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Showing 9 results for Haghparast

Abbas Haghparast, Amir-Mohammad Alizadeh, Fereshteh Motamedi,
Volume 12, Issue 2 (Summer 2008)

Introduction: Although formalin-induced activity in primary afferent fibers and spinal dorsal ‎horn is well described, the midbrain neural basis underlying each phase of behavior in ‎formalin test has not been clarified. The present study was designed to investigate the nucleus ‎cuneiformis (CnF)‎‏ ‏neuronal responses during two phases after subcutaneous injection of ‎formalin into the hind paw of rat.‎ Materials & Methods: In this study, seventy six male NMRI adult rats, weighing 230-320 g ‎were used. Control group (n=24), which was tested merely for determining spontaneous firing ‎rate of CnF neurons. Saline group (n=15) which received saline (50µl s.c.) instead of ‎formalin into the plantar surface of hind paw after 15 min baseline recording. Formalin group ‎that formalin-induced neural activity of 37 cells simultaneously recorded from the CnF during ‎first phase (0-5 min) and second phase (15-60 min) of formalin test in 5-min intervals, using ‎an extracellular single unit recording technique.‎ Results: The‏ ‏baseline firing rate of neurons in the CnF varied between 1.2 and 39.2 spikes/sec ‎and the average frequency of spontaneous activity over 1 h was 11.8 ± 1.1 spikes/sec. There ‎were three neural clusters after formalin injection. Neurons in cluster 1 (46%) exhibited ‎severe, transient excitatory response in the first (acute) phase while neurons in cluster 2 (35%) ‎exhibited tonic but long-lasting excitatory response in the second (chronic) phase. Cluster 3, a ‎small portion of neurons (about one fifth) which failed to show any evident responses to ‎formalin test. ‎ Conclusion: Our findings suggest that alteration of neural activity and pattern in the ‎spontaneous background of CnF neurons can be mediated a role in the transmission of ‎nociceptive information induced by the peripheral injection of formalin and can be discussed ‎in light of the role of these neurons in nociceptive information processing following ‎peripheral stimuli.‎
Masoumeh Sabetkasaei, Amin Ataie, Abbas Haghparast, Akbar Hajizadeh Moghaddam, Ramin Ataie, Shiva Nasiraei,
Volume 13, Issue 3 (Fall 2009)

Introduction: Aging is the major risk factor for neurodegenerative diseases and oxidative stress is involved in the pathophysiology of these diseases. Oxidative stress can induce neuronal damages and modulate intracellular signaling, ultimately leading to neuronal death by apoptosis or necrosis. Methods: In this study, we investigated the possible antioxidant and neuroprotective properties of the polyphenolic antioxidant compound, Curcumin against homocysteine (Hcy) neurotoxicity. Curcumin (5, 15, 45 mg/kg) was injected intraperitonealy once daily for a period of 10 days beginning 5 days prior to Hcy (0.2 μmol/μl) intracerebroventricular injection in rats. Biochemical and behavioral studies, including passive avoidance learning and locomotor activity tests were studied 24 h after the last curcumin or its vehicle injection. Also Histopathological studies and cell dencity in different regions of hippocampus was investigated. Results: Hcy could induce lipid peroxidation and increase MDA and SOA levels in rats' brain. Additionally, Hcy impaired memory retention in passive avoidance learning test. However, Curcumin treatment decreased MDA and SOA levels significantly as well as improved learning and memory in rats. Histopathological analysis also indicated that Hcy could decrease hippocampus cell count and Curcumin inhibited this toxic effect. Conclusion: These results suggest that Hcy may induce lipid peroxidation in rats' brain and decrease hippocampus cells. Also polyphenol treatment (Curcumin) has the ability to improve learning and memory deficits by protecting the nervous system against Oxidative stress. Keywords: Homocysteine, Curcumin, Lipid peroxidation, Oxidative Stress
Mir-Shahram Safari, Abbas Haghparast, Saeed Semnanian, Abolhassan Ahmadiani,
Volume 15, Issue 1 (Spring 2011)

