2024-03-29T13:58:23+03:30 http://ppj.phypha.ir/browse.php?mag_id=31&slc_lang=en&sid=1
31-443 2024-03-29 10.1002
Physiology and Pharmacology Physiol Pharmacol 24765236 24765244 10.61186/phypha 2008 12 3 Effect of Intra-CA1 injection of estrogen on spatial memory and learning in rats Farshad Moradpour Nasser Naghdi naghdi@Pasteur.ac.ir Yaghob Fathollahi Introduction: Sexhormones are one of most important factors in difference of learning and memory between tow sexes (male & female). High concentration of estrogen and androgen receptors and mechanism of testosterone and estrogen production in learning and memory center, especially in hippocampus show the role of this receptors, sexhormons and P450 enzymes in spatial memory. Consequently, in this study we evaluate effect of estradiol valerat and aromatase inhibitor (Anasterazole) on spatial learning and memory in Morris Water Maze. Materials and methods: Adult male rats were bilaterally connulated into CA1 region. After recovery period, control groups received DMSO 0/5µl and DMSO 0/5µl + DMSO 0/5µl. Different doses of estradiol valerat (EV) (1, 2.5, 5, 10 and 15µg / 0.5µl), anastrozole (An) (0.25, 0.5, 1µg / 0.5µl) and EV 15µg / 0.5µl +An 0.5µg / 0.5µl were microinjected all days before training. EV was injected 30-35 min before training and anastrozol was injected 25-30min before training. Result: Our results have showen EV 0.15µl / 0.5µl group increase escape latency and traveled distance. Also we have showen that anastrosole dose dependently decrease escape latency and traveled distance. Conclusion: We resulted that EV impaired acquisition of spatial learning and memory but anastrozole improved it. Anastrozole also couldn't be buffered EV – induced impairment. Estradiol valerat Anastrazole Hippocampus Memory &Learning 2008 11 01 159 169 http://ppj.phypha.ir/article-1-443-en.pdf
31-533 2024-03-29 10.1002
Physiology and Pharmacology Physiol Pharmacol 24765236 24765244 10.61186/phypha 2008 12 3 Protective effect of Saffron extract on morphine–induced inhibition of spatial learning and memory in rat Haydeh Haghighizad h_haghighizad@yahoo.com Ali Pourmotabbed Hedayat Sahraei Mohammad Rasoul Ghadami Sara Ghadami Mohammad Kamalinejad Introduction: It has been reported that acute administration of morphine impairs learning and memory processes in rats. Furthermore, recent studies showed that Saffron extract improved ethanol-induced impairments of learning behaviors in mice, and also prevented ethanol-induced inhibition of hippocampal long-term potentiation. It can be postulated that there are some common mechanisms responsible for the morphine and ethanol-induced impairments of spatial learning and memory. Therefore in the present study we investigated the effects of Saffron extract on morphineinduced learning and memory impairments in rat using Morris water maze (MWM). Methods: In the current study, male rats received Saffron extract (10, 30 or 50 mg/kg, i.p.) 30 minutes before injection of morphine (10 mg/kg, i.p.) or saline for 5 consecutive days. Animals of two control groups received only morphine or saline. Spatial learning and memory parameters in the same days in the (MWM) were tested and subjected to the ANOVA and followed by Tukey’s test for multiple comparisons. Results: The data indicated that administration of morphine impaired formation of spatial learning and memory processes. Application of Saffron extract can improve adverse effects induced by morphine in a dose-dependent manner. Conclusion: It could be concluded that the extract of Saffron can inhibit morphine-induced impairments on spatial learning and memory in rats. morphine Saffron extract spatial learning and memory Morris water maze. 2008 11 01 170 179 http://ppj.phypha.ir/article-1-533-en.pdf
31-388 2024-03-29 10.1002
