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Showing 16 results for Motamedi

Farshad Alizadeh Mansouri, Fereshteh Motamedi, Fereshteh Fathollahi, Nafiseh Atapour, Saeed Semnanian,
Volume 1, Issue 1 (Spring and Summer 1997)
Abstract

The effects of chronic morphine administration on the development of long-term potentiation (LTP) were investigated at the Schaffer collateral-CA1 pyramidal cell synapses of the rat hippocampal slices using primed-bursts tetanic stimulation. Significant enhancement of orthodromic population spike (OPS) was found for all stimulus intensities after tetanic stimulation. OPS enhancement was greatest when tested with low to mid-range stimulus intensities (25, 50 and 100 µA). There was also significant decrease in OPS delay. These responses were similar in slices from both control and morphine dependent rats. At all delivered stimulus intensities, the amount of LTP of OPS in slices from dependent rats was larger than that of control slices. However, these differences in LTP of OPS were significant at low stimulus intensities. These findings suggest that chronic morphine administration had induced changes in CA1 neurocircuitry which modulated synaptic plasticity during high frequency stimulation and appeared as augmented LTP and also inhibition of LTP decay.
Farshad Alizadeh Mansouri, Fereshteh Motamedi, Fereshteh Fathollahi, Nafiseh Atapour, Saeed Semnanian,
Volume 1, Issue 1 (Spring and Summer 1997)
Abstract

  The effects of chronic morphine administration on the development of long-term potentiation (LTP) were investigated at the Schaffer collateral-CA1 pyramidal cell synapses of the rat hippocampal slices using primed-bursts tetanic stimulation. Significant enhancement of orthodromic population spike (OPS) was found for all stimulus intensities after tetanic stimulation. OPS enhancement was greatest when tested with low to mid-range stimulus intensities (25, 50 and 100 µ A). There was also significant decrease in OPS delay. These responses were similar in slices from both control and morphine dependent rats. At all delivered stimulus intensities, the amount of LTP of OPS in slices from dependent rats was larger than that of control slices. However, these differences in LTP of OPS were significant at low stimulus intensities. These findings suggest that chronic morphine administration had induced changes in CA1 neurocircuitry which modulated synaptic plasticity during high frequency stimulation and appeared as augmented LTP and also inhibition of LTP decay.


Fereshteh Motamedi, Ali Pourmotabbed, Yaghub Fathollahi, Farshad Alizadeh Mansouri, Saeed Semnanian,
Volume 1, Issue 2 (Fall and Winter 1997)
Abstract

  The involvement of NMDA receptors and voltage-dependent calcium channels in augmentation of long-term potentiation (LTP) was investigated at the Schaffer collateral CA1 pyramidal cell synapses in hippocampal slices of morphine dependent rats, using primed-burst tetanic simulation. The amplitude of the population spike and its delay were measured as indices of increase in postsynaptic excitability. D,L-APV and nifedipine were used as an NMDA receptor antagonist and a voltage-dependent calcium channel blocker, respectively. The amount of LTP of the orthodromic population spike (OPS) was higher in slices from dependent rats. Perfusion of slices from control and dependent rats with ACSF containing D,L-APV (25 µ M) and delivering tetanic simulation showed that D,L- APV completely blocked the LTP of OPS in slices from both control and dependent rats, while nifedipine (10 µ M) attenuated the amount of LTP of OPS in dependent slices and had no effect on controls. The results suggest that the enhanced LTP of OPS in the CA1 area of hippocampal slices from morphine-dependent rats is primarily induced by NMDA receptor activity, and the voltage-dependent calcium channels may also be partially involved in this phenomenon.


