Notes

Clinicopathologic investigation of people starting replicate transurethral resection involving kidney tumor right after an initial proper diagnosis of urothelial carcinoma along with lamina propria breach along with variant/divergent histology.
more tightly linked to D2 than D1 receptor manipulation, suggesting D2-like receptors as a possible therapeutic target for maladaptive biases toward risk-taking over effort.
The EvP clearly demonstrates that rats can evaluate distinct effortful or risky costs associated with rewards of comparable magnitude, and shift preference away from either option with increasing cost. This preference is more tightly linked to D2 than D1 receptor manipulation, suggesting D2-like receptors as a possible therapeutic target for maladaptive biases toward risk-taking over effort.
After alcohol ingestion, the brain partly switches from consumption of glucose to consumption of the alcohol metabolite acetate. selleck products In heavy drinkers, the switch persists after abrupt abstinence, leading to the hypothesis that the resting brain may be "starved" when acetate levels suddenly drop during abstinence, despite normal blood glucose, contributing to withdrawal symptoms. We hypothesized that ketone bodies, like acetate, could act as alternative fuels in the brain and alleviate withdrawal symptoms.

We previously reported that a ketogenic diet during alcohol exposure reduced acute withdrawal symptoms in rats. Here, our goals were to test whether (1) we could reproduce our findings, in mice and with longer alcohol exposure; (2) ketone bodies alone are sufficient to reduce withdrawal symptoms (clarifying mechanism); (3) introduction of ketogenic diets at abstinence (a clinically more practical implementation) would also be effective.

Male C57BL/6NTac mice had intermittent alcohol exposure for 3 weeks using liquid diet. Somatic alcohol withdrawal symptoms were measured as handling-induced convulsions; anxiety-like behavior was measured using the light-dark transition test. We tested a ketogenic diet, and a ketone monoester supplement with a regular carbohydrate-containing diet.

The regular diet with ketone monoester was sufficient to reduce handling-induced convulsions and anxiety-like behaviors in early withdrawal. Only the ketone monoester reduced handling-induced convulsions when given during abstinence, consistent with faster elevation of blood ketones, relative to ketogenic diet.

These findings support the potential utility of therapeutic ketosis as an adjunctive treatment in early detoxification in alcohol-dependent patients seeking to become abstinent.

clinicaltrials.gov NCT03878225, NCT03255031.
clinicaltrials.gov NCT03878225, NCT03255031.
Systemic administration of the tobacco smoke constituent nicotine stimulates brain reward function in rats. However, it is unknown if the inhalation of tobacco smoke affects brain reward function.

These experiments investigated if exposure to smoke from high-nicotine SPECTRUM research cigarettes increases reward function and affects the rewarding effects of nicotine in adult male and female Wistar rats.

Reward function after smoke or nicotine exposure was investigated using the intracranial self-stimulation (ICSS) procedure. A decrease in reward thresholds reflects an increase in reward function. In the first experiment, the rats were exposed to tobacco smoke for 40min/day for 9days, and the rewarding effects of nicotine (0.03-0.6mg/kg) were investigated 3weeks later. In the second experiment, the dose effects of tobacco smoke exposure (40-min sessions, 1-4 cigarettes burnt simultaneously) on reward function were investigated.

Tobacco smoke exposure did not affect the nicotine-induced decrease in reward thresholds or response latencies in male and female rats. Smoke exposure lowered the brain reward thresholds to a similar degree in males and females and caused a greater decrease in latencies in females. There was a positive relationship between plasma nicotine and cotinine levels and the nicotine content of the SPECTRUM research cigarettes. Similar smoke exposure conditions led to higher plasma nicotine and cotinine levels in female than male rats.

These findings indicate that tobacco smoke exposure enhances brain reward function but does not potentiate the rewarding effects of nicotine in male and female rats.
These findings indicate that tobacco smoke exposure enhances brain reward function but does not potentiate the rewarding effects of nicotine in male and female rats.
Mu opioid receptor agonists are indispensable for the treatment of pain, but clinical use carries the inherent risk of transition from effective treatment to abuse. Abuse potential appears to increase rapidly during periods of initial opioid exposure in humans, and this increase in opioid reward during initial opioid exposure can be modeled in rats using an intracranial self-stimulation (ICSS) procedure.

The goal of the present study was to examine temporal parameters of this phenomenon.

Adult male Sprague-Dawley rats responded for electrical brain stimulation using a frequency-rate ICSS procedure. In the first experiment, rats received daily morphine injections for 6days, and morphine effects on ICSS were re-determined 1day, 1week, or 1month after the repeated morphine treatment regimen to evaluate the persistence of enhanced opioid reward. In the second experiment, rats received six repeated morphine injections with different interdose intervals (two per day, one per day, every other day, every fourth day), and morphine effects were re-determined 1day after the last dose to determine dosing frequencies sufficient to produce enhanced opioid reward.

Results of the first experiment indicated that enhanced opioid reward was greatest 1day after the morphine treatment regimen and completely dissipated after 4weeks. The second experiment indicated that all dosing frequencies tested were sufficient to produce enhanced reward.

Taken together, these results suggest that enhancement of opioid reward after initial opioid exposure is relatively transient but can be produced by a range of different dosing frequencies.
Taken together, these results suggest that enhancement of opioid reward after initial opioid exposure is relatively transient but can be produced by a range of different dosing frequencies.
Reduced motivation is one of the main symptomatic features of inflammation-induced depression. However, the exact nature of inflammation-induced alterations in motivation remains to be fully defined. As inflammation has been shown to increase sensitivity to negative stimuli, the present series of experiments was initiated to determine whether systemic inflammation induced by infra-septic doses of lipopolysaccharide (LPS) in mice influences consummatory and instrumental responding to successive negative contrast.

Successive negative contrast was operationally defined by a shift to a lower value reward than the one mice were trained with. Mice were trained to drink a high sucrose concentration solution and exposed to an acute shift to a lower concentration of sucrose. In another series of experiments, mice were trained to nose poke for chocolate pellets according to a fixed reinforcement schedule 10 (10 nose pokes for the food reinforcement) and exposed to a shift to a lower reward value (decreased number of chocolate pellets or replacement of chocolate pellets by less preferred grain pellets).
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