Introduction: Previous studies have shown that stimulation of lateral hypothalamus (LH) produces antinociception. Orexin-A (OXA) receptor is strongly expressed in the nucleus locus coeruleus (LC) and orexinergic fibers densely project from LH to LC. In this study, we assessed the role of LC and its OXA receptors in antinociceptive response induced by LH chemical stimulation in the rat. Methods: The cholinergic agonist carbachol (125nmol/0.5μl saline) and lidocaine (2% 0.5μl) were unilaterally microinjected into the LH with the concurrent LC inactivation. In another set of experiments, SB-334867 an OXA selective antagonist or its vehicle were unilaterally infused in LC to study its effect on LH stimulation-induced antinociception. Antinociceptive responses were obtained by the tail flick test and were presented as maximal possible effect (MPE) at 5, 10, 15, 20, 30 and 60 min after drug administrations. Results: The results showed that microinjection of carbachol into the LH significantly induced antinociception at 5 and 10 min (p<0.001). This effect was significantly blocked by microinjection of lidocaine into the LC. Additionally, intra-LC administration of SB-334867 (4.5 μg) could suppress the LH stimulation-induced antinociception by carbachol at 5 and 10 min post-injection times (p<0.001). Conclusion: Our findings showed that analgesic response induced by LH stimulation is mediated in part by the subsequent activation of LC neurons and results from the activation of orexinergic inputs into the LC that can modulate the pain processing.
Pegah Azizi, Mojtaba Kermani, Abbas Haghparast,
Volume 15, Issue 3 (Fall 2011)

Introduction: Nitric oxide (NO) is a neuronal messenger molecule in the central nervous system, which is generated from L-arginine by nitric oxide synthase (NOS) and involves in many important opioid-induced effects. Our previous studies revealed that Cuminum cyminum interestingly reduces morphine sensitization, tolerance and dependency in male mice. Therefore, in the present study, the effect of intraperitoneal (ip) administration of different doses of cumin fruit essential oil (FEO) on the acquisition of morphine-induced conditioned place preference (CPP) in L-arginine treated mice was investigated. Methods: In this study, the CPP paradigm was done on 231 adult male albino Wistar mice and conditioning scores and locomotor activity were recorded by the Ethovision software. Results: The results showed that solely administration of different doses of cumin FEO (0.01, 0.1, 0.5, 1 and 2% ip) or L-arginine (50, 100 and 200 mg/kg ip) during CPP protocol could not induce CPP. Nonetheless, morphineinduced CPP was significantly decreased by two higher doses of cumin FEO (1% and 2% P<0.05), while it was increased by L-arginine (100 and 200 mg/kg) when they were injected before morphine (5 mg/kg) during the acquisition period (P<0.001). Additionally, cumin FEO (0.01-2%) could interestingly attenuate the increasing effect of L-arginine (200 mg/kg) on morphine-induced CPP in a dose-dependent manner. Conclusion: In conclusion, it could be suggested that some components of cumin FEO attenuate the excessive effect of L-arginine on morphine-induced CPP through inhibitory mechanisms on NO pathway. It seems that cumin FEO possibly acts as a NOS inhibitor.
Leila Ahmad-Molaei, Mehdi Ordikhani-Seyedlar, Maryam Ziaei, Raha Khademi, Pegah Rouzmeh, Abbas Haghparast ,
Volume 15, Issue 3 (Fall 2011)

