OTHERS_CITABLE Effect of Norepinephrine depletion on induction of experience dependent plasticity in male rat barrel cortex Introduction: Barrel cortex of rats is a part of somatosensory cortex, which receives information from facial whiskers. Vibrisectomy by sensory deprivation leads to some changes in the barrel cortex, which have been known as experience dependent plasticity. On the other hand, Norepinephrine (NE) and locus coeruleus, which is the main source of NE, influenced response properties of cortical barrel neurons. In this study, the effect of NE depleted and sensory deprivation on induction of experience dependent plasticity was investigated. Materials and methods: In this study sixty wistar rats (250±25gr) were used. Rats were divided into four groups: 1.Control group (Intact). 2. NE depleted group in which Norepinephrine was selectively depleted by IP injection of DSP4. 3. Sensory deprivation group that all whiskers (except the whisker D2) on the left side were trimmed every other day. 4. NE depleted + sensory deprivation group. By using extracellular single unit recordings, the excitatory (magnitude and latency) and initiatory (Conditioning Test Ratio, CTR index) receptive fields of barrel cortical neurons were calculated. Results: Sensory deprivation led to an increase both in the response magnitude to principle whisker deflection (spared whisker) and in the CTR. In NE depleted + sensory deprivation group, the response magnitude and CTR index were the same as control group. Conclusion: The result showed that experience dependent plasticity has a facilitating effect on excitatory receptive field while decreasing the inhibitory circuits in the brain. When NE content of the brain was depleted before sensory deprivation, these changes were not seen. We conclude that NE depletion inhibits the plastic changes in the response properties of neurons following sensory deprivation. http://ppj.phypha.ir/article-1-370-en.pdf 2014-05-15 244 251 Barrel Cortex Norepinephrine Rat Sensory Deprivation Vahid Sheibani Vsheibani2@yahoo.com 1 Neuroscience research center,Kerman university of Medical Sciences AUTHOR Somaye Arabzadeh 2 Neuroscience research center,Kerman university of Medical Sciences AUTHOR Mohamadreza Afarineshkhaki reza.afarinesh@gmail.com 3 Neuroscience research center,Kerman university of Medical Sciences AUTHOR Ali Shamsizadeh alishamsy@yahoo.com 4 Neuroscience research center,Kerman university of Medical Sciences AUTHOR Hossein Aminizadeh 5 Neuroscience research center,Sheed Beheshti university of Medical Sciences AUTHOR Saeed Azizolahi 6 Neuroscience research center,Kerman university of Medical Sciences AUTHOR
OTHERS_CITABLE Assessment of the effect of nitric oxide within hippocampal CA1 area on spatial learning and memory in morphine dependent rats Introduction: There are evidences showing the role of nitric oxide in the opiate reward properties. The role of nitric oxide signaling pathway as an intracellular mechanism on augmentation of long term potentiation in hippocampal CA1 area of rats is also confirmed. It has been also reported that oral morphine dependence facilitates formation of spatial learning and memory via activation of NMDA receptors located in hippocampal CA1 area of rats. The effect of nitric oxide within hippocampal CA1 area on the spatial learning and memory processes in morphine dependent rats is unclear. Methods: 33 N-MRI male rats (250-350 g) were divided into 4 experimental groups. Two cannulae were stereotaxically implanted bilaterally into hippocampal CA1 area. After 5 days recovery, animals received morphine sulfate or sucrose for 30 consecutive days in drinking water. Morris water maze (MWM) studies were performed from day 26 to 30. In this period animals received bilateral intra-hippocampal CA1 injection of 3μg/ 2 μl L-NAME (NOS inhibitor) or 2 μl saline (1 μl/site), 1 min before daily experimentation. Spatial learning and memory parameters were subjected to analysis of variance (ANOVA). Results: Morphine dependence facilitated spatial learning and memory in rats. This effect was inhibited with local administration of L-NAME in hippocampal CA1 area. Conclusion: Activation of intracellular NO signaling pathway in the pyramidal cells of hippocampal CA1 area may involve in facilitating spatial learning and memory in morphine dependent rats. http://ppj.phypha.ir/article-1-464-en.pdf 2014-05-15 252 260 Nitric oxide morphine hippocampal CA1 spatial learning and memory rat Ali Pourmotabbed apourmotabbed@yahoo.com 1 AUTHOR Parychehr Yaghmaei 2 AUTHOR Parviz Imani 3 AUTHOR Seyed Ershad Nedaei 4 AUTHOR Atefeh Touhidi 5 AUTHOR
