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Showing 18 results for Janahmadi

Mahyar Janahmadi, Toorandokht Baluchnejad Mojarad,
Volume 3, Issue 2 (Fall and Winter 1999)
Abstract

  While the effect of changes of stimulus waveform (quasitrapezoidal and rectangular current pulses) on nerve activation is clear, but there is no evidence on the effect of quasitrapezoidal pulses on ionic currents of cellular membrane. In the present study, the effect of depolarizing quasi-trapezoidal current pulses, in comparison with that of depolarizing rectangular current pulses, on firing behavior of isolated Fl neuron in Helix aspersa was investigated using intracellular recording technique (current clamp). In standard ringer, increasing the intensity of quasi-trapezoidal pulses, in comparison with rectangular pulses, caused a considerable rise of the amplitude and the duration of elicited action potential. The reduction of time constant of fast afterhyperpolarization (fAHP) and post-stimulus hyperpolarization (PSH) after injection of low intensity of quasi-trapezoidal pulses was significantly more than that of rectangular pulses. After elimination of K+ and Na+ currents, a low intensity of quasi-trapezoidal stimulus caused a 12 % decrease in the amplitude of high-threshold Ca2+ spikes. On the other hand, with an increase in the threshold of action potential, the time constant of PSH and reduction in the threshold latency through quasi-trapezoidal pulses was more than rectangular pulses. In the presence of nifedipine (1 mM), no significant differences were observed between the effects of two waveforms of stimulus on firing behavior. The results of this study showed that two waveforms of stimulus have different effects on firing behavior and ionic nonlinear currents in FI neuron. It seems that the quasitrapezoidal pulses, through slowing hyperpolarization of membrane potential can increase the cell excitability.


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.
Jafar Vatanparast, Mahyar Janahmadi, Houri Sepehri, Ali Haeri-Rohani, Ali Reza Asgari,
Volume 10, Issue 1 (Spring 2006)
Abstract

Introduction: Since organophosphorus compounds (OP) are toxic and designed to destroy insects and pest species, there are many hazards associated with their use. Although, the main target site of these compounds is acetylcholinesterase (AChE), however it has become increasingly evident that OPs have also other direct effects on cellular processes. In the present study, the effects of low concentrations of paraoxon and its interaction with forskolin, an activator of protein kinase A (PKA), were studied on Ca2+ spike configuration and frequency in neurons of snail Caucasotachea atrolabiata. Methods: Subesophageal ganglia neurons were recorded in current clamp mode in Na+ free Ringer solution that contained voltage dependent potassium channel blockers, 4AP and TEA. Results: Paraoxon (0.3-0.6 μM) decreased the duration of spontaneous Ca2+ spikes. This effect was seen with a suppression of single spike AHPs, leading to an increment in firing rate. Paraoxon induced hyperactivity appeared to be a consequence of decrease in Ca2+ influx during spikes which is the main determinant of AHP duration by activating Ca2+ dependent potassium channels. Forskolin (25 μM), in the absence of a significant change in spike duration, decreased the duration of single spike AHPs and increased the frequency of spikes. After forskolin application, paraoxon decreased the duration of Ca2+ spikes and AHPs, and increased the activity. However, these effects, especially on spike duration, were not as pronounced as in the absence of forskolin. Conclusion: These findings suggest that although forskolin, similar to paraoxon, decreases the AHP and increases the frequency of spikes but it employs mechanism(s) different from paraoxon which also oppose the effects of paraoxon on Ca2+ spikes configuration and frequency.
Ghola Ali Hamidi, Homa Manaheji, Mahyar Janahmadi, Mahmood Salami,
Volume 10, Issue 1 (Spring 2006)
Abstract

