62 research outputs found
Hybrid Elephant Herding and Particle Swarm Optimizations for Optimal DG Integration in Distribution Networks
In this article, the amalgamation of two well-established meta-heuristic optimization methods is presented to solve the multi-objective distributed generation (DG) allocation problem of distribution systems. To overcome some of the shortcomings of newly developed elephant herding optimization (EHO), an improvement is suggested and then, a prominent feature of particle swarm optimization is introduced to the modified version of EHO. The suggested modifications are validated by solving a single objective DG integration problem where various performance parameters of the proposed hybrid method are compared with their individual standard variants. After validation, the proposed technique is exploited to solve a multi-objective DG allocation problem of distribution systems, aiming to minimize power loss and node voltage deviation while simultaneously maximizing the voltage stability index of three benchmark distribution systems namely, 33-bus, 69-bus and 118-bus. The obtained simulation results are further compared with that of the same available in the existing literature. This comparison reveals that the proposed hybrid approach is promising to solve the multi-objective DG integration problem of distribution systems as compared to many existing methods
Streptozotocin-Induced Early Thermal Hyperalgesia is independent of Glycemic State of Rats: Role of Transient Receptor Potential Vanilloid 1(TRPV1) and Inflammatory mediators
<p>Abstract</p> <p>Background</p> <p>Streptozotocin (STZ) is used as a common tool to induce diabetes and to study diabetes-induced complications including diabetic peripheral neuropathy (DPN). Previously, we have reported that STZ induces a direct effect on neurons through expression and function of the Transient receptor potential vanilloid 1 (TRPV1) channel in sensory neurons resulting in thermal hyperalgesia, even in non-diabetic STZ-treated mice. In the present study, we investigated the role of expression and function of TRPV1 in the central sensory nerve terminals in the spinal cord in STZ-induced hyperalgesia in rats.</p> <p>Results</p> <p>We found that a proportion of STZ-treated rats were normoglycemic but still exhibited thermal hyperalgesia and mechanical allodynia. Immunohistochemical data show that STZ treatment, irrespective of glycemic state of the animal, caused microglial activation and increased expression of TRPV1 in spinal dorsal horn. Further, there was a significant increase in the levels of pro-inflammatory mediators (IL-1β, IL-6 and TNF-α) in spinal cord tissue, irrespective of the glycemic state. Capsaicin-stimulated release of calcitonin gene related peptide (CGRP) was significantly higher in the spinal cord of STZ-treated animals. Intrathecal administration of resiniferatoxin (RTX), a potent TRPV1 agonist, significantly attenuated STZ-induced thermal hyperalgesia, but not mechanical allodynia. RTX treatment also prevented the increase in TRPV1-mediated neuropeptide release in the spinal cord tissue.</p> <p>Conclusions</p> <p>From these results, it is concluded that TRPV1 is an integral component of initiating and maintaining inflammatory thermal hyperalgesia, which can be alleviated by intrathecal administration of RTX. Further, the results suggest that enhanced expression and inflammation-induced sensitization of TRPV1 at the spinal cord may play a role in central sensitization in STZ-induced neuropathy.</p
Expression of Transient Receptor Potential Ankyrin 1 (TRPA1) and Its Role in Insulin Release from Rat Pancreatic Beta Cells
<div><h3>Objective</h3><p>Several transient receptor potential (TRP) channels are expressed in pancreatic beta cells and have been proposed to be involved in insulin secretion. However, the endogenous ligands for these channels are far from clear. Here, we demonstrate the expression of the transient receptor potential ankyrin 1 (TRPA1) ion channel in the pancreatic beta cells and its role in insulin release. TRPA1 is an attractive candidate for inducing insulin release because it is calcium permeable and is activated by molecules that are produced during oxidative glycolysis.