Mahmood Salami Zavareh, Yaghub Fathollahi, Hossein Esteky, Fereshteh Motamedi, Nafiseh Atapour,
Volume 2, Issue 2 (Fall and Winter 1998)
Abstract


Mahmood Salami, Yaghub Fathollahi, Fereshteh Motamedi, Hossein Esteky,
Volume 3, Issue 1 (Spring and Summer 1999)
Abstract

  The effectiveness of θ pattern primed-bursts (PBs) on development of primed-burst (PB) potentiation was investigated in layer II/III of the adult rat visual cortex in vitro. Experiments were carried out in the visual cortical slices. Population excitatory post-synaptic potentials (pEPSPs) were evoked in layer II/III by stimulation of either white mater or layer IV. To induce long-term potentiation (LTP), eight episodes of PBs were delivered at 0.1 Hz. Regardless of stimulation site, field potential recorded in layer II/III consisted of two components: a short latency and high amplitude response called pEPSP1, and a long latency and low amplitude response called pEPSP2. The incidence of LTP produced by PBs of layer IV was higher than that of the white mater tetanization. In contrast, PBs of both layer IV and white mater reliably induced LTP of pEPSP2 in layer II/III. It is concluded that PBs, as a type of activity pattern, of either white mater or layer IV can gain access to the modifiable synapses that are related to pEPSP2 in layer II/III, but accessibility of the modifiable synapses that are related to pEPSP1 depends on tetanization site. Relevancy of the results to the plasticity gate hypothesis is also discussed.

 


Esmaeil Akbari, Fereshteh Motamedi, Mohamamd Reza Vaez-Mahdavi,
Volume 4, Issue 1 (Spring and Summer 2000)
Abstract

Amitriptyline, a tricyclic antidepressant agent is used as one of the analgesic drugs in different kinds of pain. In the present study the effect of local (subcutaneous) injection of amitriptyline (50 and 100 µg) on the acute and chronic pain using formalin test, was investigated. Our data show that local injection of amitriptyline to the paw receiving formalin, causes a decrease in pain in both phasic and tonic phases of formalin test. On the other hand, in the group that this drug was injected (100 µg) to the contralateral paw, no significant change was observed in the pain score with respect to the control group. Therefore, it seems that the observed effect is due to the local action of amitriptyline and not as a result of its systemic effect. Considering the above-mentioned results, it is concluded that: 1) Amitriptyline acts like a local anesthetic in both acute and tonic phases of formalin test. 2) The mechanism of analgesia in the acute phase is probably caused by sodium channel blockade. 3) The analgesic effect of amitriptyline in the tonic phase of formalin test might be due to its antihistaminic and anti-inflammatory effects at the peripheral level, and also is due to the changes in the CNS plasticity which occurs during the acute phase.
Parvin Zareian, Mahyar Janahmadi, Seyed Mohamamd Firoozabadi, Fereshteh Motamedi,
Volume 4, Issue 2 (Fall and Winter 2000)
Abstract

Ion channels are responsible for control of cell function in excitable tissues such as heart and brain and also in organs and tissues traditionally thought to be non- excitable including liver and epithelium. In the present research, the effect of lead (Pb2+) on Ca2+ -dependent action potential and currents was studied in F77 neuronal soma membrane of Helix aspersa. For this purpose, action potential generation and Ca2+ currents were investigated in the absence and presence of Pb2+ using two-electrode voltage clamp and current clamp methods. Two distinct types of high voltage activated (HVA) calcium currents were recorded. In this respect, one of them was sensitive to nifedipine (1 µM) and the other one was resistant to nifedipine. Extracellular application of Pb2+ at concentrations of 0.6 and 3 µM suppressed the firing behavior of F77 neurons. It also decreased the amplitude and the duration of calcium action potentials. The voltage clamp findings demonstrated that lead blocked more than 50% of HVA Ca2+ currents. The blocking effect of Pb2+ on Ca2+ was time-dependent. Therefore, it can be concluded that Pb2+ may alter the bioelectrical properties of F77 neuron through blocking high voltage activated Ca2+ currents, particularly L-type that are nifedipine sensitive.
Fereshteh Motamedi, Samira Danyali, Mohammad Reza Vaez Mahdavi,
Volume 6, Issue 1 (Spring and Summer 2002)
Abstract