Introduction: Neuropathic pain syndromes are changes resulting from damage to neuronal pathways that are characterized by spontaneous burning sensation with accompanying allodynia and hyperalgesia. Since the treatments of neuropathic pain are poorly understood and existing treatments are often ineffective, it is important to increase our understanding of the neuropathic pain states in order to identify strategies for the development of effective therapies. The purpose of this study was to investigate the involvement and pre-emptive treatment of morphine and / or NMDA receptor antagonist MK-801, and co-administration of both drugs on behavioural responses in an experimental model of neuropathic pain (CCI). Methods: Experiments were performed on six groups (n=8) of male Sprague-Dawley rats (230-280g). In the groups that received drugs, two groups were injected with MK-801 (0.3 mg/kg, 20 min before, and 6 h after the operation) or morphine (8 mg/kg, 30 min prior to the operation). Another group received both drugs with the same doses and protocols. Finally, one group received normal saline in same volumes. The animals were tested for allodynia and hyperalgesia reactions at 0, 3, 7, 14, 21 and 28 days after CCI of the sciatic nerve. Results: Our data revealed that the CCI produces mechanical and cold allodynia and a hypersensitivity to noxious stimulations. MK-801 and morphine produced only a slight cold anti-allodynic response. On the other hand, co-injection of morphine and MK-801 markedly reduced cold allodynia at the days 7 (P<0.01), 14 (P<0.05) and 21 (P<0.05) when compared with the saline group. However, there was slight alleviation of the mechano allodynia, and, heat- and mechano-hyperalgesia. Results demonstrate that the CCI model importantly influences the behavioural responses to both the thermal and mechanical stimulations. Conclusion: We conclude that co-administration of both drugs can be more effective than MK-801 and morphine administered alone in the induced neuropathic pain.
Ali Rastqar, Mahyar Janahmadi, Yaghub Fathollahi, Mahyar Janahmadi,
Volume 10, Issue 3 (Fall 2006)
Abstract

Introduction: The functional effects of orexin-B on the calcium spikes and excitability of the neuronal soma membrane of garden snail, Helix aspersa were studied. Methods: Conventional intracellular recording, under the current clamp conditions was performed to examine the effects of orexin-B on the configuration and electrophysiological properties of calcium spikes. Results: Application of orexin-B (300 nM) led to a membrane depolarization and thereby the increase in excitability of neurons. It also decreased the duration and the amplitude of calcium spikes. On the other hand, orexin-B had a dual effect on the amplitude of afterhyper polarization (AHP) in a time dependent manner. The maximum reduction of the amplitude of AHP was recorded within 10 min of orexin-B exposure. However a maximum increase in AHP amplitude was observed later (15 min after exposure to orexin-B). Inactivation of G-proteins by pertussis toxin (100 nM) was used to test the involvement of Gi/Go in the orexin-B induced modulation of calcium channels. Pre-incubation of ganglia for 3-6 h with PTX blocked the depolarization effect of orexin-B on the resting membrane potential. Orexin-B on pretreated neuronal cells with PTX did not statistically change the calcium spike parameters, unless the peak amplitude of AHP increased remarkably. Conclusion: In conclusion, these data suggest that orexin-B (300 nM) may affect the membrane excitability and modulates the activity of calcium and calcium activated potassium channels in snail neurons.
Mohammad Shabani, Masoud Haghani, Vahid Sheibani, Mahyar Janahmadi,
Volume 13, Issue 2 (Summer 2009)
Abstract

Abstract* Introduction: Cannabis consumption during pregnancy may affect fetal growth, motor performance, memory and cognitive functions. Methods: Primiparous pregnant Wistar rats were randomly assigned to 4 treatment groups (6 rats per group) consisting of control and sham groups as well as 2 groups treated with Win. Win treated groups received daily s.c. injections of 0.5 or 1 mg/kg WIN suspended in 1% Tween 80 saline in a volume of 1 ml/kg from days 5 to 20 of pregnancy. Sham treated rats were given daily injections of 1% Tween 80 saline on the same days of pregnancy. Body weight, mortality, memory function and motor performance were assessed in the infants on the third, fifth and seventh weeks after birth. Righting responses in rat pups were also compared on the second day after birth. Results: Offsprings from Win (1mg/kg) treated rats exhibited a significant loss in the righting reflex on the 2nd day after birth, when compared to other groups. However, there was no statistically significant difference between groups regarding motor coordination assessed by rotarod test on the 3rd and 5th weeks after birth. Passive avoidance learning (PAL) test on 50-day-old rats showed that during the acquisition trials, approach latencies were not significantly different among all groups. However, in retention trials, which were performed 24 h and 7 days later, the avoidance latencies of rats exposed to 0.5 mg/Kg Win were significantly shorter than those of the control and sham animals. Win consumption during pregnancy did not induce significant changes in the body weight of pregnant rats on the first day and three weeks after pregnancy. Litter size (number of pups per delivery) was significantly reduced in 1 mg/kg Wintreated compared to 0.5 mg/kg Win-treated, sham treated and control groups (p<0. 001). The length of pregnancy in 1 mg/kg Win-exposed rats was also significantly shorter compared to control (p<0.001), 0.5 mg/kg win-treated (p<0.01), and sham (p<0.0001) rats. Conclusion: These findings suggest that prenatal exposure to Win, a cannabinoid agonist, probably induces a longterm alteration of the endocannabinoid system, which in turn affects learning and motor coordination ability. Keywords: Cannabinoids, Maternal Consumption, motor performance, memory.
Roghaieh Khakpay, Saeed Semnanian, Mohammad Javan, Mahyar Janahmadi,
Volume 14, Issue 3 (Fall 2010)
Abstract

