Publications by authors named "Masoud Haghani"

30 Publications

  • Page 1 of 1

Progesterone and anandamide diminish the inhibitory effect of zinc on mature human sperm.

Reprod Fertil Dev 2021 Jul 30. Epub 2021 Jul 30.

Zinc ion (Zn2+) homeostasis is very important for sperm capacitation and hyperactivation. Zn2+ is a specific inhibitor of the voltage-dependent proton channel (Hv1). Intracellular alkalisation of human spermatozoa is mainly dependent on opening of Hv1. Anandamide may affect spermatozoa through activation of Hv1. An increase in intracellular pH and progesterone (P4) activate cation channels of spermatozoa (CatSper). This study was designed to elucidate the interaction between ZnCl2, P4 and anandamide on human sperm function and intracellular calcium concentrations ([Ca2+]i). Human normal semen samples (n=30) were diluted (20×106 spermatozoa mL-1) and divided into control and ethanol (0.01%)-, anandamide (1nM)-, ZnCl2 (1mM)-, P4 (10µM)-, anandamide+ZnCl2- and P4+ZnCl2-treated groups. Sperm kinematics, viability, acrosome status and [Ca2+]i were assessed. The percentage of viable and motile spermatozoa and sperm velocity was reduced in the ZnCl2-treated groups. Anandamide and P4 attenuated the inhibitory effects of ZnCl2 on sperm kinematics. Loss of the acrosome membrane was observed in all experimental groups. P4 and anandamide are present naturally in secretions of the female reproductive tract and modulate the inhibitory effects of ZnCl2 on sperm kinematics. This attenuation is probably due to a change in [Ca2+]i and prevention of Hv1 inactivation by P4 and anandamide respectively.
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http://dx.doi.org/10.1071/RD21043DOI Listing
July 2021

Treatment with edaravone improves the structure and functional changes in the hippocampus after chronic cerebral hypoperfusion in rat.

Brain Res Bull 2021 Sep 9;174:122-130. Epub 2021 Jun 9.

Histomorphometry and Stereology Research Centre, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address:

This study aimed to find out cellular and electrophysiological effects of the edaravone (EDR) administration following induction of vascular dementia (VaD) via bilateral-carotid vessel occlusion (2VO). The rats were randomly divided into control, sham, 2VO + V (vehicle), and 2VO + EDR groups. EDR was administered once a day from day 0-28 after surgery. The passive-avoidance, Morris water-maze, and open-field tests were used for evaluation of memory, locomotor, and anxiety. The field-potential recording was used for assessment of electrophysiological properties of the hippocampus; and after sacrificing, the cerebral hemispheres were removed for stereological study and evaluation of MDA levels. The long-term potentiation (LTP), paired-pulse ratio (PPR), and input-output (I/O) curves were evaluated as indexes for long-term and short-term synaptic plasticity, and basal-synaptic transmission (BST), respectively. The 2VO led to increases in MDA level with considerable neuronal loss and decreases in the volume of the hippocampus, along with a reduction in the BST and LTP induction which was associated with a decrement in PPR and ultimate loss in memory with higher anxiety behavior. However, administration of EDR caused a decline in MDA and prevented the neural loss and volume of the hippocampus, rescued BST and LTP depression, improved memory and anxiety without any effects on PPR. Therefore, most likely through the improvement of MDA level, and the hippocampal cell number and volume, EDR leads to recovery of synaptic plasticity and behavioral performance. Because of the LTP rescue, without recovery of PPR, it is likely that the EDR improved LTP through the post-synaptic neurons.
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http://dx.doi.org/10.1016/j.brainresbull.2021.06.006DOI Listing
September 2021

Co-treatment of vitamin D supplementation with enriched environment improves synaptic plasticity and spatial learning and memory in aged rats.

Psychopharmacology (Berl) 2021 Aug 15;238(8):2297-2312. Epub 2021 May 15.

Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran.

Rationale And Objective: Environmental enrichment (EE) has been shown in old rats to improve learning and memory. Vitamin D (VitD) has also been shown to modulate age-related, cognitive dysfunction. As both EE and VitD could work to improve cognition via enhancement of neurotrophic factors, their effects might occlude one another. Therefore, a clinically relevant question is whether noted cognition-promoting effects of EE and VitD can co-occur.

Methods: Aged rats were housed for 6 weeks in one of three housing conditions: environmentally enriched (EE), socially enriched (SE), or standard condition (SC). Further, a 4th group was co-treated with VitD supplementation (400 IU kg daily, 6 weeks) under EE conditions (EE + VitD).

Results: Treatment with VitD and EE housing were associated with higher score on measures of learning and memory and exhibited lower anxiety scores compared to EE alone, SE or SC as assayed in the elevated plus maze, Morris water maze, passive avoidance, and open field tasks. Additionally, in the EE + VitD group, mRNA expression levels of NGF, TrkA, BDNF, Nrf2, and IGF-1 were significantly higher compared to expression seen in the EE group. Furthermore, field potential recordings showed that EE + VitD resulted in a greater enhancement of hippocampal LTP and neuronal excitability when compared to EE alone.

Conclusions: These findings demonstrate that in aged rats exposure to EE and VitD results in effects on hippocampal cognitive dysfunction and molecular mechanisms which are greater than effects of EE alone, suggesting potential for synergistic therapeutic effects for management of age-related cognitive decline.
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http://dx.doi.org/10.1007/s00213-021-05853-4DOI Listing
August 2021

The emerging role of FTY720 as a sphingosine 1-phosphate analog for the treatment of ischemic stroke: The cellular and molecular mechanisms.

Brain Behav 2021 06 10;11(6):e02179. Epub 2021 May 10.

Histomorphometry and Stereology Research Centre, Shiraz University of Medical Sciences, Shiraz, Iran.

