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.
Basal forebrain (BF) plays an important role in the regulation of cortical activation. Somatostatin (SOM) is present both in local neurons as well as in fibers in the BF. In previous studies, SOM axons were found to innervate corticopetal cholinergic cells and SOM was found to presynaptically modulate GABA and glutamate release onto cholinergic neurons in the BF. However, no systematic analysis is available about the EEG effects of SOM or its analog, octreotide (OCTR) injected directly into the BF. In the present experiments, EEG changes were examined following an OCTR injection (0.5 microliter, 500 nmol) into the BF areas containing several choline acetyl transferase-immunoreactive neurons of urethane-anaesthetized rats. Fronto-occipital EEG was recorded on both sides and relative EEG power was calculated in the delta (0–3 Hz), theta (3–9 Hz), alpha (9–16 Hz) and beta (16–48 Hz) frequency bands. OCTR injected to the BF failed to induce significant EEG changes and did not affect tail pinch-evoked cortical activation. Lack of effect may be attributed to the urethane anaesthesia as well as to the possible complex interactions between SOM and BF cholinergic and GABAergic neurons.
Authors:Ilona Banczerowski-Pelyhe, L. Détári, Ildikó Világi and et al
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.
Authors:Attila Toth, B. Balatoni, T. Hajnik and L. Detari
Orexin A and orexin B are neuropeptides produced by a group of neurons located in the lateral hypothalamus which send widespread projections virtually to the whole neuraxis. Several studies indicated that orexins play a crucial role in the sleep-wake regulation and in the pathomechanism of the sleep disorder narcolepsy. As no data are available related to the EEG effects of orexin A in healthy, freely moving rats, the aim of the present experiments was to analyze EEG power changes in the generally used frequency bands after intracerebroventricular orexin A administration.Orexin A administration (0.84 and 2.8 nM/rat) differently affected fronto-occipital EEG waves in the different frequency bands recorded for 24 hours. Delta (1–4 Hz) and alpha (10–16 Hz) power decreased, while theta (4–10 Hz) and beta (16–48 Hz) power increased. Decrease of the delta power was followed by a rebound in case of the higher orexin A dose. This complex picture might be explained by the activation of several systems by the orexin A administration. Among these systems, cortical and thalamic circuits as well as the role of the neurons containing corticotrophin-releasing factor might be of significant importance.
Authors:T Hajnik, A Tóth, Ö Szalontai, M Pethő and L Détári
Sleep is homeostatically regulated suggesting a restorative function. Sleep deprivation is compensated by an increase in length and intensity of sleep. In this study, suppression of sleep was induced pharmacologically by drugs related to different arousal systems. All drugs caused non-rapid eye movement (NREM) sleep loss followed by different compensatory processes. Apomorphine caused a strong suppression of sleep followed by an intense recovery. In the case of fluoxetine and eserine, recovery of NREM sleep was completed by the end of the light phase due to the biphasic pattern demonstrated for these drugs first in the present experiments. Yohimbine caused a long-lasting suppression of NREM sleep, indicating that either the noradrenergic system has the utmost strength among the examined systems, or that restorative functions occurring normally during NREM sleep were not blocked. Arousal systems are involved in the regulation of various wakefulness-related functions, such as locomotion and food intake. Therefore, it can be hypothesized that activation of the different systems results in qualitatively different waking states which might affect subsequent sleep differently. These differences might give some insight into the homeostatic function of sleep in which the dopaminergic and noradrenergic systems may play a more important role than previously suggested.