</p> <h3>Methods</h3><p>Immunohistochemistry, RT-PCR, and Western blot techniques were used to determine the expression of TRPA1 channel. Ca<sup>2+</sup> fluorescence imaging and electrophysiology (voltage- and current-clamp) techniques were used to study the channel properties. TRPA1-mediated insulin release was determined using ELISA.</p> <h3>Results</h3><p>TRPA1 is abundantly expressed in a rat pancreatic beta cell line and freshly isolated rat pancreatic beta cells, but not in pancreatic alpha cells. Activation of TRPA1 by allyl isothiocyanate (AITC), hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), 4-hydroxynonenal (4-HNE), and cyclopentenone prostaglandins (PGJ<sub>2</sub>) and a novel agonist methylglyoxal (MG) induces membrane current, depolarization, and Ca<sup>2+</sup> influx leading to generation of action potentials in a pancreatic beta cell line and primary cultured pancreatic beta cells. Activation of TRPA1 by agonists stimulates insulin release in pancreatic beta cells that can be inhibited by TRPA1 antagonists such as HC030031 or AP-18 and by RNA interference. TRPA1-mediated insulin release is also observed in conditions of voltage-gated Na<sup>+</sup> and Ca<sup>2+</sup> channel blockade as well as ATP sensitive potassium (K<sub>ATP</sub>) channel activation.</p> <h3>Conclusions</h3><p>We propose that endogenous and exogenous ligands of TRPA1 cause Ca<sup>2+</sup> influx and induce basal insulin release and that TRPA1-mediated depolarization acts synergistically with K<sub>ATP</sub> channel blockade to facilitate insulin release.</p> </div
Anti-nociceptive effect of duloxetine in mouse model of diabetic neuropathic pain
193-197The involvement of adenosinergic pathway in the anti-nociceptive effect of duloxetine, a balanced 5-HT/NE reuptake inhibitor, was evaluated in streptozotocin induced diabetic male albino mice of Laca strain. After four weeks of single injection of streptozotocin (200 mg/kg, ip), mice were tested in the tail immersion and hot-plate assays. Cerebral adenosine levels were measured by high-performance liquid chromatography (HPLC/PDA detector). Diabetic mice exhibited significant hyperalgesia along with increased plasma glucose, decreased body weights and reduced cerebral adenosine levels. Administration of duloxetine (5, 10 and 20 mg/kg, ip) to diabetic mice produced dose-dependent anti-nociceptive effect in both tail-immersion and hot-plate assays. Adenosine levels were also significantly and dose-dependently increased by different doses of duloxetine. The results demonstrated the involvement of adenosinergic pathway in duloxetine mediated anti-hyperalgesia in diabetic neuropathic pain
Comparative behavioural profile of newer antianxiety drugs on different mazes
633-638Anxiety is associated with diverse range of psychiatric conditions. In the present study, antianxiety effect of fluoxetine, citalopram (SSRI’s), gabapentin (antiepileptic drugs), venlafaxine (SNRI), clozapine and resperidone (atypical antipsychotics) and a herbal preparation ashwagandha on elevated zero maze and elevated plus maze paradigms was examined. Anti-anxiety potentials of these drugs were compared with diazepam. The drugs tested i.e. fluoxetine (10 mg/kg), citalopram (10 mg/kg), clozapine (0.25, 0.5, 1 mg/kg), resperidone (0.5, 1 mg/kg), venlafaxine (4, 8, 16 mg/kg), citalopram (10 mg/kg), fluoxetine (10 mg/kg), gabapentin (10, 20 mg/kg) and ashwagandha (100, 200 mg/kg) significantly increased the number of open arm entries and time spent in open arm. These drugs also decreased the latency to enter in open arm as compared to control in both the paradigms. Present study confirms the antianxiety activity of different newer classes of drugs and found some of them comparable to diazepam in both the elevated zero maze and elevated plus maze paradigm
Age-related susceptibility to chronic haloperidol-induced orofacial dyskinesia: Biochemical and neurochemical evidence
Objective: Aging is a continuous and intrinsic process of systems
deterioration with time. Although the mean prevalence of tardive
dyskinesia (TD), a neurological disorder associated with chronic
haloperidol administration, is 20-25%, the cumulative rate of this
disorder increases significantly in patients aged 55 years or more. The
present study investigated the effect of aging on spontaneous
development of orofacial dyskinesia and tried to find out the
interactive substrate which is activated by chronic neuroleptic
treatment and results in premature emergence of TD in adult animals.