Various physiological parameters including level of sex steroids undergo alterations following chronic administration of morphine. In this study, the effect of chronic administration of morphine on phasic and tonic pain was studied in morphine-dependent male and female rats in the presence and absence of gonads using formalin test. In addition, for evaluation of differences in dependency, withdrawal signs were observed using naloxone hydrochloride. For dependency induction, morphine sulphate was administered in drinking water for a period of 30 days. The results showed that although chronic pain is significantly greater in female rats than male ones but this pain increases in male dependent rats and decreases in female dependent animals. Thus, no gender differences were found between male and female dependent rats. Furthermore, gonadectomy led to a significant decrease in chronic pain only in male dependent rats. Meanwhile, withdrawal signs were significantly greater in female dependent rats than male ones and gonadectomy did not influence these signs. It can be concluded that following morphine addiction, pain increases in male and decreases in female rats and morphine dependency is not affected by sex hormones.
Mohammad Javan, Fereshteh Motamedi, Abolhasan Ahmadiani, Fatemeh Masoudnia,
Volume 7, Issue 1 (Spring and Summer 2003)
Abstract

It has been reported that morphine tolerance does not develop in the presence of chronic pain. Therefore, this study was conducted to find out whether chronic inflammatory pain is able to eliminate or attenuate the developed tolerance to analgesic effect of morphine and also to investigate the role of lumbar spinal cord as a candidate site for this interaction. Tolerance was induced in adult male NMRI rats using daily injection of morphine at a dose of 20 mg/kg (i.p.) for 4 days, or using daily injection of morphine at a dose of 15 pg/rat (i.t.) for 7 days. Chronic inflammatory pain was induced using 50 µl of 5% formalin, injected into the hind paws. The antinociceptive effect of morphine at a dose of 10 mg/kg on day 5 (for i.p. treated rats) or morphine at a dose of 15 pg/rat on day 8 (for i.t. treared rats) were assessed using tail flick test. The results showed that those animals receiving saline (i.t. or i.p.) have potent analgesia (p<0.001), while animals treated with chronic morphine have only a weak analgesia for i.p. treatment (p<0.05). In addition, animals treated with both repeated morphine and 5% formalin (s.c.) into the hind paw showed potent analgesia (p<0.01). Meanwhile, the developed tolerance was reversed by chronic pain induction in the following days (p<0.01). It is concluded that chronic formalin-induced inflammatory pain, not only could prevent tolerance development, but also is able to reverse the developed tolerance to antinociceptive effect of morphine. Since in i.t.-treated animals, tolerance was induced in lumbar spinal cord level, it can be concluded that chronic formalin-induced inflammatory pain, as a stress (through HPA axis) or as a factor which directly exerts some modulations on pain transmission system, is able to prevent tolerance to analgesic effect of morphine through lumbar spinal cord.
Mojtaba Dolatshahi-Somesofla, Fereshteh Motamedi, Abolhasan Ahmadiani, Saeed Esmaili-Mahani,
Volume 11, Issue 3 (Fall 2007)
Abstract

Nimodipine, an L-type calcium channel blocker, can induce analgesia. However, it is not clear that this analgesic effect is at the level of spinal or supraspinal pain pathway. In addition, it has been reported that the analgesic effect of nifedipine, another L-type calcium channel blocker is related to the HPA axis, but there is no report indicating the role of this axis in the analgesic effect of nimodipine. Methods: Analgesia was measured by tail-flick (TF) test involving spinal reflexes and by hot-plate (HP) requiring an intact central nervous system. Assays were done before and 15, 30, 60 and 120 min after drug administration in the intact, sham operated and adrenalectomized rats. To identify the interaction between nimodipine and HPA axis, plasma corticosterone level was measured using the radioimmunoassay. Results: Nimodipine significantly decreased the plasma corticosterone level, and showed significant antinociception in both tests. Adrenalectomy potentiated the analgesic effect of nimodipine which was reversed by corticosterone replacement. Furthermore, nimodipine analgesic effect in ADX rats was more potent in HP test (compared to TF test). Nimodipine, at mentioned doses, did not alter animal’s movement indices in activity monitoring test. Conclusion: Nimodipine involves both spinal and supraspinal sites to control thermal pain transmission in presence of adrenal gland. It seems that there is a mutual interaction between nimodipine and HPA axis, especially at supraspinal levels.
Leila Satarian, Mohammad Javan, Fereshteh Motamedi,
Volume 12, Issue 1 (Spring 2008)
Abstract

