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C Portas

Publications and source records attributed to C Portas.

5 recordsLinked to original sources

Chronic low-amplitude electrical stimulation of the laterodorsal tegmental nucleus of freely moving cats increases REM sleep.

While cholinergic stimulation of the PRF evokes a REM-like state, electrical stimulation of LDT/PPT neurons has not been used to test the hypothesis of mesopontine cholinergic control of REM sleep. Adult cats were implanted for electrographic recording and with bipolar unilateral stimulating electrodes, either in the LDT or within the PRF (stimulation control). Baseline recordings of the normal sleep-wake cycle were carried out for 5 h. On the next day, continuous stimulation of the LDT or mPRF was carried out during the same time period (0.5 ms pulses, 1 microA, 8 Hz) and with post-stimulation recording for 3 h. A second baseline recording day followed with same protocol as the first baseline day. This 3-day sequence, separated by 3 days, was repeated three times in each of the three LDT and the three medial PRF cats. Five hours of chronic low-amplitude stimulation of the LDT induced a highly significant increase in total REM and in the duration of REM sleep bouts. Stimulation of the mPRF did not affect any of the behavioral states. This study, the first to our knowledge to use low-amplitude stimulation of LDT in freely moving cats, indicates the importance of mesopontine cholinergic neurons in REM sleep.

Animals↗

Microdialysis measurement of cortical and hippocampal acetylcholine release during sleep-wake cycle in freely moving cats.

The variations of Acetylcholine (ACh) release in the cerebral cortex and dorsal hippocampus were monitored by microdialysis during the electroencephalographically recorded sleep-waking cycle in freely moving cats. The results show a state-dependent variation in ACh output in both the cortex and the hippocampus. ACh release increased by approximately 100% during quiet waking (QW) and by 175% during active waking (AW) as referred to slow wave sleep (SWS) baseline. In contrast, a clear difference between the two areas was observed during REM sleep. During this stage ACh release in the cortex reached approximately the same values observed during QW, while in the hippocampus ACh release rose to about 4-fold the level obtained during SWS or twice that of QW. The results support the idea that the increase in ACh release in the cortex reflects the desynchronized EEG of wakefulness and REM sleep, while the marked increase of ACh during REM in the hippocampus may be related to the sustained theta activity in this area.

Acetylcholine↗

Stress increases noradrenaline release in the rat frontal cortex: prevention by diazepam.

Foot-shock produced a more than 2-fold increase in noradrenaline (NA) release from the frontal cortex of freely moving rats. The effect of acute stress was almost completely prevented by the administration of diazepam (5 mg/kg i.p.). Diazepam alone inhibited cortical NA release, the maximal inhibition (-57%) being observed 90 min after the injection. Cortical NA release therefore appears to be a reliable index of central noradrenergic activity in response to stressful conditions.

Animals↗

Rat liver model for testing intraoperative echo contrast sonography.

The present animal experimental study showed that intraoperative hepatic ultrasonography using an echo contrast medium can visualize small hepatomas (with a diameter of between 3 and 15 mm) induced in the rat liver, although they were not recognizable with plain ultrasonography. A homogeneous increase in the echogenicity of the liver tissue was achieved by using an echo contrast medium (Echovist) based on galactose microparticles. Self-made bubble preparations such as those used in echocardiography were far less effective. When the dosage was optimal (0.01-0.003 ml/g liver weight with concentrations of 200 and 300 mg/ml Echovist), homogeneous contrast enhancement of the liver was achieved for at least 10 min after a single bolus injection via all routes of contrast administration (hepatic artery, portal vein, bile duct). As a result, hepatomas appeared as hypodense formations (portal vein and bile duct) or as hyperdense zones (hepatic artery).

Animals↗