Introduction: Estradiol is a neuroactive steroid, which is found in several brain areas such as locus coeruleus (LC). Estradiol modulates nociception by binding to its receptors and also by allosteric interaction with other membranebound receptors like glutamate and GABAA receptors. LC is involved in noradrenergic descending pain modulation. Methods: In order to study the effect of 17β-estradiol on both acute and persistent pain modulation and its mechanisms, formalin was injected into the hind paw of male rats. Formalin-induced responses including licking and flexing duration and paw jerking frequency were recorded for 60 min after injection of 50 μl of 2% formalin. Also, the expression of α2 and γ1 subunits of GABAA receptor genes were examined by RT-PCR technique. Results: The results of the current study showed that intra-locus coeruleus injection of 17β-estradiol attenuated the second phase, but not the acute phase of formalin induced pain (P< 0.05). GABAA receptor antagonist (bicuculline) reversed the antinociceptive effect of 17β-estradiol, but the expression level of α2 and γ1 subunits of GABAA receptor genes were not significantly changed. Conclusion: It may be concluded that the analgesic effect of 17β-estradiol in formalin induced inflammatory pain is possibly mediated through the interaction with membrane-bound GABAA receptors, however this effect is not exerted at the gene expression level.
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.
Parviz Shahabi , Ali Gorji , Yaghoub Fathollahi , Mahyar Janahmadi , Javad Mirnajafi-Zade , Jalil Arabkheradmand , Marius Alexander Eickhoff ,
Volume 15, Issue 1 (Spring 2011)
Abstract

Introduction: A close link between spreading depression (SD) and several neurological diseases such as epilepsy could be demonstrated in many experimental studies. Epilepsy is among the most common brain disorders. Despite a large number of investigations, its mechanisms have not been yet well elucidated. Hippocampus is one of the important structures involved in seizures. The aim of this study is to get an insight into the patho-physiological processes induced by SD that lead to the generation of epileptiform field potentials. Methods: The horizontal amygdala-hippocampus-neocortex slices of rat brain in which SD was induced by KCl application in each brain structure were used. Following GABAA receptor antagonist bicuculline superfusion (1.25 μmol/L, for 45 min), SD induced epileptic activity in all tested slices was monitored. Results: The induction of SD in the hippocampus resulted in interictal and ictal epileptiform field potentials and intracellular paroxysmal depolarization shifts (PDS). After SD, RMP slightly depolarized and the threshold of AP decreased, while the frequency of AP significantly increased. Amplitude of depolarization and also amplitude of discharges were also significantly increased. ISI significantly decreased and the most of neurons shifted from FA to SA indicating an enhanced excitability. Conclusion: SD may cause pathological changes in brain structures such as increased excitation and/or decreased inhibition. Propagation of SD over epileptogenic areas may trigger seizure attacks in some patients and our findings provide evidence on the role of SD in temporal lobe epilepsy.
Zahra Ghasemi, Majid Hassanpour-Ezatti, Mohammad Kamalinejad, Mahyar Janahmadi,
Volume 15, Issue 1 (Spring 2011)
Abstract