Finding novel and effective drugs for the treatment of ischemic stroke is warranted because there is not a definitive treatment for this prevalent disease. Due to the relevance between the sphingosine 1-phosphate (S1P) receptor and several neurological diseases including ischemic stroke, it seems that fingolimod (FTY720), as an agonist of S1P receptor, can be a useful therapeutic strategy in these patients. FTY720 is the first oral drug approved by the US food and drug administration for the treatment of multiple sclerosis. Three important mechanisms for neuroprotective effects of FTY720 have been described. First, the functional antagonistic mechanism that is associated with lymphopenia and reduced lymphocytic inflammation. This effect results from the down-regulation and degradation of lymphocytes' S1P receptors, which inhibits lymph node lymphocytes from entering the bloodstream. Second, a functional agonistic activity that is mediated through direct effects via targeting S1P receptors on the membrane of various cells including neurons, microglia, oligodendrocytes, astrocytes, and endothelial cells of blood vessels in the central nervous system (CNS), and the third, receptor-independent mechanisms that are displayed by binding to specific cellular proteins that modulate intracellular signaling pathways or affect epigenetic transcriptions. Therefore, we review these mechanisms in more detail and describe the animal model and in clinical trial studies that support these three mechanisms for the neuroprotective action of FTY720 in ischemic stroke.
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http://dx.doi.org/10.1002/brb3.2179DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8213944PMC
June 2021

Chronic exposure to 2.45 GHz microwave radiation improves cognition and synaptic plasticity impairment in vascular dementia model.

Int J Neurosci 2021 Mar 11:1-12. Epub 2021 Mar 11.

Department of Physiology, the Medical School, Shiraz University of Medical Sciences, Shiraz, Iran.

In this study, we evaluated the effects of 2.45 GHz microwave radiation on cognitive dysfunction induced by vascular dementia (VaD). The VaD was induced by bilateral-common carotid occlusion (2-VO). The rats were divided into 4 groups including: control ( = 6), sham ( = 6), 2-VO ( = 8), and 2-VO + Wi-Fi ( = 10) groups. Wi-Fi modem centrally located at the distance of 25 cm from the animal's cages and the animals were continuously exposed to Wi-Fi signal while they freely moved in the cage (2 h/day for forty-five days). Therefore, the power density (PD) and specific absorption rate value (SAR) decreased at a distance of 25 to 60 cm (PD = 0.018 to 0.0032 mW/cm, SAR = 0.0346 to 0.0060 W/Kg). The learning, memory, and hippocampal synaptic-plasticity were evaluated by radial arm maze (RAM), passive avoidance (PA), and field-potential recording respectively. The number of hippocampal CA1 cells was also assessed by giemsa staining. Our results showed that VaD model led to impairment in the spatial learning and memory performance in RAM and PA that were associated with long-term potentiation (LTP) impairment, decrease of basal-synaptic transmission (BST), increase of GABA transmission, and decline of neurotransmitter release-probability as well as hippocampal cell loss. Notably, chronic Wi-Fi exposure significantly recovered the learning-memory performance, LTP induction, and cell loss without any effect on BST. The LTP recovery by Wi-Fi in the 2-VO rats was probably related to significant increases in the hippocampal CA1 neuronal density, partial recovery of neurotransmitter release probability, and reduction of GABA transmissiSon as evident by rescue of paired-pulse ratio 10 ms.
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http://dx.doi.org/10.1080/00207454.2021.1896502DOI Listing
March 2021

Effect of Dimethyl Fumarate on the Motor Function and Spatial Arrangement of Primary Motor Cortical Neurons in the Sub-Acute Phase of Stroke in a Rat Model.

J Stroke Cerebrovasc Dis 2021 Apr 23;30(4):105630. Epub 2021 Jan 23.

Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran; Histomorphometry & Stereology Research Centre, Shiraz University of Medical Sciences, Shiraz, Iran; Department of Anatomical Sciences, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address:

Background: The therapeutic effects of dimethyl fumarate (DMF) in patients with multiple sclerosis and animal models of neurologic disease were reported. The density and the distribution pattern of motor neurons are important in transmitting the signal and controlling the movement-related functions. The present study evaluated the effects of DMF treatment on the neurological functions, infarct volume, and spatial distribution of the neurons in the primary motor cortex after cerebral ischemia.

Methods: Thirty-three Sprague-Dawley rats were randomly divided into three groups: The sham group underwent surgery without middle cerebral artery occlusion (MCAO) and drug. The vehicle and treatment groups after MCAO received a vehicle or DMF for three consecutive days. Post-stroke neurological and motor functions were assessed. At the end of the third day, the brains were removed, and the cerebral infarct volume was evaluated. We used cresyl violet staining to analyze the density and the spatial arrangement of motor cortical neurons using Voronoi tessellation.

Results: Treatment of the brain ischemia for three days with DMF could not significantly reduce the neurological and motor function deficits and infarct volume. However, it reduced the neuronal area and death and preserved their spatial distribution in the normal regular pattern.

Conclusion: Cerebral ischemia decreased the neuronal density of the primary motor cortex and changed their distributions to a random pattern. DMF treatment during sub-acute ischemic stroke did not significantly improve the neurological deficit scores. However, it could prevent neuronal swelling and death and preserved the spatial distribution of the cortical neurons in their normal pattern.
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http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2021.105630DOI Listing
April 2021

Intranasal insulin improves mitochondrial function and attenuates motor deficits in a rat 6-OHDA model of Parkinson's disease.

CNS Neurosci Ther 2021 Mar 26;27(3):308-319. Epub 2021 Jan 26.

Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Aims: Experimental and clinical evidences demonstrate that common dysregulated pathways are involved in Parkinson's disease (PD) and type 2 diabetes. Recently, insulin treatment through intranasal (IN) approach has gained attention in PD, although the underlying mechanism of its potential therapeutic effects is still unclear. In this study, we investigated the effects of insulin treatment in a rat model of PD with emphasis on mitochondrial function indices in striatum.

Methods: Rats were treated with a daily low dose (4IU/day) of IN insulin, starting 72 h after 6-OHDA-induced lesion and continued for 14 days. Motor performance, dopaminergic cell survival, mitochondrial dehydrogenases activity, mitochondrial swelling, mitochondria permeability transition pore (mPTP), mitochondrial membrane potential (Δψ ), reactive oxygen species (ROS) formation, and glutathione (GSH) content in mitochondria, mitochondrial adenosine triphosphate (ATP), and the gene expression of PGC-1α, TFAM, Drp-1, GFAP, and Iba-1 were assessed.

Results: Intranasal insulin significantly reduces 6-OHDA-induced motor dysfunction and dopaminergic cell death. In parallel, it improves mitochondrial function indices and modulates mitochondria biogenesis and fission as well as activation of astrocytes and microglia.

Conclusion: Considering the prominent role of mitochondrial dysfunction in PD pathology, IN insulin as a disease-modifying therapy for PD should be considered for extensive research.
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http://dx.doi.org/10.1111/cns.13609DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7871791PMC
March 2021

Time-dependent effects of platelet-rich plasma on the memory and hippocampal synaptic plasticity impairment in vascular dementia induced by chronic cerebral hypoperfusion.