Introduction: The antinociceptive effect of morphine is, in part, mediated through the activation of a descending pathway. One of the major components of this pathway is the nucleus raphe magnus (NRM). Our previous study demonstrated the involvement of NRM in the analgesic effect of morphine microinjected into the nucleus cuneiformis (NCF) in a descending manner. The aim of the current study was to investigate another aspect of the interaction between these two nuclei in both acute and chronic inflammatory pain models. Methods: In order to calculate 50% effective dose (ED50) of morphine, animals received bilateral morphine injections (1, 2.5, 5 and 10 μg/0.5 μl saline) into the NRM. The obtained ED50 of morphine was applied into the NRM with/without bilateral electrolytic lesion (500 μA, 30 sec) of the NCF. Tail-flick and formalin tests were applied as behavioral analgesic tests in this study. Results: Results interestingly showed that the intra-NRM morphine injection (ED50 1 μg/0.5 μl saline) resulted in an increase in tail flick latencies (morphine-induced antinociception) at 30-min intervals, while bilateral electrolytic lesions in the NCF could notably decreased the morphine-induced antinociception during 30-90 min after the injection of morphine. Data also showed that bilateral morphine microinjected into the NRM, dose-dependently increases the antinociceptive responses during both early and late phases of formalin test. The antinociceptive effect of morphine microinjected into the NRM was significantly attenuated at the late phase but not early phase following the bilateral destruction of NCF in formalin test. Conclusion: It could be concluded that there is a reciprocal interaction between NRM and NCF during morphine - induced antinociception in both acute and chronic inflammatory pain models in rat.
Samad Nazemi, Homa Manaheji, Abbas Haghparast, Jalal Zaringhalam Moghadam , Mehdi Sadegi,
Volume 15, Issue 4 (Winter 2012)

Introduction: Pharmacological blockage of glial activity has been proved useful for treatment of neuropathic pain by lowering proinflammatory cytokines. The present study is to confirm the effect of post-injury administration of pentoxifylline on chronic constriction injury (CCI)-induced neuropathic pain symptoms_ and improved the efficacy of morphine anti-nociception. Methods: Male Wistar rats (230-270 g) underwent surgery for induction of CCI model of neuropathy. In the sham group the nerve was exposed but not ligated. In 5 groups (n=8) morphine (2.5, 5, 7.5, 10, 15 mg/kg s.c.) was administered in post-operative days (POD) 0, 6 and 14. To evaluate the analgesic effect of different doses of morphine, Von Frey and Hargreaves tests were performed before and 30 minutes after morphine administration. In different groups, pentoxifylline (8, 15, 30 mg/kg i.p.) or normal saline (vehicle) were administered from POD6 to POD13. Behavioral tests were utilized after last dose of pentoxifylline and also on POD14 again after injection of a single dose of morphine (5 mg/kg, s.c.). Results: The analgesic effect of morphine (5 mg/kg) on POD6 and morphine (5, 7.5, 10, 15 mg/kg) on POD14 was significantly decreased in comparison to POD0. Pentoxifylline effectively attenuated thermal hyperalgesia (at 15 and 30 mg/kg) and mechanical allodynia (at 30 mg/kg) on POD13. However, pentoxifylline (15, 30 mg/kg) improved the antihyperalgesic effect of morphine (5 mg/kg s.c.) on POD14. Conclusion: Analgesic effect of morphine was reduced after nerve injury and it may be due to the activation of glia. Inhibition of glial activity is an effective way to attenuate CCI-induced neuropathic pain and also to improve the antihyperalgesic effect of morphine, without significant effect on its anti-allodynic effect.
Najmeh Katebi, Yasaman Razavi, Shabnam Zeighamy Alamdary, Shiva Irani , Fariba Khodagholi, Abbas Haghparast,
Volume 17, Issue 1 (Spring 2013)

Introduction: Nucleus accumbens (NAc) plays a critical role in neuronal reward circuits that are responsible for motivated and goal-directed behaviors. Some data suggest that morphine induces apoptosis in neurons, while other evidences show that morphine could have beneficial effects against neuronal cell death. This study was designed to evaluate the effect of morphine on apoptosis in the NAc in rat brain by assessing the changes in apoptotic factors. Methods: To investigate the effects of 3 different doses (0.5, 5 and 10 mg/kg) of morphine on induction of apoptotic factors in the NAc after its sub-chronic consumption, conditioned place preference paradigm was used in three groups of rats compared with the control group that received saline, and then the changes in apoptotic factors caspase-3, PARP and Bax/Bcl-2 ratio were assessed by western blot technique. Results: Our results showed that apoptotic factors increase in all three groups treated with morphine. In the nucleus accumbens, morphine induced significant increase (p<0.01) in caspase-3, PARP and Bax/Bcl-2 ratio, in the lowest dose (0.5 mg/kg) compared with the control group that received saline instead of morphine. Conclusion: Increase in apoptotic factors by low dose morphine in the nucleus accumbens of morphine-treated rats shows that morphine can affect the molecular mechanisms which interfere with apoptosis through one kind of its receptors with high affinity. However, with increase in dose of morphine, it seems that other kinds of opioid receptors have been involved which exert some neuroprotective effects of morphine against apoptosis.
Marzieh Moradi, Mohammad Reza Yazdian, Abbas Haghparast,
Volume 18, Issue 1 (Spring 2014)