OTHERS_CITABLE The role of Na+-K+-ATPase in the basic and rate-dependent properties of isolated perfused rabbit Atrioventricular Node Introduction: Ouabaine is a well-known atrioventricular (AV) node depressant agent, but its effects on functional properties of the AV node have not been cleared. The aim of the present study was to determine how ouabaine administration modifies the rate-dependent properties of the AV node. Methods: Selective stimulation protocols were used to quantify independently electrophysiological properties of the Node. Ouabaine was added directly to superfusion tyrods in a cumulative model (0.05, 0.1, 0.2, 0.25 μM) . The same stimulation protocols were repeated before and after ouabaine addition. Comparisons among multiple groups were made by two-way analysis of variance. P<0.05 was considered significant. Results: Ouabaine decreased fatigue in low concentration (0.05μM), whereas at high concentrations increased the magnitude of fatigue. Ouabaine (0.2, 0.25 μM) caused significant increase in basic properties of the AV-Node (AVCT, WBCL, ERP, FRP). WBCL was prolonged by ouabaine (0.25 μM) from 147.5 ± 8.9 to 194 ± 13 msec. Also amount of facilitating decreased by 0.2 μM ouabaine from 43.3 ± 5 to 38.8 ± 5 msec. Conclusion: The paradoxical effects of ouabaine on the fatigue indicate potential role of Na+-K+-ATPase in the protective mechanism of the AV-node. http://ppj.phypha.ir/article-1-463-en.pdf 2014-05-15 261 269 Isolated heart rabbit AV Nod Ouabaine Na+-K+ ATPase Khoori Vahid 1 AUTHOR Nayebpour Mohsen m_nayeb_2000@yahoo.com 2 AUTHOR Naseri Mohsen 3 AUTHOR Hoseinkhalehjir Seyedgholamreza 4 AUTHOR Salehi Aref 5 AUTHOR
OTHERS_CITABLE Investigation on the vasodilatory effect of insulin through KATP channels and NO pathway in the skin vessels of native and diabetic rats Introduction: Endothelium and smooth muscle dysfunction are the most important complications of diabetes. In type 1 diabetic patients, absence of insulin leads to vasoconstriction and lower skin blood perfusion. Release of some mediators by endothelium which is induced by insulin causes vasodilation, but the exact mechanism of insulin vasodilatory effect is not detected properly. At present study we investigated the role of NO as a vasodilator and KATP channels and their intraction in the vasodilatory effect of insulin on the skin vessles. Methods: Male wistar rats (200-250 gr) were made diabetic by streptozocin (50mg/kg, s.c). After 40 days of diabetes induction, skin blood flow was measured by Laser Doppler Flowmetry technique (LDF). Insulin, LNNA (NO blocker) and Glibenclamide (KATP blocker) infusion were made by infusion pump subcutaneousely. Results: 1- Insulin increases skin blood flow in both control and diabetic groups and this increase was significantly higher in diabetic group. 2- Insulin vasodilatory effect was decreased by LNNA. 3- The vasodilatory effect of insulin was decreased by Glibenclamide. 4- Simultaneous block of both NO and KATP was more effective. Conclusion: Insulin induces vasodilation in part by NO release and partly by activation of K ATP channels. However some interaction has been seen between both routes. Although by block of both these routes, blood flow has not been completely inhibited. So it is supposed that other factors may be involved in this effect and yet to be illucidated. http://ppj.phypha.ir/article-1-282-en.pdf 2014-05-15 270 275 Insulin Diabetes skin blood flow NO KATP channels. zahra Barabadi zbarabadi@yahoo.com 1 Tabiat Modares University AUTHOR Sohrab Hajizadeh hajizads@modares.ac.ir 2 Tabiat Modares University AUTHOR mohammad Javan mjavan@modares.ac.ir 3 Tabiat Modares University AUTHOR batool Erfani batoolerfani@yahoo.com 4 Tabiat Modares University AUTHOR ali Heidarian pour hei 5 Tabiat Modares University AUTHOR