Physiology and Pharmacology Physiol Pharmacol 24765236 24765244 10.61186/phypha 2008 12 3 Dehydroepiandroesteron increased proliferation of neural progenitor cells derived from p19 embryonal carcinoma stem cells. hossein azizi hosseinazizi58@yahoo.com Narges Zare Mehrjerdy Saeed Kasemi Ashtiani MirzaKhalil Bahmani Hossein Baharvand baharvand@royanInstitute.org Introduction: The p19 line of embryonal carcinoma cells develops into neurons, astroglia and fibroblasts after aggregation and exposure to retinoic acid (RA). Dehydroepiandroesteron (DHEA) is a neurosteroid, can increase proliferation of human neural stem cell (NSC) and positively regulated the number of neurons produced. This study was initiated to assess the effect of DHEA on neural progenitor cells derived from p19 embryonal carcinoma stem cells. Methods: p19 cells suspended in DMEM contain 5%FBS into bacterial-greade Petri dishes in the presence RA and DHEA in different concentration for 6 days. Serum concentration decrease to 3% in days 5 and 6. Then collected aggregate and processed for flowcytometry, immunocytochemistery and RT-PCR analysis. Cells were trypsinized for dispersion and replaced in poly L- lysine (10µg/ml) coated tissue culture dishes without RA and DHEA for 4 days. And then difference cells were evaluated by phase contrast microscopy. Results: Flowcytometry analyses of Nestin and Brdu/Nestin showed percent Nestin positive and proliferation Nestin positive cells in different groups DHEA and RA. Brdu/Nestin immunochemistry confirmed proliferation of Nestin positive cells and also RT-PCR analysis show expression of proneural marker and estrogen receptor gens.Result showed that RA +DHEA(1μM) significantly increased the number of Nestin positive and newly formed Nestin positive cells than other groups. Conclusion: Result showed DHEA accompanied RA significantly increased the number of Nestin positive and newly formed Nestin positive cells derived from p19 embryonal carcinoma cells but in comparison to RA cannot induce neural progenitor cells. DHEA RA neuron differentiation p19 embryonal carcinoma stem cells 2008 11 01 180 187 http://ppj.phypha.ir/article-1-388-en.pdf
31-465 2024-03-29 10.1002
Physiology and Pharmacology Physiol Pharmacol 24765236 24765244 10.61186/phypha 2008 12 3 Comparing the analgesic effects of periaqueductal gray matter injection of orexin A and morphine on formalin- induced nociceptive behaviors. Hassan azhdari Zarmehri azhdariz@yahoo.com Saead Semnanian ssmnan@modares.ac.ir Yaghoub Fathollahi Introduction: Orexin-A and B (Hypocretin 1 and 2) are neuropeptides that are mostly expressed in the posterior and lateral hypothalamus (LH). Intracisternal (ICV) and intratechal (IT) injections of orexin-A (hypocretin-1) have been shown to elicit analgesic responses in formalin test. However, the locations of central sites that may mediate these effects have not been clearly elucidated. Orexin-containing fibers are projected to periaqueductal gray matter (PAG), which is involved in pain modulation. Methods: Behavioral study was done on male Sprague Dawley rats (200-300 g) in formalin induced nociceptive behaviour. Results: Intra-PAG microinjection of orexin-A produced a dose-dependent inhibition of formalin-evoked behaviour in interphase and phase 2, but not in phase 1, indicating an antinociceptive role of exogenous orexin-A in the PAG. Analgesic effect of orexin-A was less than and specific to inter- and late phase of formalin test, when compared with that of morphine (5 μg/0.5μl) after intra-PAG administration. Conclusion: The obtained results suggest that orexin-A plays an anti-nociceptive role in PAG, on the interphase and late phase of formalin test in rats. So it is possible that orexin-A might be involved in the mechanisms of inter- and last phases of formalin induced behaviours. orexin-A analgesic periaqueductal gray matter formalin test morphine 2008 11 01 188 193 http://ppj.phypha.ir/article-1-465-en.pdf
31-298 2024-03-29 10.1002
Physiology and Pharmacology Physiol Pharmacol 24765236 24765244 10.61186/phypha 2008 12 3 Behavioral study of effects of mesenchymal stem cells transplant on motor deficits improvement in animal model of Huntington\'s disease Mohammad Amin Edalatmanesh Ahmad Reza Bahrami Ar-Bahrami@um.ac.ir Morteza Behnam Rasuli Ali Moghimi Maryam Moghadam Matin Fatemeh Naseri Introduction: As an inherited neurodegenerative disease, Huntington's disease is accompanied with wide neuronal degeneration in neostriatum and neocortex. Progress of the disease causes disabling clinical effects on movements, recognition and physiology of the body, and finally results in death. At this stage of knowledge we are, there is no effective therapeutic strategy for diminishing the motor disorders of Huntington's disease. In recent years, cellular transplantation has been an effective therapeutic method for neurodegenerative disease. Material and methods: In this paper, the effects of bone marrow derived mesenchymal stem cells were assessed in animal model of Huntington disease. After causing ipsilateral lesion in striatum with Quinolinic acid, bone