Introduction: Stimulation or inactivation of the lateral hypothalamus (LH) produces antinociception. Studies showed a role for the ventral tegmental area (VTA) in the antinociception induced by LH chemical stimulation through the orexinergic receptors. In this study, we assessed the role of intra-VTA dopamine D1 and D2 receptors in antinociceptive effects of cholinergic agonist, carbachol, microinjected into the LH in the tail-flick test. Methods: Rats were unilaterally implanted with two separate cannulae into the VTA and LH. Intra-VTA infusions of selective D1 receptor antagonist SCH-23390 (0.125, 0.25, 1 and 4 μg/0.3 μl saline) and selective D2 receptor antagonist sulpiride (0.125, 0.25, 1 and 4 μg/0.3 μl DMSO) 2 min before microinjection of carbachol (125 nmol/rat effective dose) into the LH was done. The antinociceptive effects of different doses of these antagonists were measured using a tail-flick analgesiometer, and represented as maximal possible effect (%MPE) at 5, 15, 30, 45 and 60 min after administration. Results: The results showed that intra-VTA administration of D1 and D2 dopamine receptors antagonists could significantly prevent the development of LH stimulation-induced antinociception. Administration of maximum doses of SCH-23390 and Sulpiride (4 μg) didn’t affect the nociceptive behaviors in acute model of pain. Conclusion: Thus dopamine receptors in the VTA play a modulating role in carbachol-induced analgesia within the LH, in acute model of pain. It is supposed that there is an interaction between VTA dopaminergic and orexinergic systems in pain modulation.
Zahra Mirmohammadsadeghi, Afsaneh Elyasi, Abbas Haghparast,
Volume 18, Issue 4 (Winter 2015)

Introduction: Dopamine plays an important role in the central nervous system for modulating food intake. Dopamine receptors are distributed within the hypothalamus, and expression of D1 receptors is significant in hypothalamic paraventricular nucleus (PVN). Therefore, the aim of this study was to find if PVN-microinjected SKF38393, D1 receptor agonist, may modulate food intake. Methods: Guide cannula directed to the PVN were implanted in male Wistar rats (220-250 g). Stereotaxic coordinates were: lateral: +0.4 mm from midline dorsoventral: 7 mm from skull surface anteroposterior: -1.8 mm from the bregma. Intra-PVN microinjections of SKF38393, SCH23390 (D1 receptor antagonist) and saline were performed after a 5-7 day recovery period. Hourly over a 3 hours period, the weight of food pellets was measured. Assessment of spontaneous activity in rat was performed in standard activity chambers interfaced with a Digiscan animal. Feeding trials were done normally from Saturday to Wednesday between 9:00 am and 12:00 on rats which were deprived of food for 24 hours. All drugs were administered in 0.9% saline. Results: Intraparaventricular injections of SKF38393 (0.06, 0.01 μg) decreased food intake in a dose-dependent manner. The PVN injection of SCH23390, D1 receptor antagonist, did not affect food intake decreased by PVNmicroinjected SKF38393 (0.01 μg). Analysis of the physical activity revealed that PVN microinjection of SKF38393 (0.01 μg) did not affect locomotor activity. Conclusion: Our results showed that PVN-microinjected SKF38393 decreases food intake. This suppressive effect is probably not mediated through D1 receptors.

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