Brain Res Bull 2020 11 8;164:299-306. Epub 2020 Sep 8.

Department of Physiology, The Medical School, Shiraz University of Medical Sciences, Shiraz, Iran; Histomorphometry and Stereology Research Centre, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address:

The present study aimed to investigate the effects of early and late administration of platelet-rich plasma (PRP) on learning-memory and hippocampal synaptic plasticity impairment in rat model of vascular dementia. Sprague-Dawley rats (6-7 weeks) were randomly divided into control, sham, 2VO + V (bilateral carotid vessel occlusion + vehicle), 2VO + E-PRP (early after 2VO), and 2VO + L-PRP (late after 2VO) groups. The injection of PRP started immediately or on the day 20 after 2VO in 2VO + E-PRP and 2VO + L-PRP, respectively, and continued until 28th day (two-time a week). The passive avoidance and Morris water maze tests were used for evaluation of fear and spatial memory formation. The in-vivo long-term potentiation (LTP) was evaluated by field-potential recording, paired-pulse ratio (PPR) and input-output (I/O) curve which were monitored as indexes for evaluation of short-term plasticity (STP) and basal-synaptic transmission (BST), respectively. The 2VO decreased PPR at inter-stimuli interval (ISI) 10 ms and BST, but injection of PRP in both treated groups rescued the PPR and BST depression. In addition, the induction of LTP, fear and spatial memory performance decreased in the 2VO + V group. However, early treatment, but not late, recovered LTP and memory. The PPR and BST improved with early and late treatment; therefore, the number and time of injection seem to be not important for recovery of BST. However, we found that LTP and memory loss rescued only with early administration. Hence, timely injection, before development of the disease, or number of injections could be critical.
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http://dx.doi.org/10.1016/j.brainresbull.2020.08.033DOI Listing
November 2020

Renal ischemia/reperfusion induced learning and memory deficit in the rat: Insights into underlying molecular and cellular mechanisms.

Brain Res 2019 09 15;1719:263-273. Epub 2019 May 15.

Department of Physiology, The Medical School, Shiraz University of Medical Sciences, Shiraz, Iran; Shiraz Nephro-Urology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address:

Distance organ dysfunction is the major cause of death in the patients with acute kidney injury (AKI). However, the neurobiological basis of AKI-induced brain disorders and their mediators are poorly understood. This study was aimed to find out the links between AKI and brain injury and also the underlying cellular and electrophysiological mechanisms of memory deficit following induction of AKI via different experimental models of renal ischemia with or without uremia and uremia without renal ischemia. Fifty four male Sprague-Dawley rats were divided into 4 groups that underwent 1-h bilateral or 2-h unilateral renal ischemia followed by 1-day reperfusion (BIR and UIR, respectively), and 1-day following bilateral nephrectomy (BNX) or sham-operation. There were 2 subgroups in each group, which blood-brain barrier (BBB) integrity was evaluated in one subgroup. The other subgroup was used for recordings electrophysiological activities of the hippocampus; and after blood sampling and sacrificing animal, the cerebral hemispheres were removed and preserved for performing stereological study and Western-blotting of caspase-3 in the left and right hippocampus, respectively. Plasma urea and creatinine and CA1 neuronal loss were largely increased by BNX and BIR, but slightly by UIR. Apoptosis was stimulated in the hippocampus intensively by BIR but moderately by UIR and BNX. However, BIR and UIR were associated with profoundly disturbed BBB, increased CA1 neuronal excitability, impaired LTP induction and memory deficit. Therefore, AKI most likely through inflammatory mediators leads to hippocampal apoptosis and electrophysiological impairments, BBB disruption and memory loss, whereas uremia may contribute to necrotic neuronal death.
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http://dx.doi.org/10.1016/j.brainres.2019.05.018DOI Listing
September 2019

Inhibition of inflammation is not enough for recovery of cognitive impairment in hepatic encephalopathy: Effects of minocycline and ibuprofen.

Brain Res Bull 2019 07 18;149:96-105. Epub 2019 Apr 18.

Neuroscience Research Centre, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran. Electronic address:

There is evidence that hyperammonia and inflammation play crucial roles in hepatic encephalopathy. This study intends to determine neuroprotective effects of minocycline (MINO) and ibuprofen (IBU), and also set out to assess whether inhibition of inflammation is enough to achieve optimal improvement of hepatic encephalopathy symptoms. The hepatic encephalopathy was induced by bile-duct ligation (BDL), and the animals received first dose of MINO and/or IBU 15 days later and then every day until the 28 day. The rats were divided into the 6 groups of control, sham, BDL + V and BDL + IBU, BDL + MINO and BDL + MINO + IBU, which each group had 3 sub-groups for evaluations of blood-brain barrier (BBB), memory performance, synaptic-plasticity and apoptosis. The long-term potentiation (LTP) and short-term potentiation were evaluated by field potential recording. The memory performance, apoptosis and BBB integrity were assessed via passive avoidance, Western-blotting of caspase-3 and Evans-blue dye extravasation, respectively. The MINO, IBU or their co-treatment in the BDL rats did not improve liver dysfunction. The BDL increased hippocampal apoptosis and BBB disruption, which were fully recovered by all three pharmacological interventions. The MINO treatment alone or combined with IBU had similar neuroprotective effects on the BDL-induced disturbances of hippocampal basal synaptic transmission, LTP and memory performance, whereas they were not ameliorated by the single IBU therapy. Therefore, it seems likely that inhibition of inflammation is not able to improve functionally impaired memory and LTP in the hepatic encephalopathy, and they may be recovered by the direct neuroprotective effects of the MINO.
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http://dx.doi.org/10.1016/j.brainresbull.2019.04.015DOI Listing
July 2019

Modulation of sphingosine-1-phosphate receptor by FTY720 contributes in improvement of hepatic encephalopathy induced by bile duct ligation.

Brain Res Bull 2019 03 17;146:253-269. Epub 2019 Jan 17.