Introduction: Stress inhibits the development of tolerance to morphine analgesia via activating Hypothalamic- Pituitary-Adrenal (HPA) axis. Modified catecholamine systems have been reported following morphine tolerance development. In the current study we tried to evaluate changes in the gene expression levels for MAO-A, MAO-B, COMT and thyrosine hydroxylase (TyH) enzymes following chronic pain, development of morphine tolerance and their combined administration. Methods: Analgesic tolerance was induced by intrapritoneal injections of morphine 20 mg/kg twice a day for 4 days. To study the effect of pain on morphine tolerance, 50 μl of formalin 5% was injected into the animal paws prior to morphine injections. Semi-quantitative RT-PCR was used to evaluate the gene expression level in lumbar spinal cord on day 5. Three separate control groups received saline or morphine injections or pain induction. Results: Chronic administration of morphine increased the expression level of MAO-B, decreased the expression of TyH and did not change the expression of COMT and MAO-A. Pain increased the expression of MAO-A, but did not change the expression of MAO-B, COMT and TyH. The combination of morphine treatment and pain induction for 4 days partially reversed the reduced expression of TyH and did not change the expression of MAO-A, MAO-B and COMT. Conclusion: Our results showed that in the context of morphine tolerance, gene expression was changed toward decreased biosynthesis and increased elimination of catecholamines. It seems that chronic administration of morphine caused lower level of catecholamines in spinal neurons and help development of morphine tolerance. Also, chronic pain partially produced compensational changes in gene expression. This may explain for its anti-tolerance effect.
Abbas Haghparast, Amir-Mohammad Alizadeh, Fereshteh Motamedi,
Volume 12, Issue 2 (Summer 2008)
Abstract

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 Motamedi Joibari, Homayoon Khazali,
Volume 14, Issue 2 (Summer 2010)
Abstract

Introduction: ghrelin is a potent orexigenic agent in rodents and humans. Some studies have shown that ghrelin participates in the adaptive response to weight loss and plasma concentration of ghrelin rises with dieting. On the other hand, weight loss and fasting is accompanied by increased levels of epinephrine and cortisol. In this study, we investigated the effects of epinephrine and cortisol on fasting-induced ghrelin secretion in rats fed different levels of their energy requirements. Methods: forty five male Wistar rats (300-350 g, 15 per group) were fed a diet containing 100%, 50% and 25% of their energy requirement for 10 days followed by 2 days of fasting. Animals were then anesthetized for carotid artery cannulation, which was used for injections and blood samplings. Rats received either 3 μg epinephrine (Ep)/Kg BW, 3 μg cortisol (Cor)/Kg BW, or a combination of these two (0.1 mg in 1 ml of PBS). Blood samples were collected before injections and 30, 60, and 120 min after injections. Results: mean plasma concentration of baseline ghrelin increased in the animals fed 50% food restriction (P≤0.01). In 100% and 50% food restricted groups, fasting ghrelin levels fell after epinephrine and combination of epinephrine and cortisol injection (P≤0.05). In contrast, the group that had 25% food restriction did not show any response to epinephrine and combination of epinephrine and cortisol (P>0.05), while the levels of the fasting ghrelin rose significantly after cortisol treatment (P≤0.01). Conclusion: These results indicate that injection of epinephrine suppresses starvation-induced secretion of ghrelin in normal (100%) and starved (50%) rats. Ghrelin secretion response to epinephrine might be affected by weight loss as it does not seem to be suppressed in starved (25%) rats.
Mitra Yousefpour, Nima Naderi, Mahyar Janahmadi, Amir Mohammad Alizadeh, Fereshteh Motamedi,
Volume 14, Issue 4 (Winter 2011)
Abstract

