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Showing 4 results for Ca1 Pyramidal Neurons

Zohre Ghotbeddin, Javad Mirnajafi-Zadeh, Saeed Semnanian, Mahyar Janahmadi,
Volume 16, Issue 1 (4-2012)
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.
Gholam Hossein Meftahi, Mahyar Janahmadi, Mohammad Javad Eslamizade,
Volume 18, Issue 2 (7-2014)
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.
Amir Shojaei, Saeed Semnanian, Mahyar Janahmadi, Homeira Moradi, Seyad Mohammad Firoozabadi, Javad Mirnajafi-Zadeh,
Volume 19, Issue 1 (3-2015)
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 (5-2016)
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.



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