OTHERS_CITABLE Comparison of pain behavior responses in two peripheral neuropathic models (SNI, CCI) in rat Introduction: Peripheral nerve injury leads to neuropathic pain syndromes and different sensation like allodynia and hyperalgesia. Different animal models of neuropathic pain are used to study the neuropathic pain mechanisms. The present study was performed on two models, (SNI). The purpose of this study was comparing the behavioral responses of yhese two models and the role of saphenous and sural nerve in SNI model. Methods: Male Wistar rats (180-220 g) were used. CCI models were made by 4 loose legations on common sciatic nerve. In SNI models, 2 of 3 terminal branches of sciatic nerve were cut and the sural nerve was remained intact. Zero, 4, 7 and 14 days after the operation, thermal hyperalgesia and mechano allodynia were assessed with radiant heat with von-frey filament. Results: The results indicated mechano allodynia and thermal hyperalgesia at days 4th, 7th and 14th. In comparison of SNI and CCI, there was no significant difference in pain behaviors however there was more sensitivity to allodynia in the SNI model and more sensitivity to hyperalgesia in the CCI model. Saphenous territory showed less allodynia and hyperalgesia than sural territory. Conclusion: behavioral testes of CCI and SNI models demonstrated the hypersensitivity to both thermal and mechanical stimuli. But there were different pain intensity between the sural and saphenous nerve territories in SNI model. It seems different neuropathy models have different mechanisms and symptoms. http://ppj.phypha.ir/article-1-259-en.pdf 2014-05-15 276 281 Thermal hyperalgesia Mechano allodynia CCI model SNI model Rat Vahide Mirzaei 1 Neuroscience research center AUTHOR Homa Manaheji hmanaheji@yahoo.com, 2 Neuroscience research center AUTHOR Keivan Keramati 3 Biology Department of Azad University of damghan AUTHOR Nader Maghsodi 4 Neuroscience research center AUTHOR Jalal Zaringhalam 5 Neuroscience research center AUTHOR
OTHERS_CITABLE Central mineralocorticoid receptors mediate impairing effects of corticosterone on memory retrieval in rats Introduction: Previous studies have indicated that stress levels of glucocorticoid hormones induce impairment of long term memory retrieval, but the underlying mechanisms (genomic or non-genomic) are not clear. To clarify this issue, we investigated the involvement of brain corticosteroid receptors and protein synthesis in the glucocorticoid-induced impairment of memory retrieval. Methods: 140 young rats were trained in the water maze (WM) task with six trials per day for six consecutive days. Retention of the spatial training was assessed 24 h after the last training session with a 60-s probe trial. Experiments included intraventricular injections of anisomycin ( 187.5 or 450 µg/5µl) , a specific protein synthesis inhibitor or specific antagonists for mineralocorticoid receptors (MR, 37.5, 75, 150 µg/5ul) or glucocorticoids receptors (GR, 75 or 150 µg/5ul) before corticosterone administration (1 mg/kg) shortly before retention testing. Results: The results showed that administration of anisomycin did not change the corticosterone response. Administration of the MR, but not GR, antagonist blocked the corticosterone-induced response. Conclusion: These findings provide evidence for the view that glucocorticoids impair memory retrieval through non-genomic mechanisms involving an interaction with central MRs. http://ppj.phypha.ir/article-1-384-en.pdf 2014-05-15 282 292 Glucocorticoids Mineralocorticoid receptor Glucocorticoid receptor Spironolactone RU 38486 Anisomycin Memory retrieval Water Maze Mehdi Khaksari 1 - AUTHOR Ali Rashidy-Pour Rashidy-Pour@sem-ums.ac.ir 2 - AUTHOR Abbas Ali Vafaei aavaf43@yahoo.com 3 - AUTHOR
OTHERS_CITABLE Effect of coadministeration of NO and morphine in CA3 of hippocampus on learning and spatial memory in morphine dependent male rats Abstract: ِIntroduction: The effect of morphine dependency on learning and spatial memory is controversial. So in this study effect of co-administeration of nitric oxide (NO) and morphine in CA3 of hippocampus on learning and spatial memory in morphine dependent rats was investigated. Methods: After anaesthetization of male rats, cannulae implanted bilaterally in CA3 of hippocampus. After recovery period (7 days), morphine dependency induced then animals divided in 6 groups that received 1μl saline (Sham), L-Arginine, L-Name and morphine individually and L-Arginine with morphine or L-Name with morphine