Introduction: Anethole is the main constituent of Pimpinella anisum L. (anise), a herbaceous annual plant which has several therapeutic effects. In the folk medicine, anise is employed as an antiepileptic drug. Specifically, this study was focused on the cellular effect of anethole, an aromatic compound in essential oils from anise and camphor. Anethole has various physiological effects on the cardiovascular system and smooth and skeletal muscles. However, despite these persistent effects, there is little information available about the actions of anethole on nerve cells. Therefore, a major goal of the present research was to investigate the possible cellular mechanisms underlying the effect of anethole on the neural excitability and action potential characteristics in snail neurons. Methods: Intracellular recordings were made under the current clamp condition on F1 cells of Helix aspersa. Following extracellular application of anethole (0.5% or 2%), changes in the firing pattern and action potential parameters were assessed and compared to control condition. Results: Application of anethole (0.5% and 2%) led to a significant increase in the action potential amplitude and a reduction in the peak area and time to peak. In the presence of 0.5% anethole, the after hyperpolarization (AHP) amplitude was significantly decreased, while the firing frequency of neurons was increased. However, 2% anethole did not affect the AHP amplitude, but significantly reduced the firing frequency of action potentials. Conclusion: Based on the effect of anethole on the action potential parameters, it can be concluded that it probably affects the voltage gated ion channels function, including Ca2+ channels and/or Ca2+ dependent K+ channels activity.
Zohre Ghotbeddin, Javad Mirnajafi-Zadeh, Saeed Semnanian, Mahyar Janahmadi,
Volume 16, Issue 1 (Spring 2012)
Abstract

Introduction: Many studies have shown that amygdala kindling produces synaptic potentiation by induction of changes in the neuronal electrophysiological properties and inward currents both in epileptic focus and in the areas which are in connection with the epileptic focus and have important role in seizure development and progression such as hippocampal CA1 region. However, cellular mechanisms of these processes are not clear. In the present study, changes in the electrophysiological properties of hippocampal CA1 pyramidal neurons following amygdala kindling were examined in rat. Methods: Animals were rapidly kindled by stimulation of right amygdala (12 stimulation per day, 1 ms pulse duration at 50Hz). Twenty-four hours after amygdala kindling, electrophysiological properties and inward currents of CA1 pyramidal neurons were assessed by using whole-cell patch clamp technique. Results: Amygdala kindling findings show that percentage broadening of the last spike compared to the first spike during a trains of action potentials was significantly increased in kindled rats (p<0.05). The number of rebound action potential was significantly increased from 1±1 in control rats to 6±1 in kindled rats (p<0.01). The amplitude of post stimulus afterhyperpolarization potential (Post AHP) following a trains of action potential was also significantly (p<0.05) increased in kindled group (-5±2mV) compared to normal rats (-3±1mV). Under voltage clamp condition, amygdala kindling produced a significantly larger inward current (-5344.25±33.19 pA, p<0.001) in CA1 pyramidal neurons compared to normal cells (-9203.6±44.99pA). Conclusion: The present findings show that amygdala kindling resulted in neuronal hyperexcitability through alteration of the electrophysiological characteristics possibly by increasing the inward currents in hippocampal CA1 pyramidal neurons.
Zahra Ghasemi, Saeedeh Fakharzadeh, Mohammad Hassan Nazaran, Mahyar Janahmadi,
Volume 16, Issue 2 (Summer 2012)
Abstract

Introduction: Oxidative stress is one of the important pathologic factors involved in the pathogenesis of neurodegenerative diseases. Antioxidants as neutralizing agents of free radicals are one of the treatment options for these diseases and antioxidant agents that can pass through blood brain barrier have beneficial effects. In the present research, the antioxidant effect of a new iron nanochelator on the electrophysiological characteristics of neural cells following H2O2– induced oxidative stress was investigated. Methods:Intracellular recordings were made under the current clamp condition on F1 cells of Helix aspersa. Effects of oxidant agent, H2O2(1 mM), in the presence of the new iron nanochelator at high (2.63 mM) and low (263 µM) concentrations were assessed on the firing pattern and action potential parameters and were compared to the control condition. Results:Application of H2O2led to a significant decrease in the firing pattern and AP amplitude and an increase in the time to peak compared with control condition. Addition of the antioxidant following H2O2treatment increased these parameters and restored them to the control condition. On the other hand, effects of H2O2 on the electrical activity of cell were modulated when the antioxidant was used earlier. Conclusion:Based on the modulating effects of the new synthesized iron nanochelator on verified action potential parameters in the presence of H2O2, it can be concluded that nanochelator probably exerts its antioxidant effects through the alterations of the function of ion channels.
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.
Gholam Hossein Meftahi, Mahyar Janahmadi, Mohammad Javad Eslamizade,
Volume 18, Issue 2 ( Summer 2014)
Abstract