Department of Physiology, The Medical School, Shiraz University of Medical Sciences, Shiraz, 71365-1689, Iran; Histomorphometry and Stereology Research Centre, Shiraz University of Medical Sciences, Shiraz, 71365-1689, Iran. Electronic address:

Hepatic encephalopathy (HE) is a complex neuropsychiatric disorder, which is associated with memory loss and behavioral abnormalities. The cellular and molecular mechanisms that led to hippocampal dysfunction in bile duct ligation (BDL)-induced HE and neuroprotective mechanisms of FTY720 administration were evaluated using whole-cell patch clamp, field-potential recording, western blot, stereology and behavioral experiments. The animals were divided into 4 groups of control (n = 24), sham (n = 21), BDL + V (n = 21) and BDL + FTY720 (n = 20), each having three subgroups. The first subgroup was used for field potential, western blot and stereology experiments. The second and third subgroups were used for behavioral experiments and whole cell patch clamp recording, respectively. The BDL led to considerable loss of hippocampal neurons and apoptosis, along with large impairments in their intrinsic electrophysiological properties, including decrease of firing frequency and increases of first spike latency (FSL), AHP amplitude, irregularity of firing, and half-width, as well as impaired long-term synaptic plasticity and memory. Importantly, FTY720 decreased AHP amplitude probably by direct inhibition of Ca channels and/or KCa currents and improved the FSL and firing irregularity and frequency possibly by decreasing A-type K currents in the BDL + FTY720 group. FTY720 administration in the BDL rats also decreased the release probability, which was evident by the increased paired-pulse ratio, but the increased number of readily releasable pool (RRP) of neurotransmitter. Moreover, the AHP improvement and RRP increment most likely led to recovery of LTP and memory performance. In total, FTY720 ameliorated brain disorders in the BDL rats via its direct neuroprotective and/or indirect anti-inflammatory effects.
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http://dx.doi.org/10.1016/j.brainresbull.2019.01.012DOI Listing
March 2019

Peroxisome proliferator-activated receptor-γ activation attenuates harmaline-induced cognitive impairments in rats.

J Clin Neurosci 2019 Jan 22;59:276-283. Epub 2018 Nov 22.

Intracellular Recording Lab, Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman.

Cognitive and motor disturbances are serious concerns of the tremors induced by motor disorders. Despite the lack of effective clinical treatment, some potential therapeutic agents have been used to alleviate the cognitive symptoms in the animal models of tremor. Recent studies have shown that PPAR-γ agonists have neuroprotective effects. In the current study, the effects of pioglitazone (PIO), a peroxisome proliferator-activated receptor gamma agonist, on harmaline-induced motor and cognitive impairment were studied. Male Wistar rats were divided into vehicle (normal saline), PIO (20 mg/kg i.p.), harmaline (10 mg/kg, i.p.) and PIO + harmaline (PIO injected 2 h before harmaline) groups. Open field, rotarod, wire grip, foot print and Morris water maze tests were used to evaluate the motor and cognitive performance. The results indicated that administration of PIO attenuated harmaline-induced locomotor, anxiety-like behaviors, and spatial learning and memory impairments, but it partially decreased the tremor score. The neuroprotective and anxiolytic effects of PIO demonstrated in the current study can offer the PPAR-γ receptor agonism as a potential therapeutic agent in the treatment of patients with tremor that manifest mental dysfunction.
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http://dx.doi.org/10.1016/j.jocn.2018.11.004DOI Listing
January 2019

2.45 GHz microwave radiation impairs learning, memory, and hippocampal synaptic plasticity in the rat.

Toxicol Ind Health 2018 Dec 21;34(12):873-883. Epub 2018 Oct 21.

Amir Oncology Hospital, Shiraz University of Medical Sciences, Shiraz, Iran.

Microwave (MW) radiation has a close relationship with neurobehavioral disorders. Due to the widespread usage of MW radiation, especially in our homes, it is essential to investigate the direct effect of MW radiation on the central nervous system. Therefore, this study was carried out to determine the effect of MW radiation on memory and hippocampal synaptic plasticity. The rats were exposed to 2.45 GHz MW radiation (continuous wave with overall average power density of 0.016 mW/cm2 and overall average whole-body specific absorption rate value of 0.017 W/kg) for 2 h/day over a period of 40 days. Spatial learning and memory were tested by radial maze and passive avoidance tests. We evaluated the synaptic plasticity and hippocampal neuronal cells number by field potential recording and Giemsa staining, respectively. Our results showed that MW radiation exposure decreased the learning and memory performance that was associated with decrement of long-term potentiation induction and excitability of CA1 neurons. However, MW radiation did not have any effects on short-term plasticity and paired-pulse ratio as a good indirect index for measurement of glutamate release probability. The evaluation of hippocampal morphology indicated that the neuronal density in the hippocampal CA1 area was significantly decreased by MW.
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http://dx.doi.org/10.1177/0748233718798976DOI Listing
December 2018

Acute bilateral common carotid arteries occlusion (2VO) alone could not be a proper method for induction of ischemia in rats.

Biomed Pharmacother 2017 Dec 21;96:1557-1558. Epub 2017 Nov 21.

Department of Physiology, Shiraz University of Medical Sciences, Shiraz, Iran; Histomorphometry and Stereology Research Centre, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address:

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http://dx.doi.org/10.1016/j.biopha.2017.11.102DOI Listing
December 2017

Structural and functional disorders of hippocampus following ischemia/reperfusion in lower limbs and kidneys.

Neuroscience 2017 09 4;358:238-248. Epub 2017 Jul 4.

Department of Physiology, The Medical School, Shiraz University of Medical Sciences, Shiraz 71365-1689, Iran; Shiraz Nephro-Urology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address:

Recent evidence suggests that ischemia/reperfusion (I/R) in an organ may have distance effect on the brain. In this study, the effects of renal I/R, limb I/R or both together on the structural and function of hippocampus were evaluated and compared. Hence, rats were subjected to 2-h bilateral lower limb ischemia, 45-min bilateral renal ischemia, or combined limb and renal ischemia followed by 1-day reperfusion. At 22-h reperfusion, each rat was fixed on a stereotaxic apparatus for performing electrophysiological study on the hippocampus. The long-term potentiation (LTP) was induced by high-frequency stimulation (HFS), and paired-pulse ratio (PPR) was also monitored before and after HFS delivery. After taking blood sample and sacrificing animal, its brain was removed and preserved for stereological study. The limb I/R reduced plasma osmolality that led to synaptic excitement in the hippocampus, where there was a considerable loss of pyramidal cells and markedly impaired short- and long-term synaptic plasticity. The renal I/R largely increased plasma creatinine that might excite basal synaptic transmission. In the rats with combined limb and renal I/R, the hippocampal neuronal loss and impaired synaptic plasticity were the same as those with limb I/R, but basal synaptic transmission was lowered. In conclusion, the 2-h lower limb ischemia compared to 45-min renal ischemia induced more injurious distant effects on the hippocampus after 1-day reperfusion. The combination of renal and limb I/R did not add or potentiate hippocampal neuronal loss and synaptic plasticity impairment, whereas it decreased the basal synaptic transmission with respect to each one alone.
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http://dx.doi.org/10.1016/j.neuroscience.2017.06.058DOI Listing
September 2017

Netrin-1 improves the amyloid-β-mediated suppression of memory and synaptic plasticity.

