Our data indicate that IV dexmedetomidine exerts pronounced antinociception against CRD-induced visceral pain and suggest that the antinociceptive effect of dexmedotimidine is mediated in part by opioid receptors, but peripheral alpha(2)-ARs are not involved.

No abstract

Epilepsy is an important problem in neurological disorders. The common features of all types of epilepsy are the synchronized and uncontrolled discharges of nerve cell assemblies. Recent studies claimed that gap junctions have a critical role in epileptic neuronal events. The aim of present study is to investigate the effects of connexin36 (Cx36) channel blocker quinine on penicillin-induced experimental epilepsy. For this purpose, 4 months old male Wistar rats were used in the present study. Permanent screw electrodes allowing EEG monitoring from conscious animals and permanent cannula providing the administration of the substances to the brain ventricle were placed into the cranium of rats under general anesthesia. At the end of the postoperative recovery period, epileptiform activity was generated by injecting 300 IU crystallized penicillin through the ventricular cannula. When the epileptiform activity, monitored from a digital recording system, reached maximal frequency and amplitude, quinine (200, 400 or 1000 nmol) was administered similar to penicillin. Effects of quinine on epileptiform activity were assessed by both electrophysiological and behavioral analysis. Quinine suppressed epileptiform activity by decreasing the amplitude and frequency of epileptiform spikes and by attenuating the epileptiform behavior. The outcomes of this study suggest that the blockade of Cx36 channels may contribute to the amelioration of epileptic activity.

These results suggested that HG may have adverse effects on both mother and baby's health. Pregnant women with HG should be provided with training and consultancy services and be closely monitored in terms of anemia and thyroid hormones.

Iron plays an important role in maintaining normal brain function. However, iron overload and enhanced hydroxyl radical formation have been implicated as the causative factors of some neurodegenerative disorders such as Parkinson's and Alzheimer's diseases. Calcium is also required for diverse physiological process including secretion of neurotransmitters, synaptic plasticity, gene expression and axonal growth. Iron and calcium are essential for neuronal function but, when present in excessive level, they induce neuronal damage and may even cause neuronal death. Some reports suggest that voltage gated calcium channels (VGCCs) are an alternate route for iron entry into neuronal cell lines under conditions of iron overload. The aim of the present study was to investigate the effects of L-type VGCCs on iron-induced neurotoxicity. Iron neurotoxicity was generated by intracerebroventricular FeCl₃ injection. Nicardipine treatment (10 mg/kg/d) was applied to block L-type VGCCs for 10 d. Rats were perfused intracardially under deep urethane anaesthesia after treatment period. Removed brains were processed using the standard histological techniques. The numbers of neurons in hippocampus and substantia nigra of all rats were estimated by stereological techniques. Results of present study show that nicardipine decreased hippocampal and nigral neuron loss from 43.9% to 18.4% and 41.0% to 12.1%, respectively. Outcomes of the present study propose that blocking of L-type VGCCs may reduce the neurotoxic effects of iron by inhibiting the cellular influx of excessive calcium and/or iron ions.