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  • Author or Editor: L Détári x
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The suprachiasmatic nuclei (SCN) constitute the principal pacemaker of the circadian timing system in mammals. The generated rhythm is forwarded mostly through projections to various hypothalamic nuclei. On the other hand, the regulated processes feedback to the SCN. One of the possible feedback pathways is the orexinergic projection from the lateral hypothalamus. Orexins are recently identified neuropeptides with an overall facilitatory effect on waking behaviors. Orexinergic fibers are widely distributed throughout the brain and are also present in the SCN. In this study we examined the effect of orexin-A on the spontaneous activity of rat SCN cell in vitro. Neurons showed 2 different firing pattern (continuous-regular, intermittent-irregular). Orexin-A increased firing rate in both cell types at 10-8 M concentration, but caused a clear supression of neuronal activity at 10-7 M. Continuously firing neurons were less responsive than those firing intermittently. These results show that orexin-A may play a role in the modulation of the circadian pacemaker function. The neuropeptide might exert both direct, postsynaptic effects on SCN neurons and indirect, presynaptic effects on excitatory and inhibitory terminals. The dose-dependent modification of the firing rate indicate that the weight of these factors changes with the concentration of orexin-A.

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Mycotoxin fumonisin B1 (FB1) a natural inhibitor of ceramide synthase contaminating mainly the cornbased food and feed may cause dysfunctions in the nervous system. In the present study peripheral neural dysfunctions were biomonitored after dietary FB1 exposure in rats. Daily oral doses of 6.2 mg/kg body weight/day FB1 were applied in rats for 2 weeks. Before and after FB1 treatment nerve conduction velocities of tibial and sciatic nerves and spinal reflexes were analyzed in vivo. Electrophysiological recordings of biphasic plantar EMG (M and H components) and evaluation of sensory and motor nerve conduction velocities were carried out. Nerve conduction velocities revealed decreasing tendencies after FB1 exposure. The flexor reflex and the H-components of the extensor reflex were significantly reduced. The proposed in vivo biomonitoring can reveal functional impairment of the peripheral nervous system caused by mycotoxin exposure. Reduction of conduction velocity and altered reflexes after FB1 exposure are suspected to be associated with modified signal transmission due to toxic systemic effects and possible changes in sphingolipid metabolism.

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