Brain Res Bull 2017 May 4;131:107-116. Epub 2017 Apr 4.

Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran. Electronic address:

The aim of this study was to investigate the effects of netrin-1 (NT-1) on amyloid-beta (Aβ)-induced impairments in learning-memory and synaptic plasticity. The NT-1 or its vehicle was administered four times into the Aβ+NT or Aβ+V groups, respectively. The Aβ+SNT group received a single dose of NT-1. The Aβ+HNT group received heat-inactivated NT-1. For the learning-memory and synaptic plasticity assessment, field potentials recording and behavioral experiment were used. Bilateral injection of Aβ inhibits induction of long-term potentiation (LTP) and decreased memory performance in all the behavioral tasks. However, only by repeated injection of NT-1, significant recovery of LTP and memory was seen. Although, the delivery of HFS to Aβ+NT group recovered EPSP slope of the maintenance phase when compared with Aβ+V, but it failed to recover the induction phase. It can be assumed that NT-1 may have regulatory effects on the synthesis of key proteins and/or structural changes that are responsible for LTP induction, since the protein synthesis and/or structural changes are required for the maintenance phase of LTP.
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http://dx.doi.org/10.1016/j.brainresbull.2017.03.015DOI Listing
May 2017

Effect of radiofrequency radiation from Wi-Fi devices on mercury release from amalgam restorations.

J Environ Health Sci Eng 2016 13;14:12. Epub 2016 Jul 13.

Ionizing and Non-ionizing Radiation Protection Research Center (INIRPRC), Shiraz University of Medical Sciences, Shiraz, Iran.

Background: Dental amalgam is composed of approximately 50% elemental mercury. Despite concerns over the toxicity of mercury, amalgam is still the most widely used restorative material. Wi-Fi is a rapidly using local area wireless computer networking technology. To the best of our knowledge, this is the first study that evaluates the effect of exposure to Wi-Fi signals on mercury release from amalgam restorations.

Methods: Standard class V cavities were prepared on the buccal surfaces of 20 non-carious extracted human premolars. The teeth were randomly divided into 2 groups (n = 10). The control group was stored in non-environment. The specimens in the experimental groups were exposed to a radiofrequency radiation emitted from standard Wi Fi devices at 2.4 GHz for 20 min. The distance between the Wi-Fi router and samples was 30 cm and the router was exchanging data with a laptop computer that was placed 20 m away from the router. The concentration of mercury in the artificial saliva in the groups was evaluated by using a cold-vapor atomic absorption Mercury Analyzer System. The independent t test was used to evaluate any significant differences in mercury release between the two groups.

Results: The mean (±SD) concentration of mercury in the artificial saliva of the Wi-Fi exposed teeth samples was 0.056 ± .025 mg/L, while it was only 0.026 ± .008 mg/L in the non-exposed control samples. This difference was statistically significant (P =0.009).

Conclusion: Exposure of patients with amalgam restorations to radiofrequency radiation emitted from conventional Wi-Fi devices can increase mercury release from amalgam restorations.
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http://dx.doi.org/10.1186/s40201-016-0253-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4944481PMC
July 2016

Development and Validation of a Persian Version of Dichotic Emotional Word Test.

Iran J Otorhinolaryngol 2016 Mar;28(85):113-9

Department of Biostatistics, School of Management and Medical Information Science, Iran University of Medical Sciences, Tehran, Iran.

Introduction: Emotional words in comparison with neutral words have different hemispheric specialization. It is assumed that the right hemisphere has a role in processing every kind of emotional word. The objective of the present study was the development of a Persian version of the dichotic emotional word test and evaluate its validation among adult Persian speakers.

Materials And Methods: The present study was done on 60 adults, with the age ranging from 18-30 years for both genders, who had no history of neurological disorders with normal hearing. The developed test included eight main lists; each had several dichotic emotional/ neutral pairs of words. Participants were asked to recall as many words in each list as they could after they listened to them. A content validity index was used to analyze the validity of the test.

Results: The mean content validity index score was 0.94. The findings showed that in the left ear, emotional words were remembered more than neutral ones (P=0.007). While in the right ear, neutral words were remembered more (P=0.009). There were no significant differences in male and female scores.

Conclusion: Dichotic emotional word test has a high content validity. The ability to remember emotional words better in the left ear supports the dominant role of the right hemisphere in emotional word perception.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4881879PMC
March 2016

Electrophysiology of cerebral ischemia and reperfusion: First evidence for the role of synapse in ischemic tolerance.

Synapse 2016 09 18;70(9):351-60. Epub 2016 May 18.

Department of Physiology, Shiraz University of Medical Sciences, Shiraz, Iran.

Objective: The subthreshold brain-damaging stimulus may protect the brain from subsequent ischemia; this phenomenon has been named "ischemic tolerance" (IT). We focused on the synaptic properties of the neurons after mild and severe ischemia to determine the association between IT and synaptic efficacy.

Experimental Design: Adult male rats were randomly divided into four experimental groups including control, sham, permanent ischemia (pI/R), and mild ischemia (mI/R). Middle cerebral artery occlusion (MCAO) method was applied to induce brain ischemia. Seven days after the insult, long-term potentiation (LTP) induced by high-frequency stimulation (HFS) and paired-pulse ratio (PPR) were monitored before and after the HFS delivery.

Results: The field potential recording demonstrated that mild ischemia significantly increased the basal synaptic transmission. Additionally, the HFS produced a significant potentiation compared to its baseline level in the mI/R group. Moreover, mild ischemia prevented depression of PPR by HFS. This effect was accompanied by a significant increase in the normalized PPR (PPR after HFS/PPR before HFS) in this group.

