Suppressive effects of resveratrol treatment on the intrinsic evoked excitability of CA1 pyramidal neurons

Objective: Resveratrol, a phytoalexin, has a wide range of desirable biological actions. Despite a growing body of evidence indicating that resveratrol induces changes in neuronal function, little effort, if any, has been made to investigate the cellular effect of resveratrol treatment on intrinsic neuronal properties. Materials and Methods: This experimental study was performed to examine the acute effects of resveratrol (100 μ M) on the intrinsic evoked responses of rat Cornu Ammonis (CA1) pyramidal neurons in brain slices, using whole cell patch clamp recording under current clamp conditions. Results: Findings showed that resveratrol treatment caused dramatic changes in evoked responses of pyramidal neurons. Its treatment induced a significant (P<0.05) increase in the after hyperpolarization amplitude of the first evoked action potential. Resveratrol-treated cells displayed a significantly broader action potential (AP) when compared with either control or vehicle-treated groups. In addition, the mean instantaneous firing frequency between the first two action potentials was significantly lower in resveratrol-treated neurons. It also caused a significant reduction in the time to maximum decay of AP. The rheobase current and the utilization time were both significantly greater following resveratrol treatment. Neurons exhibited a significantly depolarized voltage threshold when exposed to resveratrol. Conclusion: Results provide direct electrophysiological evidence for the inhibitory effects of resveratrol on pyramidal neurons, at least in part, by reducing the evoked neural activity

Intracerebroventricular administration of adiponectin attenuates streptozotocin-induced memory impairment in rats

Alzheimer’s disease (AD) has been reported to be linked with diabetes mellitus and insulin resistance. Adiponectin (ADN), an adipocytokine secreted from adipose tissue, is involved in the regulation of insulin sensitivity, energy homeostasis, and mitochondrial dysfunction. In this study, we examined the effect of ADN on passive avoidance memory in animal model of sporadic AD (sAD). On days 1 and 3 after cannulation, rats received intracerebroventricular (icv) injection of streptozotocin (STZ) (3 mg/kg). Thirty minutes before the learning process, animals received saline or ADN in different doses (6, 60, and 600 µg). The step-through latency (STL) and total time spent in the dark compartment (TDC) were recorded and analyzed. In STZ-treated rats, STL was significantly decreased, whereas TDC showed a dramatic increase. In ADN-treated rats, STL was significantly increased (P < 0.01) in all treatment doses. The number of entries was decreased in all applied doses; however, TDC was reduced only by the application of 6 ng of ADN (P < 0.05). It can be concluded that ADN is useful to improve the STZ-induced memory impairment. This study showed, for the first time, that icv administration of ADN could improve the memory acquisition in animal model of sAD

Rapid synthesis of LiCr0.15Mn1.85O4 by glycine-nitrate method

LiCr0.15Mn1.85O4 spinel has been successfully synthesized by glycine-nitrate method (GNM). The presence of pure spinel phase was confirmed by long term XRPD measurements and the Rietveld structural refinement. Lattice parameter was estimated to be 8.2338 angstrom. Average particle size of prepared powder material is below 500nm. The BET surface area is 9.6m(2)g(-1). As a cathode material for lithium batteries LiCr0.15Mn1.85O4 shows initial discharge capacity of 110mA h g(-1) and capacity retention of 83% after 50 cycles. (c) 2006 Elsevier B.V. All rights reserved

Evaluation of the L5 spinal nerve ligation on Aδ- and C-fibers activation threshold and also LTP-induced by electrical high frequency stimulation of sciatic nerve in spinal dorsal horn of rats