individually. Morphine dependency was induced by subcutaneous injection of morphine(10mg/kg first day and 20mg/kg for four days). Last dose of morphine(20mg/kg) was injected daily to maintain morphine dependency during test period (5 days) in morris water maze Results: Results showed that L-Name decreased learning in morphine dependent rats although was ineffective on retention of memory. Morphine did not affect learning and spatial memory. Co-administeration of L-Arginine and morphine not only improved the effect of morphine on learning and memory but also promote the effect of L-Arginine on learning and spatial memory. Conclusion: Thus co-administeration of NO and morphine in morphine dependent rats can improve learning and spatial memory differently from using them individually. http://ppj.phypha.ir/article-1-239-en.pdf 2014-05-15 293 299 Keywords:Learning SpatialMemory Morphinedependency Hippocampus NO Mahshid Hoseinzadeh Hosseinzadehmahshid@yahoo.com 1 AUTHOR Iran Pouraboli pouraboli_i@mail.uk.ac.ir 2 AUTHOR Mehdi Abbasnejad mabbas@mail.uk.ac.ir 3 AUTHOR Batool Pouraboli 4 AUTHOR
OTHERS_CITABLE Central administration of Peganum harmala seeds methanolic extract increases fear behavior in rats Traditionally, Peganum harmala seeds (P.h) have been extensively used in the Asia region. We have previously reported the increase of fear behavior by systemic administration of P.h extract. Here, we evaluated the effect of central administration of the extract on the fear behavior. Method: Methanolic extract of the plant's seeds (37% humidity) was prepared for the investigation. Elevated plusmaze apparatus was used for evaluating the fear behavior. Adult male rats were categorized in 7 main groups (n=6). 1) Sham control (saline 1 ul/rat, i.c.v) 2) Harmaline treated group (50 ug/rat, i.c.v). 3) Extract treated groups (10, 20, 25, 50, 100 ug/rat i.c.v respectively). Results: All the doses of the P.h Methanolic extract as like as harmaline caused fear behavior (p<0.05). There was no significant difference between the effects of harmaline and the doses of the plant extract. Discusion: Overall, it is possible that the main alkaloid of the P.h (harmaline) is responsible for the increasing of fear behavior. The effect seems to be done trough the central nervous system neurochemical mechanisms. http://ppj.phypha.ir/article-1-69-en.pdf 2014-05-15 300 305 Peganum harmala i.c.v plus-maze ethanolic extract rat. Vaezi Gholamhassan 1 AUTHOR Masoud Fereidoni 2 AUTHOR Leila Etemadi ll_etemadi@yahoo.com 3 AUTHOR Maryam Sabzali 4 AUTHOR
OTHERS_CITABLE Effect of Dexamethasone on Preventing Tibial Nerve Conduction Velocity Loss in Tourniquet Neurepathic Rat Introduction: Ischaemic-reperfusion nerve injury has been suggested as the mechanism for post-tourniquet limb paralysis. As dexamethasone (Dex) has been shown to Prevent ischaemic-reperfusion process in some tissues, we tested the hypothesis that this drug would reduce tourniquet induced nerve injury. Methods: 36 male Wistar rats (200-250 gr) were chosen and divided randomly into 6 equal groups as Sham Operated, Vehicle, Control and treatments (Dex1, Dex2 and Dex3). Tourniquet was applied to the right hind limb of all Animals except of Sham and Vehicle groups for 3 hours at the beginning of experiments. Animals of Control and Vehicle groups were injected by 1 cc vehicle (Normal saline containing 4% ethanol). Animals of Dex1, Dex2 and Dex3 groups were injected by 1mg/kg, 2mg/kg and 3mg/kg dexamethasone solution respectively 30 min before fastening tourniquet, 30 min after releasing tourniquet and daily during the week of experiment. Motor nerve conduction velocity (MNCV) was measured one week after releasing the tourniquet. Results: MNCV of tibial nerve in response to nerve stimulation were measured at 1 week post-tourniquet release. Application of the tourniquet for 3 h decreased significantly (p<0.001) MNCV in all animals. Dexamethasone administration in doses of 2mg/kg and 3mg/kg (Dex2 and Dex3 groups) resulted in a significant improvement of MNCV (p<0.001) in comparison to Control group. Conclusion: These data indicated that dexamethasone administration in doses of 2mg/kg and 3mg/kg could prevent nerve conduction velocity loss in tourniquet neurepathic rat. http://ppj.phypha.ir/article-1-256-en.pdf 2014-05-15 306 311 Tourniquet Neuropathy-Ischaemic-Reperfusion Injury-Dexamethasone- Rat Morteza Jarrahi jarrahi44@yahoo.com 1 AUTHOR Ali Rashidipour 2 AUTHOR