Materials and Methods: Various behavioral (orofacial dyskinetic
movements, stereotypy, locomotor activity, and percent retention);
biochemical (lipid peroxidation, reduced glutathione levels, and
antioxidant enzyme levels: SOD and catalase); and neurochemical
(neurotransmitter levels) parameters were assessed in young (60-80 gm),
matured adult (180-200 gm), and aged (380-400 gm) rats. Results: Aging
resulted in significant increase in hyperkinetic motor activities,
vacuous chewing movements (VCMs), tongue protrusions, facial jerking,
and development of dopamine supersensitivity (increased locomotor
activity and stereotypy); there was also associated oxidative damage in
all regions of the brain. The extracellular dopamine levels were also
significantly decreased (45%) in the forebrain of aged animals. Chronic
administration of haloperidol to aged animals further significantly
increased all the parameters as compared to age-matched control
animals. Chronic administration of haloperidol to matured adult animals
showed similar changes, especially hyperkinetic movements, and
oxidative damage in different parts of the brain. There was no
significant change in young animals on chronic administration of
haloperidol. Conclusion: The findings of the present study suggest
that free radical generation and development of dopamine
supersensitivity are the prime interactive substrates that are
activated by chronic neuroleptic treatment in matured animals and are
responsible for the development of TD, whereas these paradigms are
increased with aging and result in spontaneous orofacial hyperkinetic
movements
Involvement of adenosinergic receptors in anxiety related behaviours
439-443In the present study, the effect of adenosine (A1 and A2 receptor agonist), caffeine (A2A receptor antagonist), theophylline (A2A receptor antagonist) and their combination was studied in anxiety related behaviours using elevated zero maze and elevated plus maze paradigms and compared their various behavioural profiles. Adenosine (10, 25, 50,100 mg/kg) significantly showed anxiolytic effect at all the doses, whereas caffeine (8, 15, 30, 60 mg/kg) and theophylline (30, 60 mg/kg) showed psychostimulatory action at lower doses and anxiogenic effect at higher doses. Pretreatment with caffeine (8, 15, 30 mg/kg) and theophylline (30 mg/kg) reversed the anxiolytic effect of adenosine. The study suggested the involvement of adenosinergic receptor system in anxiety related behaviours
In vivo microdialysis studies of striatal level of neurotransmitters after haloperidol and chlorpromazine administration
91-97Therapeutic success of atypical antipsychotics has focused the attention on the role of receptor systems other than dopaminergic system in the pathophysiology of neuroleptics-associated acute (Parkinson’s like syndrome) and chronic (tardive dyskinesia) extrapyramidal side effects. This study was planned to investigate changes in striatal levels of norepinephrine, dopamine and serotonin after acute and chronic administration of classical neuroleptics (haloperidol and chlorpromazine). These changes were correlated with behavioural alterations in rats. In vivo microdialysis with HPLC/ECD system revealed that there was a marked decrease in striatal neurotransmitter contents (NE, DA and 5-HT), which was also correlated with severe cataleptic response in rats after acute administration of haloperidol (2 mg/kg) and chlorpromazine (20 mg/kg). Chronic administration of haloperidol (1 mg/kg for 21 days) and chlorpromazine (5 mg/kg for 21 days) resulted in time dependent increase in orofacial hyperkinetic movements. The microdialysis studies also showed a significant decrease in the striatal levels of all the neurotransmitters. The results provide evidence for the involvement of striatal adrenergic and serotonergic systems, besides dopaminergic system in neuroleptic-induced acute and chronic extrapyramidal symptoms
Copyright © 2007 by Institute of Pharmacology Polish Academy of Sciences
adenosine receptor antagonist prevents behavioral, biochemical and neurochemical changes associated with an animal model of tardive dyskinesi
- …