Introduction: The magnocellular neurons (MCNs) of the supraoptic nucleus (SON) play a crucial role in control of physiological and pathophysiologiccal condition due to two peptides that they synthesize, i.e. Oxytocin (OXT) and Vasopressin (AVP). The activity of MCNs is regulated by a variety of excitatory and inhibitory inputs. Opioid receptors are one of the important receptors in SON synapses. The aim of the present study is to evaluate the effect of acute morphine application on SON synapses and AVP release in rats. Methods: In this study, whole cell patch clamp recording of neurons in rat (70-100 g, 3–4 weeks old) brain slice preparations consisting of SON was used to investigate the effect acute of lowest effective dose of morphine (25μM) administration on spontaneous inhibitory and excitatory post synaptic currents (sIPSCs and sEPSCs) in MCNs. Also, AVP levels were measured in blood samples of rats using ELISA technique after the Morphine injection (30 mg/kg, ip). Results: Bath application of morphine produced an increase in sEPSCs and a decrease in sIPSCs frequencies. Measurement of plasma AVP revealed an increase in hormone levels 45 min after systemic administration of morphine. P-values of less than 0.05 were considered statistically significant. Conclusion: It is suggested that acute administration of morphine stimulates the MCNs and AVP secretion.
Jafar Doost Mohammad Pour, Narges Hosseinmardi, Mahyar Janahmadi, Yaghoub Fathollahi, Fereshteh Motamedi, Mehdi Hooshmandi,
Volume 17, Issue 3 (Fall 2013)
Abstract

Introduction: The prostaglandin E2 (PGE2), a cyclooxygenase (COX) product, play critical roles in the synaptic plasticity. Therefore, long term use of COX inhibitors may impair the synaptic plasticity. Considering the wide clinical administration of aspirin and its unknown effects on information processing in the brain, the effect of aspirin and sodium salicylate on the short term synaptic plasticity was investigated. Methods: Field excitatory post synaptic potential (fEPSP) from stratum radiatum of CA1 neurons were recorded following Schaffer collateral stimulation in rats receiving aspirin in drinking water (2 mg/ml) for 6 weeks or sodium salicylate (six injection of 300 mg/kg, IP, twice daily) for 3 days. In order to examine the short-term synaptic plasticity, paired pulse stimulations with inter pulse intervals (IPI) of 20, 80, and 200 ms were applied and paired pulse index (PPI) was calculated. Results: The data showed that both sodium salicylate and aspirin decreased basal synaptic responses, although this change was significant in the sodium salicylate group, but not in aspirin treated rats (ANOVA P<0.001). Sodium salicylate significantly increased PPI at 20 ms IPI (%90.7±1.6, n=5Vs. control: %76.1±1.5, n=5). Also significant increase in PPI was observed in aspirin treated rats (%125.9±6.6, n=5) at 20 ms IPI compared to control ones (%76.3±2.4, n=5, P<0.05, unpaired t-test). Conclusion: In summary, our study suggests that aspirin and sodium salicylate may affect synaptic transmission and short term synaptic plasticity in the rat hippocampus.
Abdolaziz Ronaghi, Nima Naderi, Fereshteh Motamedi,
Volume 19, Issue 1 (March 2015)
Abstract

Introduction: The effects of cannabinoids (CBs) on synaptic plasticity of hippocampal dentate gyrus neurons have been shown in numerous studies. However, the effect of repeated exposure to cannabinoids on hippocampal function is not fully understood. In this study, using field potential recording, we investigated the effect of repeated administration of the nonselective CB receptor agonist WIN55212-2, and the CB1 receptor antagonist AM251, on both short- and long-term synaptic plasticity in dentate gyrus (DG) of hippocampus. Materials and Methods: Drugs were administered three times daily for seven consecutive days into lateral ventricle of rats. Short term synaptic plasticity was assessed by measuring paired-pulse index (PPI) in DG neurons after stimulation of perforant pathway. Long-term plasticity was assessed through measurement of both population spike (PS) amplitude and field excitatory postsynaptic potential (fEPSP) slope after high frequency stimulation (HFS) of DG neurons. Results: Repeated administration of WIN55212-2 not only significantly decreased PPI in 20, 30 and 50 ms intervals but also blocked LTP. This effect was reversed by pretreatment of rats with CB1 receptor antagonist AM251. Moreover, AM251 by itself increased PPI in 10 and 20 ms interval stimulations, but had no effect on HFS-induced PS amplitude and fEPSP slope. Conclusion: These results suggest that repeated administration of cannabinoids could impair short term and long term synaptic plasticity that may be due to desensitization of cannabinoid receptors and/or changes in synaptic spine density of hippocampus which leads to alteration in short and long term memories that remains to be elucidated.

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