Caffeine - treat or trigger? Disparate behavioral and long-term dopaminergic changes in control and schizophrenia-like Wisket rats.

The influence of caffeine on behavioral functions in both healthy and schizophrenic subjects is controversial. Here we aimed to reveal the effects of repeated caffeine pre- and post-training treatments on motor and exploratory activities and cognitive functions in a reward-based test (Ambitus) along with a brain region-specific dopamine D2 receptor profile in control and schizophrenia-like WISKET model rats. In the control animals, pre-treatment caused temporary enhancement in motor activity, while permanent improvement in learning function was detected in the WISKET animals. Post-treatment produced significant impairments in both groups. Caffeine caused short-lasting hyperactivity followed by a rebound in the inactive phase determined in undisturbed circumstance. Caffeine treatment substantially enhanced the dopamine D2 receptor mediated G-protein activation in the prefrontal cortex and olfactory bulb of both groups, while it increased in the dorsal striatum and cerebral cortex only in the WISKET animals. Caffeine enhanced the maximal binding capacity in the hippocampus and cerebral cortex of WISKET animals, but it decreased in the prefrontal cortex of the control animals. Regarding the dopamine D2 receptor mRNA expression, caffeine treatment caused significant enhancement in the prefrontal cortex of WISKET animals, while it increased the hippocampal dopamine D2 receptor protein amount in both groups. This study highlights the disparate effects of caffeine pre- versus post-training treatments on behavioral parameters in both control and schizophrenia-like animals and the prolonged changes in the dopaminergic system. It is supposed that the delayed depressive effects of caffeine might be compensated by frequent coffee intake, as observed in schizophrenic patients.

Haemodynamic parameters and cognitive function during modeled acute volume loss.

PURPOSE: The purpose of the present study was to find a noninvasive way of detecting even smaller volume loss which is easier to carry out and possibly more precise than the currently used (mostly sphygmomanometer-based) methods. Haemodynamic and EEG measurements were carried out in simulated volume loss, involving blood donation and orthostatic challenges to assess adaptive responses and cognitive performance. Cognitive performance was assessed in an oddball task and changes of the evoked potential P300 were analyzed. Both haemodynamic and cognitive parameters were recorded in 'pre-donation' and 'post-donation' conditions for purposes of comparison. RESULTS: Cognitive performance (as reflected by P300 changes) was found to be a poor marker of volume loss. Difference between the two conditions in none of the parameters reached the level of statistical significance (defined as p < 0.05) RR mean, baroreceptor sensitivity and pulse pressure were rather sensitive to the relatively mild volume loss (p < 0.01 between pre- and post-conditions). CONCLUSION: Our study indicates that traditional sphygmomanometer based values can safely be replaced by values yielded by finger plethysmography, combined with brief orthostatic challenges and that P300 as a cognitive marker cannot be used to assess volume loss.

Inhibition of itch-related responses at spinal level in rats.

The goal was to develop a rat model for determination of the effects of intrathecally administered drugs on the peripherally induced pruritic behaviors. After chronic intrathecal catheterization, a serotonin derivative (5-methoxytryptamine: MeOT, 200 µg on both sides) was injected into the lower leg skin. After the first period (phase 0: 0-30 min) MeOT injection was repeated and opioid antagonist naltrexone (10 µg), NMDA receptor antagonists ketamine (10-100 µg), kynurenic acid (1-10 µg) or their combinations were injected intrathecally. The second observational period lasted for 60 min (phases I and II, 30-60 and 60-90 min, respectively). MeOT produced pruritic behavior with high degree of interindividual differences. The second MeOT injection caused an enhanced pruritic behavior in Phase I. Naltrexone decreased the pruritic activity, while neither doses of ketamine influenced the effects of MeOT. The higher doses of kynurenic acid resulted in notable decreases in the pruritic behavior. The combinations of naltrexone with ketamine or kynurenic acid produced a prolonged antipruritic effect. Our data suggest an important direction for the development of a new itch model in rats that focuses on the spinal mechanism of itching. Besides, the results revealed the role of the spinal opioid and NMDA receptors in this process.