Conclusions: Our data indicated that a mild reduction in brain perfusion without permanent lesion can dramatically increase the basal synaptic transmission. This effect may be associated with an increase in the neurotransmitter content of the pre-synaptic neurons. This hypothesis could provide a new insight into the relationship between IT and synaptic efficacy. Synapse 70:351-360, 2016. © 2016 Wiley Periodicals, Inc.
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http://dx.doi.org/10.1002/syn.21910DOI Listing
September 2016

Fingolimod (FTY720) improves hippocampal synaptic plasticity and memory deficit in rats following focal cerebral ischemia.

Brain Res Bull 2016 06 8;124:95-102. Epub 2016 Apr 8.

Department of physiology, Shiraz University of Medical Sciences, Shiraz, Iran; Histomorphometry and Stereology Research Centre, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address:

Fingolimod (FTY720) is a known sphingosine-1-phosphate (S1P) receptor agonist. Several studies have shown the therapeutic efficacy of FTY720 in neurodegenerative disorders. However, the neuroprotective mechanisms in brain ischemia have not been adequately studied. Therefore, the present study aimed to investigate the effects of FTY720 on the impairment of learning and memory and hippocampal synaptic plasticity induced by middle cerebral artery occlusion (MCAO) in ischemic brain injury. Twenty eight male rats were randomly divided into four groups of control (n=7), sham (n=8), ischemic-reperfusion+vehicle (I/R+V; n=7), and I/R+FTY720 (n=6). After 1h of the occlusion of artery, the filament was gently withdrawn to allow reperfusion for the next 7 days. The animals first received a dose of FTY720 (0.5mg/Kg) or its vehicle (intra-peritoneal) twenty-four hours before surgery in I/R+FTY720 and I/R+V groups, respectively. The administration of FTY720 or its vehicle continued every other day. The passive avoidance test and field potential recording were used for evaluation of learning, memory and synaptic plasticity. The brain infarct volume was measured by triphenyltetrazolim hydrochloride (TTC) staining. MCAO caused infarct damage in the rat's brain tissue. The administration of FTY720 significantly reduced the size of the lesion, improved the memory impairment of MCAO rats, and increased the STL time. In addition, the field potential recording demonstrated a marked reduction in induction of long-term potentiation of MCAO animals. However, administration of FTY720 recovers the magnitude of the LTP without any effects on presynaptic plasticity and neurotransmitter release probability. The results of this study demonstrated that MCAO in rats impairs the retention of passive avoidance tasks and multiple injection of FTY720 improved the memory performance after MCAO by LTP induction via post-synaptic mechanisms.
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http://dx.doi.org/10.1016/j.brainresbull.2016.04.004DOI Listing
June 2016

Alterations in the intrinsic electrophysiological properties of Purkinje neurons in a rat model of hepatic encephalopathy: Relative preventing effect of PPARγ agonist.

Brain Res Bull 2016 Mar 17;121:16-25. Epub 2015 Dec 17.

Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman 76198-13159, Iran. Electronic address:

Patients suffering from hepatic cirrhosis (HC) have been shown to have motor and cognitive impairments. The cerebellum, which controls coordinated and rapid movements, is a potential target for the deleterious effects of hyperammonemia induced by bile duct ligation. Therefore, the aim of this study was to determine the mechanisms of motor impairments observed in a rat model of HC and second objective of the current study was to evaluate the possible protective effect of pioglitazone (PIO) on these impairments. Male Wistar rats were used in the current study. Bile duct ligation (BDL) surgery was performed and pioglitazone administration was started two weeks after the surgery for the next four weeks. The effects of pioglitazone on BDL-induced electrophysiological changes of the Purkinje cerebellum neurons were evaluated by Whole-cell patch clamp recordings. Purkinje neurons from the BDL group exhibited significant changes in a number of electrophysiological properties and some alterations partially were counteracted by activation of peroxisome proliferator-activated receptor-γ. Purkinje cells from BDL groups showed a significant increase in the spontaneous firing frequency followed by a decrease in the action potential duration of half-amplitude and spike interval. Chronic administration of pioglitazone could contract this effect of BDL on event frequency and interevent interval, though the difference with the sham group was still significant in the duration of action potential. Results of the current study raise the possibility that BDL may profoundly affect the intrinsic membrane properties of the cerebellar Purkinje neurons and PIO administration can counteract some of these effects.
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http://dx.doi.org/10.1016/j.brainresbull.2015.12.002DOI Listing
March 2016

Enriched environment improves synaptic plasticity and cognitive deficiency in chronic cerebral hypoperfused rats.

Brain Res Bull 2015 Oct 22;119(Pt A):34-40. Epub 2015 Oct 22.

Kerman Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran. Electronic address:

Recent studies have indicated that environmental enrichment (EE) increases the sensorial and social stimulations and leads to strengthened plastic changes in the brain. In models of chronic cerebral hypoperfusion, the ability of an EE to restore the cognition depends on hippocampal synaptic plasticity. The mechanisms for this effect have not, however, been adequately studied. Thus, the aim of the present study was to evaluate the neuroprotective effects and underlying mechanism of environmental enrichment by assessment of spatial memory tasks as well as parameters of synaptic plasticity in rats subjected to occlusion of the bilateral common carotid arteries (2-VO) model. Male Sprague-Dawley rats were used in this study. The model group was established by occlusion of the bilateral common carotid arteries. The animals were tested for learning, memory performance and synaptic plasticity using Morris water maze (MWM), 8-arm Radial Maze (RM), and field potential recording, respectively. The rats subjected to 2-VO in EE exhibited a significantly lower number of working errors and reference errors in RM. Moreover, the enriched environment recovered the memory performance of hypoperfused rats and decreased the swimming time to reach the platform in MWM. In addition, conditions of the environment did not have any effect on baseline synaptic transmission and presynaptic plasticity, but housing the animals in EE rescued the impairment of LTP induction induced by 2-VO. These results suggest that EE ameliorates the LTP and spatial memory impairment induced by 2-VO. Our data indicated that the LTP recovery by EE in the rat models of 2-VO is probably mediated by post-synaptic mechanisms.
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http://dx.doi.org/10.1016/j.brainresbull.2015.10.001DOI Listing
October 2015

The therapeutic potential of berberine against the altered intrinsic properties of the CA1 neurons induced by Aβ neurotoxicity.

Eur J Pharmacol 2015 Jul 8;758:82-8. Epub 2015 Apr 8.

