage.

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Objective: The objective of the study was to determine whether physician-scientists in psychiatry in Canada are in decline, as was reported for medicine overall during the 1990s in the United States.

Design: Federal databases were searched to study grant applications in the area of mental health submitted by physician-scientists compared with PhD-scientists for the period 1985-2001. A survey of Canadian Residency Training Program Directors was carried out for the graduating class of 2000.

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Administration of opiate agonists and antagonists has been shown to increase and decrease alcohol consumption, respectively. Because opioids can affect gastric emptying and decrease intestinal motility, the present experiments were done to determine whether changes in alcohol consumption following opioid administration might be due to opioid-induced changes in the pharmacokinetics of alcohol. In experiment 1, morphine in doses ranging from 1.

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Kindled and control rats were exposed to either ethanol or dextrose solutions in the limited access paradigm, a paradigm that allows access to the test solution for only 1 h each day. Limited access trials were initiated either 24 h or 30 days after the fifth stage 5 seizure had been elicited in the kindled subjects. As previously reported, increased voluntary ethanol selection was observed in the limited access paradigm.

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Previous experiments have shown that systemically administered low doses of opioid agonists increase subsequent alcohol consumption by rats. In this experiment, 10 micrograms of morphine were infused intracerebroventricularly (ICV) in free-feeding rats, daily for 6 days, 30 min prior to one-hour access to a 12% alcohol solution. Alcohol consumption was significantly increased in the morphine-treated group compared to that of a saline-treated control group, confirming that the locus of the effect is within the central nervous system.

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The present study investigated a possible role for neural signals sent from the liver and stomach to the brain in the regulation of alcohol intake. Experiment 1 showed that gastric vagotomy (GVX) reduced the intake of 3% alcohol and 6% alcohol, while water intake was increased. This effect was not due to an alteration in pharmacokinetics, although an alteration in taste function could not be ruled out.

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The effects of several dopaminergic drugs on alcohol consumption were studied in free-feeding rats using a limited access paradigm. Ascending doses of amphetamine (0.1, 0.

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Although there is considerable evidence that pretreatment with low doses of opioid agonists can enhance, and opioid antagonists can reduce alcohol consumption in rats, little is known about the locus or mechanism of these effects. As a first approximation as to where the effect may occur, we compared the effects of an opioid agonist morphine (1, 3 and 10 mg/kg) and antagonist naltrexone (1, 3 and 10 mg/kg) that are known to act within the brain as well as the periphery, to those of an agonist-like drug loperamide (0.3, 1 and 3 mg/kg) and an antagonist methylnaltrexone (3, 10 and 30 mg/kg) that are known to act peripherally only.

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A number of different studies have suggested that the amount of alcohol consumed in a single bout by free-feeding rats is regulated by its pharmacological consequences. The present experiments were designed to test the limits of this apparent pharmacological regulation by examining the effect of weight restriction and enhanced palatability, two variables that have been shown to increase alcohol consumption when the alcohol is continuously available, on amount of alcohol consumed in a single bout. Increasing the palatability of the alcohol solution by the addition of saccharin enhanced consumption substantially such that the blood alcohol levels (BALS) achieved were more than twice those of animals which had drunk unadulterated alcohol.

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Weight restriction has frequently been used to induce consumption of pharmacologically significant amounts of alcohol by rats. When previously weight-restricted rats are fed ad lib., however, their alcohol consumption is substantially reduced.

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The general properties of the heat shock response in Pseudomonas aeruginosa were characterized. The transfer of cells from 30 to 45 degrees C repressed the synthesis of many cellular proteins and led to the enhanced production of 17 proteins. With antibodies raised against the Escherichia coli proteins, two polypeptides of P.

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A number of recent studies have shown that free-feeding rats will consume pharmacologically significant amounts of alcohol when given access to alcohol for short periods of time daily. The present experiment was designed to examine the role of taste in inducing alcohol consumption in this type of periodic availability paradigm, by comparing amounts drunk thereby to amounts of another bitter solution, sucrose octa acetate (SOA), presented on a similar schedule. In contrast to alcohol, which was consistently preferred to water, at a concentration as high as 12% (w/v), preference for SOA diminished across days, indicating that the bitter taste alone was insufficient to increase consumption of this solution.

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Unilateral microinjections of morphine sulphate into the rat hippocampus were found to produce a conditioned place preference, whereas equi-volume saline injections into the same region in a separate control group were without effect. The results are discussed in terms of possible reward or habituation functions of the hippocampus.

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Although the presence of several types of opiate receptors and ligands has been demonstrated within the hippocampus, little is known about the circumstances in which endogenous opiates may be released. Previous studies have suggested that opiates may be involved in producing seizure activity within the hippocampus, or alternatively, that they may be released by seizure activity within the limbic system to prolong the period of postictal depression and thereby prevent the recurrence of seizures during this period. In this experiment we examined the effect of opiate receptor blockade produced by 20 mg/kg ip naloxone on the duration of afterdischarge produced by high-frequency hippocampal stimulation and on inhibition of subsequent seizure activity in male Sprague-Dawley rats.

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Voluntary consumption of alcohol by rats (i.e. in the absence of food or water deprivation, sweetening of the alcohol solution, etc.

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A previously reported paradigm in which rats run down a runway for food reward followed by morphine injection was analyzed to assess the utility of the paradigm in studies of opiate reinforcement. One experiment replicated the original report that post-trial morphine caused both an increase in runway speed and a decrease in food consumption (taste aversion) over successive trials, and showed in addition that the increase in runway speed did not occur as a result of food deprivation alone, but required the animals to have consumed food in the goal box. A second study using the quaternary opiate antagonist methyl naltrexone to block the peripheral effects of morphine suggested that the increase in runway speed has a peripheral locus while the taste aversion has a central one.

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The effect of IV morphine, 2, 6 and 15 mg/kg, on hilar-evoked CA3 field potentials was studied to determine if this area would be more sensitive to mu-type opiate agonists than the CA1 or dentate regions. In addition, the effect of IV naloxone, 2 and 25 mg/kg, on the same responses was studied to determine if endogenous opiates reported to be present in the mossy fibers are released by electrical stimulation of this pathway. Neither morphine nor naloxone had an effect on CA3 field potentials at any dose used.

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Hippocampal field potentials were recorded in vitro before and after a series of incremental doses of morphine (2, 6 and 15 mg/kg i.v.) and after a subsequent infusion of 2 mg/kg naloxone.

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Changes in hippocampal CA1 field potentials during and after tetanic stimulation were studied in rats pretreated with 5 mg/kg s.c. naloxone or saline.

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The effect of morphine (0.5-50 microM) was examined on CA1 field potentials in the tranverse hippocampal slice. Morphine consistently produced an augmentation of evoked activity manifest as (i) a decrease in the threshold for generation of a population spike and (ii) generation of an additional population spike(s) whose amplitude was proportional to the position of the sampled response on its input/output curve.

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Urethane is often used as a central anaesthetic in neurophysiological studies of drug effects. In this experiment, the effect of morphine on cortical EEG and single units of hippocampus and medial thalamus were compared in urethane-anaesthetized and paralyzed-awake rats. In each case, there was evidence of a morphine-urethane interaction, suggesting caution in the interpretation of drug studies using urethane-anaesthetized animals.

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Medial thalamic (MT), and hippocampal (HPC) EEG, and single unit activity, and frontal cortical (CTX) EEG were recorded following IV infusions of 0.625 mg morphine/kg in drug-naive, and following 0.0125 mg naloxone/kg in morphine-dependent paralyzed rats.

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