marrowe derived mesenchymal stem cells which had been isolated and purified from 4-6 weeks old rats, transplanted into damage striatum. The efficiency of cellular transplantation for improvement of motor disorder was assessed by cylinder test and Apomorphin induced rotation tests, during eight weeks after engraftment. Results: Results show significant improvement (p ≤ 0.0001) in motor disorders and striatal atrophy percent. Conclision: According to results of this assay, cell therapy by means of bone marrow derived adult stem cells promises for treatment of neurodegenerative diseases, especially Huntington's disease. Huntington\'s disease mesenchymal stem cells cell therapy drug induced rotation test. 2008 11 01 194 200 http://ppj.phypha.ir/article-1-298-en.pdf
31-461 2024-03-29 10.1002
Physiology and Pharmacology Physiol Pharmacol 24765236 24765244 10.61186/phypha 2008 12 3 Changes in plasma nitric oxide metabolites concentration during glucose tolerance test in type 2 diabetic rats Asghar Ghasemi Ghaseni@endocrine.ac.ir Hamid Farahani Hamid_farahani2001@yahoo.com Saleh Zahedi Asl Zahedi@endocrine.ac.ir Introduction: Repeated hyperglycemia play an important role in the development of atherosclerosis in diabetic patients. Endothelium is the organ of the first-line defense against atherosclerosis and nitric oxide has a major role in this task. The aim of this study was to determine changes in plasma nitric oxide metabolites concentration during glucose tolerance test in type 2 diabetic rats. Methods: Male neonate Wistar rats divided into control and diabetic groups. Type 2 diabetes was induced by administration of Streptozotocin (100 mg/kg) to neonate rats at day 2. Plasma glucose and nitric oxide concentration were measured at 7, 30, 45, 60, and 75 days. Intravenous glucose tolerance test was done in adults rats and blood samples were collected in 0 and 5, 10, 30, and 60 min after glucose infusion for determining plasma glucose, insulin, and nitric oxide metabolites. Two-way mixed (between-within) ANOVA was used for comparing data. Results: In control group plasma glucose was returned to basal values 60 min after glucose injection while in diabetic rats it was higher than basal levels (P<0.001). After glucose injection, plasma insulin concentration was increased to 4.5 and 1.9 folds in control and diabetic groups respectively. Basal nitric oxide metabolites concentration was higher in diabetic rats (50.4 ± 6.4 vs. 28.8 ± 3.8 mol/l, P<0.05). During glucose tolerance test there was 35 and 62 % fall in plasma nitric oxide concentration in control and diabetic groups respectively. This reduction return to basal values after 30 min in control group while, in diabetic rats it was 17% less than basal levels in 60 min after glucose injection. Conclusions: Decreased nitric oxide production or increased its degradation may be underlying endothelium dysfunction and atherosclerosis in type 2 diabetes. Nitric oxide type 2 diabetes glucose tolerance test rat. 2008 11 01 201 208 http://ppj.phypha.ir/article-1-461-en.pdf
31-479 2024-03-29 10.1002
Physiology and Pharmacology Physiol Pharmacol 24765236 24765244 10.61186/phypha 2008 12 3 Structural-functional studies of peptides derived from a long-chain snake neurotoxin Naja naja oxiana Adak Nasiripourdori nasiripour@modares.ac.ir Bijan Ranjbar ranjbarb@modares.ac.ir Hossein Naderi-manesh naderman@modares.ac.ir Faramarz Mehrnejad mehrnejadf@yahoo.com Safie Soofian sofian@modaes.ac.ir Goudarz Sadeghi gsadeghi@ut.ac.ir Saeed Kolahian saeedkolahian@yahoo.com Introduction: The design and structural characterization of mini-proteins with a compact, folded structure provide insight into the complex architecture of proteins today and has long been a challenging issue in structural- functional studies. Alpha neurotoxins from snake venom have a distinct folded structure comprised of a disulphide core and three loops or “fingers” each of these loops are considered as a separate functional domain. Because of selectivity and specificity of snake alpha neurotoxins, they are ideal candidates for structural-functional studies. Method: With the assumption that each "loop" in the structure of alpha neurotoxin is able to fold as a structurally independent unit and could possibly have functional properties, we have minimized the structure of a long-chain alpha neurotoxin into 18 and 31 amino acid peptides using solid-phase synthesis and cloning methods, respectively. The