Background: The underlying central mechanisms for the development and maintenance of neuropathic pain are unknown. The current study aimed to evaluate the long-term potentiation (LTP) changes in spinal dorsal horn wide dynamic range (WDR) neurons following a peripheral neuropathy model. Materials and Methods: This study was conducted on 26 male Wistar rats. The spinal nerve ligation (SNL) model was performed to induce neuropathy. After surgery, thermal hyperalgesia and mechanical allodynia were evaluated one day before neuropathy, and then on days 2, 5, 7, 14, 21 and 28 after neuropathy. Single-unit recording was used to study the changes of LTP. The changes of LTP and Aδ- and C-fiber evoked responses by high-frequency stimulation (100 Hz and current intensity six times that of the threshold for activation of C- fibers) of sciatic nerve in spinal WDR synapses were studied on day 14 after surgery up to 2 hours. Results: Neuropathy was induced thermal hyperalgesia and mechanical allodynia on day 2 and persisted for 28 days after neuropathy. Electrophysiological recording revealed that HFS induced LTP either in the Aδ- or in the C-fibers in both sham and neuropathy groups up to 2 hr on day 14 after neuropathy. Neuropathy also significantly decreased the threshold of these fibers.Conclusion: LTP-induced HFS in spinal WDR neurons can be one of the underlying central mechanisms in the maintenance of neuropathic pain

Ameliorating Effects of Dorema ammoniacum on PTZ-Induced Seizures and Epileptiform Brain Activity in Rats

The objective of the current study was to investigate the anti-epileptogenic and anticonvulsant effects of Dorema ammoniacum gum, which is used in Iranian traditional medicine for the treatment of seizures. Animals received pentylenetetrazol (IP, 30 mg/kg/48 h) for inducing seizures. Five different seizure stages were evaluated for 20 min and parameters including maximum seizure stage, the latency to the onset of stage 4, stage 4 duration, and seizure duration were measured. D. ammoniacum (50 and 100 mg/kg) or its vehicle was administered 30 min before or after pentylenetetrazol injection in different groups. In addition, the effective dose of D. ammoniacum (100 mg/kg) on different seizure stages was compared with the common antiseizure drug phenobarbital. In another set of experiments, we investigated the effective dose of D. ammoniacum on fully kindled animals in which an interictal electroencephalogram was recorded by superficial electrodes placed on the skull. The results showed that D. ammoniacum administration, before and after pentylenetetrazol injections, significantly decreased seizure stage, seizure duration, stage 4 duration, and 1/stage 4 latency. The anti-epileptogenic effect of D. ammoniacum was about 50 to 60 of phenobarbital. In addition, D. ammoniacum significantly decreased seizure stage, seizure duration, stage 4 duration, and 1/stage 4 latency when administered to fully kindled animals but had no effect on the power of EEG sub-bands. These results indicate that D. ammoniacum has anti-epileptogenic and anticonvulsant effects in a chemical kindling model of seizures. © 2020 Georg Thieme Verlag. All rights reserved

Alterations in ca1 pyramidal neuronal intrinsic excitability mediated by iH channel currents in a rat model of amyloid beta pathology

Amyloid beta (Aβ) accumulation plays an important role in the pathogenesis of Alzheimer's disease (AD) by changing the neuronal excitability. However, the cellular mechanisms by which accumulation of Ab affects intrinsic neuronal properties are not well understood. The effect of bilateral intra-frontal cortex Aβ (1-42) peptide injection on the intrinsic excitability of hippocampal CA1 pyramidal neurons with particular focus on the contribution of hyperpolarization-activated (Ih) channel currents was examined using whole-cell patch-clamp recording. Passive avoidance memory impairment and morphological changes in rats receiving intra-frontal Aβ treatment were observed, which was associated with significant changes both in passive and active intrinsic electrical membrane properties of CA1 pyramidal neurons. Electrophysiological recording showed a significant decrease in neuronal excitability associated with an augmentation in the first spike after-hyperpolarization (AHP) amplitude. In addition, the depolarizing sag voltage was altered in neurons recorded from Ab-treated group. In voltage-clamp condition, a hyperpolarizing activated inward current sensitive to ZD7288 and capsaicin was significantly increased in neurons from Aβ-treated rats. The Ih current density was increased and the activation curve was shifted toward less negative potential in the Aβ-treated group as compared to control group. The enhancing effect of Aβ treatment on Ih current was confirmed by showing upregulation of the mRNA of HCN1 channel in the CA1 pyramidal layer of hippocampi. These findings suggest the contribution of Ih and possibly TRPV1 channel currents to the changes induced by Aβ treatment in the intrinsic membrane properties, which, in turn, may provide therapeutic targets for treatment of AD. © 2015 IBRO