OTHERS_CITABLE The effect of amygdala lesion on anterior claustrum kindled seizures in rats Introduction: The claustrum interconnects with the allocortical and neocortical regions and also projects to the hippocampus and the amygdala. .The role of claustrum in the complex partial seizure is not clear. Thus in this study the effect of amygdala lesion on anterior claustrum kindled seizures in rat were investigated. Methods: Male Wistar rats, weighting 250-300 g, were received DC current via a bipolar electrode which is inserted in right basolateral amygdala. A tripolar electrode for stimulation and electroencephalography recording in the right anterior claustrum has been fixed. After a 10 days period of surgical recovery, animals were received kindling stimulation (60Hz, 2s, 1 ms pulse duration) daily, and kindling parameters were measured. In the control group animals did not receive DC current. In the lesion groups (2 groups) animals received DC current both before kindling stimulation and after full kindled statement respectively. Results: Our result showed that amygdala lesion, were capable of delaying claustrum kindling. The delay in kindling was due to an increase in the stimulation trials required to kindle to seizure stages. Furthermore the effect of this lesion on established kindled seizures reduced the severity of claustrum by decrease the stage 5 duration and after discharge duration. Conclusion: amygdale lesion had no effect on the expression of generalized seizures and claustrum play an important role in the propagation of epileptic seizure. Whereas the amygdala has a facilitators role in propagation claustrum kindled seizure. http://ppj.phypha.ir/article-1-258-en.pdf 2014-05-15 312 319 Anterior claustrum kindling Amygdala lesion. Fariba Zafari 1 Neuroscience research center.Cellular and malecular research center AUTHOR Masome Sabetkasaei kasai@sbmu.ac.ir 2 Neuroscience research center AUTHOR Yousef Sadeghi 3 Cellular and malecular research center AUTHOR Mohammad Mohammad-zade 4 Department od physiology,Tarbiat modares university. AUTHOR Fateme Deljo 5 Pasture institute AUTHOR
OTHERS_CITABLE Study of the effects of maternal hypothyroidism and thyroxin therapy on the neuronal density of subiculum in rat newborns Introduction: It is well established that thyroid hormones are essential for normal development of mammalian brain. Thyroid hormone deficiency during critical period of brain development can exert devastative and irreversible effects on neuronal functions as well as on learning abilities and memory. The aim of the present investigation was to investigate the effects of maternal hypothyroidism on the neuronal structures of the subiculum in an experimental model of cretinism. Methods: Twenty five female Wistar rats were divided into experimental groups 1 and 2 and control. The experimental groups were made hypothyroid (500 mg/L PTU in drinking water). The experimental group 2 received PTU+Levothyroxin (1mg/L in drinking water). The controls only received drinking water. After two weeks the animals were mated. During pregnancy and lactation, the treatment regime of all groups was continued as above. The brain of 20 days old newborns were dissected and fixed for histological preparation. The numerical density (NV) of subicular neurons was estimated by applying a stereological technique "dissector". Results: In addition to the effects of maternal hypothyroidism on the litter size and offspring weights, the results showed significant increase of subicular neuronal density in experimental group 1 when compared with control (p<0.001). There was also a significant difference (p<0.001) between the Nv of experimental groups 1 and 2. Conclusion: The increased of neuronal Nv in hypothyroid rats was probably due to the retardation of the neuronal normal growth and extension of their dendritic arborization. It seems that thyroxin therapy can improve the effects of hypothyroidism on the neuronal structure of subiculum. http://ppj.phypha.ir/article-1-72-en.pdf 2014-05-15 320 326 Maternal hypothyroidism subiculum PTU rat Zahra Delshad zahradelshad@myway.com 1 AUTHOR Morteza Behnam Rasouli behnam@ferdowsi.um.ac.ir 2 AUTHOR Alireza Fazel 3 AUTHOR