molecules are structurally studied using circular dichroism spectroscopy and also in vitro using organ bath apparatus and chick biventer cervicis muscle (CBCM). Results: The 18 and 31-mer peptides form predominant beta structures (-turn and -sheet/alpha helix) in aqueous solutions which vary with solvent ionic strength. Data from in vitro and in silico studies indicate that these minimized structures block the twitches in chick biventer cervices muscle with concentrations higher than 0.5 M and this effect is absolutely dose dependent. On the other hand, the long-chain alpha neurotoxin completely and irreversibly blocks the CBCM even at 50 nanomolar concentration and both effects are post synaptic. Conclusion: These data support the primary assumption that the peptides derived from the second loop of snake alpha neurotoxin can have a distinct folded structure and furthermore, exist as an independent biological unit. Keywords: Protein design Neurotoxin Acetylcholine Receptor 2008 11 01 209 220 http://ppj.phypha.ir/article-1-479-en.pdf
31-365 2024-03-29 10.1002
Physiology and Pharmacology Physiol Pharmacol 24765236 24765244 10.61186/phypha 2008 12 3 Decrease of the responsiveness of beta-2 adrenoceptors of diabetic rat knee joint blood vessels in acute inflammation Sohrab Hajizadeh hajizads@modares.ac.ir Batool Erfani S. Mohammad Faghihi Zahra Barabadi Marzeieh Hosseini Beta-2 adrenoceptors in blood vessels are one of the active factors that play a role in regulation of tissue blood flow. in diabetic angiopathy, responsiveness of these receptors is decreased, while that is increased in inflammation. According to these opposite effects, the aim of this study was to investigate the vasodilatory response of knee joint blood vessels to salbutamol (Beta-2 adrenoceptor agonist) in IDDM with combination of acute inflammation. Acute knee joint inflammation was induced by intraarticular injection of kaolin 4% and induction of diabetes was performed by streptozotocine (55 mg/kg). Wistar rats weighting 200-300 gr were used. The animals divided in 5 groups as: the control, saline, diabetic, inflammatory and diabetic- inflammatory. Blood flow of knee joint was measured using Laser Doppler Flowmeter Technique (LDF). Vasodilatation of articular micro vascular was measured in response to topical application of different concentration (10 -11 -10 -1) of salbutamol. Results obtained in this study showed that: 1- Increased knee joint diameter and perimeter due to acute inflammation in diabetic rat knee joint were significantly lesser than that of inflammatory rats. 2- Responsiveness of Beta-2 adrenoceptors were increased in kaolin- induced acute inflammation. 3- In diabetic rats, kaolin- induced acute inflammation could not increase the responsiveness of Beta-2 adrenoceptors. Based on above mentioned results, we conclude that diabetes inhibits the increasing effects of acute inflammation on responsiveness of Beta-2 adrenoceptors. کلمات کلیدی: دیابت التهاب حاد گیرنده‌های بتا- دو آدرنرژیک- مفصل زانو 2008 11 01 221 226 http://ppj.phypha.ir/article-1-365-en.pdf
31-460 2024-03-29 10.1002
Physiology and Pharmacology Physiol Pharmacol 24765236 24765244 10.61186/phypha 2008 12 3 The Effect of ascorbic acid injection into lateral ventricle on spatial learning and memory on adult male rats mehdi abbasnejad Mabbas@mail.uk.ac.ir Sima Nasri Habib Nazem Mehri Bahaaddini Introduction: Ascorbic acid (AA) acts as an antioxidant in the Central nervous system (CNS) of the mammalians. It is released from the some nerve ending together with neurotransmitters. The results have shown that Ascorbic acid could affect learning as well as memory. In this study, we examined the effect of ICV injection of ascorbic acid on learning and memory by Morris water maze. Method: In the present study, 42 adult male rats weighing 250-300 g were used. then cannula implanted bilaterally in LV (AP=-0.8, LA=±1.5, DV=3.4).After recovery period, the animals were divided into 6 groups including control group(no injected), 4 groups as experimental groups (received different doses of ascorbic acid 25, 50, 100, 150 mg/kg), 5th group as Sham-operated group (received normal saline as vehicle). Injection period has taken five consecutive days. 30 min after each injection they were trained in Morris Water Maze (MWM). Spatial learning and memory parameters recorded and then were analyzed. Results: These results showed that ICV injection of ascorbic acid decreased learning and spatial memory in rats. Ascorbic acid (100 mg/kg) significantly decreased learning and spatial memory. Conclusion: It can be concluded that ascorbic acid decreased learning and spatial memory, directly or indirectly through interference to the neurotransmitters effects. Keywords: Spatial learning and memory Ascorbic acid Lateral ventricle Morris Water Maze 2008 11 01 227 237 http://ppj.phypha.ir/article-1-460-en.pdf
