Dreaming and REM sleep are controlled by different brain mechanisms

The paradigmatic assumption that REM sleep is the physiological equivalent of dreaming is in need of fundamental revision. A mounting body of evidence suggests that dreaming and REM sleep are dissociable states, and that dreaming is controlled by forebrain mechanisms. Recent neuropsychological, radiological, and pharmacological findings suggest that the cholinergic brain stem mechanisms that control the REM state can only generate the psychological phenomena of dreaming through the mediation of a second, probably dopaminergic, forebrain mechanism. The latter mechanism (and thus dreaming itself) can also be activated by a variety of nonREM triggers. Dreaming can be manipulated by dopamine agonists and antagonists with no concomitant change in REM frequency, duration, and density. Dreaming can also be induced by focal forebrain stimulation and by complex partial (forebrain) seizures during nonREM sleep, when the involvement of brainstem REM mechanisms is precluded. Likewise, dreaming is obliterated by focal lesions along a specific (probably dopaminergic) forebrain pathway, and these lesions do not have any appreciable effects on REM frequency, duration, and density. These findings suggest that the forebrain mechanism in question is the final common path to dreaming and that the brainstem oscillator that controls the REM state is just one of the many arousal triggers that can activate this forebrain mechanism. The “REM-on” mechanism (like its various NREM equivalents) therefore stands outside the dream process itself, which is mediated by an independent, forebrain “dream-on” mechanism.

Verapamil-induced kinetics of ion flux in oat seedlings

Verapamil application in ion transport studies on plant cells is widespread; however, the mechanism of its action is still poorly understood. Net flux of Ca 2+ , K + , Na + , H + and Cl – were measured in solution around oat seedlings using the non-invasive ion-selective microelectrode MIFE technique. The verapamil effect on intact plant tissues was a distinct immediate influx of monovalent cations, H + , K + or Na + . Pre-treatment with tetraethyl-ammonium, Cs + , Ba 2+ or Ca 2+ did not affect K + flux changes, whereas DMSO, Cd 2+ and vanadate increased verapamil-induced K + influx. Verapamil-induced K + flux increased with increased external KCl concentration or pH. Verapamil concentration up to 1 mM failed to shift Ca 2+ flux to efflux. Pre-treatment with adrenaline and dopamine agonists and antagonists led to changes in verapamil-induced ion flux, especially for Ca 2+ . We suggest that a transporter that allows entry of K + and Na + was the main system providing monovalent ion influx after verapamil application.

Moderators and mechanisms relating personality to reward and dopamine: Some findings and open questions

Data from further human experiments touch four open questions in the target article. (1) Extinction of reward acquisition postulated by Depue & Collins's model could not be confirmed if correlating craving for, liking of, and satisfaction from smoking. (2) Intraindividual correspondence between responsivity to dopamine agonists and antagonists could likewise not be confirmed. (3) Nicotine craving and drug-induced hormone responses were not substantially correlated. (4) Low serotonin can be the cause and not just the moderator of dopaminergic sensitivity, and personality correlates of low dopamine/low MAO (aggressive impulsive traits) can hardly be related to the positive emotion associated with dopaminergic activity.