Introduction: Resveratrol (3,5,4-trihydroxystilbene) a non-flavonoid polyphenol found in some plants like grapes, peanuts and pomegranates, possesses a wide range of biological effects. Evidence indicates that resveratrol has beneficial effects on nervous system to induce neuroprotection. However, the cellular mechanisms of the effects are not fully determined. In the present study, the cellular actions of resveratrol on intrinsic electrophysiological properties of the rat hippocampal CA1 pyramidal neurons were examined. Materials and Methods: The spontaneous and evoked firing properties of CA1 pyramidal neurons in adult rats exposed to resveratrol (100 µM) were examined using whole cell patch clamp recording under current clamp condition and the results were compared with control and vehicle treated groups. Results: Treatment with resveratrol caused changes in neuronal firing characteristics. Application of resveratrol shifted the resting membrane potential (RMP) toward hyperpolarizing voltage (from -58.62±0.89 mV in control to -67.06±0.89 mV after resveratrol). The after hyperpolarization potential (AHP) amplitude was significantly (P < 0.001) increased following extracellular application of resveratrol. In addition, resveratrol treatment caused changes in evoked responses of pyramidal neurons. Its treatment induced a significant (P<0.05) increase in the peak amplitude of action potential in response to 100-300pA depolarizing current pulses. Furthermore, resveratrol-treated neurons displayed a significantly (P<0.05) increased time to peak in response to 400 and 500 pA depolarizing currents, when compared with either control or vehicle-treated groups. In addition, rise time to half-amplitude, rise tau and decay tau of action potential were significantly (P<0.01, P<0.01 and P<0.01, respectively) increased following resveratrol application. Conclusion: Resveratrol treatment changes the action potential parameters, hyperpolarizes the RMP and reduces the neuronal excitability and probably thereby may induce neuroprotective effects.
Mahtab Bahrami, Zahra Ghasemi, Mahyar Janahmadi,
Volume 18, Issue 3 (Fall 2014)
Abstract

Introduction: Epilepsy is a neurological disorder that affects 1-2% of the world population and about 30% of patients are resistant to antiepileptic drug therapy. Therefore, new treatment alternatives are needed. In the present study, the possible neuroprotective effect of minocycline against epileptiform activity induced by pentylenetetrazole (PTZ) was assessed. Methods: Conventional intracellular recordings were taken from F1 cells of Helix aspersa, under the current clamp condition. Following extracellular application of minocycline alone (300 and 600 μM) or in combination with PTZ (25 mM), alterations in the firing pattern and action potential wave forms were studied and compared to the control group and the group treated with PTZ alone. Results: In the presence of PTZ alone (25mM), neurons displayed paroxysmal depolarization shift (PDS)-like events and produced burst activity. When PTZ was applied following minocycline pretreatment, it did not produce burst activity, and even reduced the firing frequency. In addition, pre-exposure to minocycline prevented almost some of the changes in the AP shape induced by PTZ treatment. Conclusion: The findings indicated that minocycline may be able to exert preventive effects against induction of epileptiform activity and could be possibly considered as a new treatment option for epilepsy.
Amir Shojaei, Saeed Semnanian, Mahyar Janahmadi, Homeira Moradi, Seyad Mohammad Firoozabadi, Javad Mirnajafi-Zadeh,
Volume 19, Issue 1 (March 2015)
Abstract