Department of Biochemistry and Molecular & Cellular Biology, School of Medicine, Georgetown University, Washington, DC, United States. Electronic address:

It was demonstrated that treatment with beta amyloid (Aβ) led to extreme alterations in the intrinsic electrophysiological properties of CA1 pyramidal neurons. Also, malfunction of the cholinergic system is correlated to the memory and cognitive impairments. Several new studies have suggested that Berberis vulgaris can act as a cholinesterase inhibitor. The present study aimed to investigate the effects of berberine (BER) on the Aβ-induced impairments in learning and memory. The male Wistar rats were divided into 4 groups of Sham, BER, Aβ and Aβ+BER. The administration of BER or its vehicle started immediately after the injection of Aβ and followed by 13 days. Then, the animals were tested for learning and memory performance using the Morris water maze (MWM) and passive avoidance tests. Then, they were sacrificed for the whole cell patch clamp recording. The results of the MWM and passive avoidance tasks indicated that administration of the BER in the Aβ+BER group prevented the memory impairment induced by Aβ. The results of the whole cell patch clamp also showed that administration of the BER restored the Aβ-induced impairments in the firing frequency, half-width and rebound action potential. These results suggested that administration of the BER could ameliorate neurotoxicity induced by Aβ. However, this neuroprotection impact could be resulted from the balance effect of the Ca(2+) entry. The optimal level of Ca(2+) entry by BER could be a major factor that modified the function of the Ca(2+)-activated K(+) channels and decreased the half-width in the Aβ treated rats.
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http://dx.doi.org/10.1016/j.ejphar.2015.03.016DOI Listing
July 2015

The therapeutic potential of Berberine chloride hydrate against harmaline-induced motor impairments in a rat model of tremor.

Neurosci Lett 2015 Mar 30;590:84-90. Epub 2015 Jan 30.

Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran. Electronic address:

Essential tremor (ET) is a progressive neurological disorder with motor and non-motor symptoms. It has conclusively been shown that modulation of glutamate receptors could ameliorate ET. Recent studies have suggested that Berberine (BBR) has an inhibitory effect on glutamate receptors. Therefore, BBR may have therapeutic effects on ET. In this study, male Wistar rats (n=10 in each group) weighing 40-60 g were divided into control, harmaline (30 mg/kg, i.p.) and berberine (10, 20 or 50mg/kg, i.p, 15 min before harmaline injection) groups. Open field, rotarod, wire grip and foot print tests were used to evaluate motor performance. The results indicated that the administration of BBR (10 and 20mg/kg) attenuated harmaline-induced tremor in rats, but the beneficial effects of BBR could not be identified at dose 50mg/kg. In addition, BBR ameliorated gait disturbance in doses of 10 and 20mg/kg. The high dose of BBR not only failed to recover step width but also showed an adverse effect on left and right step length. The results indicate that BBR only in dose of 20mg/kg recovers mobility duration. The current study found a dose-dependent manner for the therapeutic effects of BBR in ET. Our study provides the initial evidence for the effects of BBR on motor function. Since BBR exerts its effects mainly through regulation of neurotransmitter release or blocke of NMDA receptors, thus, it is predicted that BBR ameliorate harmaline effect through blockade of NMDA receptors or glutamate release. This is an important issue for future research to evaluate the possible mechanisms involved.
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http://dx.doi.org/10.1016/j.neulet.2015.01.078DOI Listing
March 2015

Erythropoietin improves synaptic plasticity and memory deficits by decrease of the neurotransmitter release probability in the rat model of Alzheimer's disease.

Pharmacol Biochem Behav 2015 Mar 29;130:15-21. Epub 2014 Dec 29.

Department of physiology, Shiraz University of Medical Sciences, Shiraz, Iran; Histomorphometry and Stereology Research Centre, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address:

Introduction: Several studies indicate erythropoietin (Epo) to have remarkable neuroprotection in various central nervous system disorders, including Alzheimer's disease (AD). Amyloid beta (Aβ) is believed to be responsible for the synaptic dysfunction that occurs in AD. Therefore, the present study is aimed to investigate the effects of Epo on the Aβ-induced impairments in learning-memory and hippocampal synaptic plasticity.

Materials And Methods: Male Sprague-Dawley rats (200-250 g) were used in this study. After the injection of Aβ, they were injected intra-peritoneal with Epo in the Aβ+Epo group or its vehicle in the Aβ+V group every other day for 12 days. A shuttle box apparatus was used for the passive avoidance learning and memory study. Moreover, paired-pulse ratio (PPR) was monitored before and after tetanic stimulation.

Results: Bilateral injection of Aβ decreased step-through latency (STL), whereas the 12 day administration of Epo significantly improved memory performance in Aβ+Epo group. The field potential recording demonstrated that the in vivo administration of Aβ25-35 led to extreme inhibition in long-term potentiation, this inhibition was accompanied by a significant increase of the normalized PPR (PPR after HFS/PPR before HFS) as an index for release probability. However, administration of Epo recovers the magnitude of the LTP and the extent of normalized PPR.

Conclusion: The results of this study demonstrated that the injection of Aβ25-35 resulted in impaired LTP and the memory process, which is likely mediated through increasing the release probability of neurotransmitter vesicles. In addition, treatment with Epo improved the Aβ-induced deficits in memory and LTP induction, probably via recovering the release probability.
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http://dx.doi.org/10.1016/j.pbb.2014.12.011DOI Listing
March 2015

Looking at the other side of the coin: the search for possible biopositive cognitive effects of the exposure to 900 MHz GSM mobile phone radiofrequency radiation.

J Environ Health Sci Eng 2014 26;12:75. Epub 2014 Apr 26.

Ionizing and Non-ionizing Radiation Protection Research Center (INIRPRC), School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran ; Department of Medical Physics and Medical Engineering, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran ; Medical Physics & Medical Engineering Department, School of Medicine, Imam Hossein, Shiraz, Iran.

