Immune and nervous systems share molecular and functional similarities: memory storage mechanism.

One of the most complex and important features of both the nervous and immune systems is their data storage and retrieval capability. Both systems encounter a common and complex challenge on how to overcome the cumbersome task of data management. Because each neuron makes many synapses with other neurons, they are capable of receiving data from thousands of synaptic connections. The immune system B and T cells have to deal with a similar level of complexity because of their unlimited task of recognizing foreign antigens. As for the complexity of memory storage, it has been proposed that both systems may share a common set of molecular mechanisms. Here, we review the molecular bases of memory storage in neurons and immune cells based on recent studies and findings. The expression of certain molecules and mechanisms shared between the two systems, including cytokine networks, and cell surface receptors, are reviewed. Intracellular signaling similarities and certain mechanisms such as diversity, memory storage, and their related molecular properties are briefly discussed. Moreover, two similar genetic mechanisms used by both systems is discussed, putting forward the idea that DNA recombination may be an underlying mechanism involved in CNS memory storage.

Saccharin effects on morphine-induced antinociception in the mouse formalin test.

This study was performed to investigate the role of sweetness and taste sensations of the non-caloric sweetener saccharin on pain and morphine antinociception by the formalin test in mice. The formalin test was chosen because it measures the response to a long-lasting nociceptive stimulus and thus may closely resemble clinical pain. The total time (seconds) spent licking and biting the injected paw (indices of nociception) during periods of 0-5 min (early phase) and 10-30 min (late phase) were measured as an indicator of pain and inflammatory responses. A 12 days pretreatment of animals with saccharin (0.04%, 0.08%, 0.16%) produced complex effects on the action of morphine. All doses significantly potentiated the low dose (1.5 mgkg(-1)) of morphine-induced analgesia in the early phase significantly but antagonized the effect of morphine (3 mgkg(-1)). The effect of high doses of morphine (6-9 mgkg(-1)) was antagonized by the low dose of saccharin (0.04%), but the effect of morphine (6 mgkg(-1)) was potentiated with high concentrations of saccharin (0.08% and 0.16%). All doses of saccharin decreased the analgesic effect of morphine at a dose of 9 mgkg(-1). Analgesic effects of low doses of morphine (1.5-3 mgkg(-1)) were decreased by all doses of saccharin in the late phase. Different concentrations of saccharin also affected the antagonistic effect of naloxone (0.4 mgkg(-1)) on morphine-induced analgesia in both phases of the formalin test. The high dose of saccharin (0.16%) potentiated the effect of naloxone in the late phase. The results obtained suggest that sweet sensation is an important factor in mediating morphine analgesic properties. It is therefore inappropriate to use different concentrations of sweet saccharin solutions interchangeably.