31-450 2024-03-29 10.1002
Physiology and Pharmacology Physiol Pharmacol 24765236 24765244 10.61186/phypha 2008 12 3 Embryonic stem cells derived cardiomyocytes are a suitable model for assessment of cardiotoxic effects of doxorubicin and other drugs Mahboobeh Farokhpour Khadijeh Karbalaie Mahmood Etebari Hamid Mirmohamad Sadeghi Mohammad Hossein Nasr-Esfahani MH_Nasr@med.mui.ac.ir Marzieh Nematolahi Hossein Baharvand Baharvand50@yahoo.com Introduction: Doxorubicin is frequently used for treatment of several types of cancer. Doxorubicin cardiac toxicity has limited the use of this drug. Corticosteroids may prevent doxorubicin induced cardiotoxicity. Therefore the aim of this study was to evaluate mouse embryonic stem cells derived cardiomyocytes as a model to evaluate the effect of Doxorubicin and dexamethasone. Methods: Mouse embryonic stem cells derived cardiomyocytes were treated with different concentration of doxorubicin for 24 hours and the results were compared with control group. In order to exam effect of dexamethasone on cardiotoxicity, mouse embryonic stem cells derived cardiomyocytes were either exposed to 0.1, 1 or 10 µM dexamethasone 24 hours prior exposure to doxorubicin or expose to dexamethasone 24 hours before and during exposure to doxorubicin . Each group were compared with only doxorubicin or dexamethasone treated cells. Results: 5µM doxorubicin was selected as the lowest dose that ceased heart beats in more than 50% of Mouse embryonic stem cells derived cardiomyocytes. Results revealed that 10 µM dexamethasone for 24 hours before treatment with doxorubicin has protective effect on doxorubicin induced cardiotoxicity. Conclusion: The overall results obtained in this model are in accordance with previous literature. Thus suggesting that mouse embryonic stem cells derived cardiomyocytes is a suitable model for assessment of cardio toxic effects of drugs. Key words: Stem cell, Cardiomyocyte, Doxorubicin, Dexamethasone Stem cell Cardiomyocyte Doxorubicin Dexametasone 2008 11 01 238 244 http://ppj.phypha.ir/article-1-450-en.pdf
31-449 2024-03-29 10.1002
Physiology and Pharmacology Physiol Pharmacol 24765236 24765244 10.61186/phypha 2008 12 3 The role of hippocampal (CA1) NMDA receptor on learning and memory in presence and absence of zinc chloride in adult male rats Zohreh Valizadeh valizadeh_z@yahoo.com Ahmad Ali Moazedi moazedi_a@yahoo.com Gholamali Parham parham_@yahoo.com Introduction: Zinc is an essential trace element that plays an important role in synaptic plasticity and modulating the activity of CNS and involve in learning and memory. Synaptic vesicle zinc in the hippocampus area exerting modulatory effects on NMDA glutamate receptor. Method: In this experiment the effects of NMDA agonist and antagonist administration intra hippocampus on passive avoidance learning and memory in adult male rats in presence and absence of Zncl2 by step down task has been investigated. Animal divided into 10 group (n=8).Control group, second group received 0.1µg/rat NMDA in 1µlit saline for 4 days. Sham group received saline in the same volume. Forth group received 1µg/rat MK-801 in 1µlit saline 10min before training for 4 days. Sham group received saline in the same volume. Five remain groups received 30mg/kg/day zncl2 in drinking water for 2 weeks. Sixth groups only received 30mg/kg/day zncl2, but others groups (7, 8, 9, and 10) in addition consumption zncl2 received drug and saline in the same condition to 2,3,4,5 groups. Result: our experiment showed that consumption of 30mg/kg/day zncl2 impair learning and memory in adult male rats (P<0.05), while administration of NMDA improve the impairment effects on zncl2 consumption (P<0.05), but administration of MK-801 increasing the impairment effects of zncl2. Concultion: It seems that zinc impaired passive avoidance learning and memory by effects on subunits of NMDA receptor in hippocampus. zinc chloride hippocampus passive avoidance learning step down 2008 11 01 245 253 http://ppj.phypha.ir/article-1-449-en.pdf