The results demonstrate the antagonistic effect of astaxanthin against the ethanol-induced facilitation of CSD propagation. Probably carotenoid antioxidant properties are involved in such effects.

The results showed an antagonistic effect of acute EtOH treatment on CSD propagation that was reverted by astaxanthin. The EtOH-astaxanthin interaction was not influenced by the age, as it was found in both young and adult animals.

As a consequence of worldwide improvement in health care, the aging portion of the human population has increased, now representing a higher proportion of the total population. This fact raises great concern regarding how to age while maintaining good brain function. Very often, alterations in brain electrophysiological signaling are associated with age-dependent functional disorders of the brain. Therefore, animal models suitable for the study of age-related changes in electrical activity of the brain can be very useful. Herein, we review changes in brain electrophysiological features as a function of age by analyzing studies in the rat brain on the phenomenon known as cortical spreading depression (CSD). Alterations in the brain’s capability to generate and propagate CSD may be related to differences in the propensity to develop certain neurological diseases, such as epilepsy, stroke, and migraine, which can biunivocally interact with the aging process. In this review, we revisit ours and others’ previous studies on electrophysiological features of the CSD phenomenon, such as its velocity of propagation and amplitude and duration of its slow negative DC shift, as a function of the animal age, as well as the interaction between age and other factors, such as ethanol consumption, physical exercise, and nutritional status. In addition, we discuss one relatively new feature through which CSD modulates brain signaling: the ability to potentiate the brain’s spontaneous electrical activity. We conclude that the CSD model might importantly contribute to a better understanding of the aging/brain signaling relationship.

No abstract

Various neurological and psychiatric diseases lead to alterations in cortical serotonergic activity as one of their underlying processes. However, the electrophysiological implication of changes in serotonergic activity remains a matter of investigation. In this study, we investigated whether brain serotonergic activity influences the excitability-related phenomenon known as cortical spreading depression (CSD). CSD parameters (propagation velocity, and amplitude and duration of the DC-shift) was evaluated in rats that received two treatments that increased cortical serotonergic activity, electrical stimulation of the raphe nuclei and subcutaneous injection of a selective serotonin reuptake inhibitor, sumatriptan. A third group of rats was tested on a low-tryptophan diet rat model of serotonin depletion. Control rats for these three groups received, respectively, sham raphe stimulation, saline injection, and a tryptophan-supplemented diet. Compared to controls, electrical stimulation of the raphe nuclei and sumatriptan administration decelerated CSD and increased the duration of the negative DC-shift of CSD, whereas the low-tryptophan diet was associated with significantly accelerated CSD propagation and shortened DC-shift of CSD (p<0.05). We concluded that serotonergic neurons are very important for stabilizing the delicate equilibrium between excitatory and inhibitory neuronal influences that determines cortical excitability and CSD propagation. Our pharmacological, electrophysiological and dietary data suggest that cortical serotonergic activity negatively modulates CSD propagation in the rat cortex. Reduced central serotonergic activity, as can be observed in several neurological and psychiatric diseases, may constitute a pathological factor for increased sensitivity to CSD.