Introduction: Considering the antiepileptogenic effects of repeated transcranial magnetic stimulation (rTMS), the effect of rTMS applied during amygdala kindling on spontaneous activity of hippocampal CA1 pyramidal neurons was investigated. Materials and Methods: A tripolar electrode was inserted in basolateral amygdala of Male Wistar rats. After a recovery period, animals received daily kindling stimulations until they reached stage 5 seizure. In one group of animals, rTMS at frequency of 1 Hz were applied to hippocampus once daily at 5 min after termination of kindling stimulations. 24 h after the last kindling stimulation, spontaneous activity of CA1 pyramidal neurons of the hippocampus was investigated using whole cell patch clamp technique. Results: Kindling-induced seizures resulted in increment of spontaneous activity of hippocampal CA1 neurons, but application of rTMS during amygdala kindling prevented it. Moreover, rTMS administration inhibited the kindling-induced enhancement of afterdepolarization (ADP) amplitude and action potential duration. Conclusion: Results of this study suggest that rTMS exerts its anticonvulsant effect, in part, through preventing the amygdala kindling-induced increase in spontaneous activity and excitability of hippocampal CA1 pyramidal neurons.
Sharareh Daryani, Alireza Farzaei, Narges Hosseinmardi, Farideh Bahrami, Mahyar Janahmadi,
Volume 20, Issue 2 (June 2016)
Abstract

Introduction: Although aging is the most important risk factor for Alzheimer's disease (AD), there is evidence indicating that neuroinflammation may contribute to the development and progression of the disease. Several studies indicated that minocycline may exert neuroprotective effects in rodent models of neurodegenerative diseases. Nevertheless, there are also other studies implying that minocycline has no positive beneficial effects. Thus, the aim of the present study was to assess the preventive effect of minocycline against Aβ-induced changes in intrinsic electrophysiological properties in a rat model of AD. Methods: The present study extended this line of research by examining whether inhibition of microglial activation may alter the intrinsic electrophysiological properties of CA1 pyramidal neurons in a rat model of Aβ neurotoxicity, using whole cell patch clamp. Results: Findings showed that bilateral injection of the Aβ (1-42) into the prefrontal cortex caused membrane hyperpolarization, action potential (AP) narrowing and after hyperpolarization (AHP) amplitude enhancement. It was also resulted in a faster decay time of AP, higher rheobase current, lower firing frequency and smaller post stimulus AHP amplitude. Administration of minocycline (45mg/kg, i.p) not only failed to prevent Aβ-induced alterations in the intrinsic electrophysiological properties, but also enhanced the effects of Aβ on neuronal firing behavior. Conclusion: It can be concluded that minocycline, as a microglial inhibitor, may enhance the disruption of electrophysiological properties of CA1 pyramidal neurons induced by Aβ neurotoxin, including AP parameters and intrinsic neuronal excitability.


Mohsen Fathi, Narges Hosseinmardi, Kambiz Rohampour, Mahyar Janahmadi, Ali Sonboli, Jalal Zaringhalam,
Volume 20, Issue 3 (September 2016)
Abstract

Introduction: The management of pain and inflammation related problem is a real challenge that people face daily. Although several drugs are available for these conditions, medicinal plants are believed to be an important source of new chemical substances with potential therapeutic effects. The objective of current study was to investigate the anti-nociceptive effect of Tanacetum Fisherae which has been traditionally used for treatment of pain. Methods: In this experimental study, formalin test was performed with drug (Tanacetum Fisherae) or DMSO pretreatment 30 min prior to formalin injection in 40 male Wistar rats. Fifty microliters of 2.5% formalin was injected into the plantar surface of the right hind paw. Immediately after injection, licking and flinching number and paw-shaking responses were observed at 5-min intervals for 1 h. Animals were divided into five experimental groups. There were 8 animals in each group. Each group received vehicle (7% DMSO) or Tanacetum Fisherae essential oil (25, 50 or 100 μg) or morphine (5 mg/kg). Two-way and one-way ANOVA were used for data analysis. Differences were considered significant at the level of P<0.05 (with 95% confidence interval). Results: Results showed that Tanacetum Fisherae essential oil dose dependently reduced licking and flinching number and also pain score in the late (15-35 min) and recovery phase (35-60 min) of formalin test (p<0.05, p<0.01, and p<0.001). It had no anti-nociceptive effect (p>0.05) in early (0-5 min) phase and interphase (5-15 min). Conclusion: Results demonstrate the effectiveness of Tanacetum Fisherae to mitigate the inflammatory pain.



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