Although exposure to electromagnetic radiation in radiofrequency range has caused a great deal of concern globally, radiofrequency radiation has many critical applications in both telecommunication and non-communication fields. The induction of adaptive response phenomena by exposure to radiofrequency radiation as either increased resistance to a subsequent dose of ionizing radiation or resistance to a bacterial infection has been reported recently. Interestingly, the potential beneficial effects of mobile phone radiofrequency radiation are not only limited to the induction of adaptive phenomena. It has previously been indicated that the visual reaction time of university students significantly decreased after a 10 min exposure to radiofrequency radiation emitted by a mobile phone. Furthermore, it has been revealed that occupational exposures to radar radiations decreased the reaction time in radar workers. Based on these findings, it can be hypothesized that in special circumstances, these exposures might lead to a better response of humans to different hazards. Other investigators have also provided evidence that confirms the induction of RF-induced cognitive benefits. Furthermore, some recent reports have indicated that RF radiation may play a role in protecting against cognitive impairment in Alzheimer's disease. In this light, a challenging issue will arise if there are other RF-induced stimulating effects. It is also challenging to explore the potential applications of these effects. Further research may shed light on dark areas of the health effects of short and long-term human exposure to radiofrequency radiation.
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http://dx.doi.org/10.1186/2052-336X-12-75DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4004454PMC
June 2014

Human-Induced Radioresistance as a Possible Mechanism for Producing Biological Weapons: A Feasible Bridge between Radiore-sistance and Resistance to Antibiotics and Genotoxic Agents.

Iran J Public Health 2014 Feb;43(2):247-8

3. The Center for Research in Radiological Sciences, School of Allied Medical Sciences, Shiraz University of Medical Sciences , Shiraz, Iran ; 4. Medical Physics and Medical Engineering Department, School of Medicine, Shiraz University of Medical Sciences , Shiraz, Iran.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4450694PMC
February 2014

CB1 cannabinoid receptor activation rescues amyloid β-induced alterations in behaviour and intrinsic electrophysiological properties of rat hippocampal CA1 pyramidal neurones.

Cell Physiol Biochem 2012 3;29(3-4):391-406. Epub 2012 Apr 3.

Neuroscience Research Centre and Dept. of Physiology, Medical School, Shahid Beheshti University of Medical Sciences, Evin, Tehran.

Background: Amyloid beta (Aβ) is believed to be responsible for the synaptic failure that occurs in Alzheimer's disease (AD), but there is little known about the functional impact of Aβ on intrinsic neuronal properties. Here, the cellular effect of Aβ-induced neurotoxicity on the electrophysiological properties of CA1 pyramidal neurons and the mechanism(s) of neuroprotection by CB1 cannabinoid receptor activation was explored.

Methods: A combination of behavioural, molecular and electrophysiological approaches was used.

Results: Bilateral injections of the Aβ peptide fragment (1-42) into the prefrontal cortex caused a significant impairment in the retention and recall capability in the passive avoidance tasks and significantly increased the level of active caspase-3 in the hippocampus. Whole-cell patch clamp recordings revealed a significant reduction in the intrinsic action potential (AP) frequency and an increase in the discharge irregularity in the absence of synaptic inputs in Aβ treated group. Aβ treatment induced also significant changes in both the spontaneous and evoked neuronal responses. However, co-treatment with ACEA, a CB1 receptor agonist, preserved almost the normal intrinsic electrophysiological properties of pyramidal cells.

Conclusions: In vivo Aβ treatment altered significantly the intrinsic electrophysiological properties of CA1 pyramidal neurons and the activation of CB1 cannabinoid receptors exerted a strong neuroprotective action against Aβ toxicity.
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http://dx.doi.org/10.1159/000338494DOI Listing
August 2012

Protective effect of cannabinoid CB1 receptor activation against altered intrinsic repetitive firing properties induced by Aβ neurotoxicity.

Neurosci Lett 2012 Jan 7;507(1):33-7. Epub 2011 Dec 7.

Neuroscience Research Centre and Department of Physiology, Medical School, Shahid Beheshti Medical Sciences University, Tehran, Iran.

The amyloid β (Aβ) protein is believed to be the key pathological mediator of Alzheimer's disease (AD) which is the first and most well known type of dementia. Despite a growing body of evidence indicating that Aβ neurotoxicity induces changes in synaptic function, little effort, if any, has been made to investigate the effect of in vivo Aβ treatment on intrinsic neuronal properties. The present study was designed to examine the effects that in vivo Aβ treatment have on the intrinsic repetitive firing properties of CA1 pyramidal neurons, using whole cell patch clamp recording. Protective effect of cannabinoid CB1 receptor activation was also investigated against Aβ-induced alterations in evoked electrophysiological activities. The findings from present study demonstrated that a bilateral injection of Aβ into the prefrontal cortex causes robust changes in activity-dependent electrophysiological responses in hippocampal CA1 pyramidal neurons. The effects of Aβ treatment alone was almost completely prevented by combined treatment with Aβ and ACEA, a selective CB1 receptor agonist. It can be concluded Aβ treatment reduces evoked neuronal activity and activation of CB1 cannabinoid receptors may have beneficial preventative effects on Aβ-induced electrophysiological changes.
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http://dx.doi.org/10.1016/j.neulet.2011.11.044DOI Listing
January 2012

Cooperative mechanisms of acute antidiuretic response to bendroflumethiazide in rats with lithium-induced nephrogenic diabetes insipidus.

Can J Physiol Pharmacol 2010 Dec;88(12):1191-201

Department of Physiology, The Medical School, Shiraz University of Medical Sciences, Shiraz 71365-1689, Iran.

The exact mechanism underlying thiazides-induced paradoxical antidiuresis in diabetes insipidus is still elusive, but it has been hypothesized that it is exerted either via Na+-depletion activating volume-homeostatic reflexes to decrease distal delivery, or direct stimulation of distal water reabsorption. This study examined how these two proposed mechanisms actually cooperate to induce an acute bendroflumethiazide (BFTZ)-antidiuretic effect in nephrogenic diabetes insipidus (NDI). Anaesthetized rats with lithium (Li)-induced NDI were prepared in order to measure their renal functional parameters, and in some of them, bilateral renal denervation (DNX) was induced. After a 30 min control clearance period, we infused either BFTZ into 2 groups, NDI+BFTZ and NDI/DNX+BFTZ, or its vehicle into a NDI+V group, and six 30 min experimental clearance periods were taken. During BFTZ infusion in the NDI+BFTZ group, transiently elevated Na+ excretion was associated with rapidly increased urinary osmolality and decreased free water clearance, but Li clearance and urine flow declined in the later periods. However, in the NDI/DNX+BFTZ group, there was persistently elevated Na+ excretion with unchanged Li clearance and urine flow during the experimental period, while alterations in free water clearance and urinary osmolality resembled those in the NDI+BFTZ group. In conclusion, BFTZ initially exerted two direct effects of natriuresis-diuresis and stimulating free water reabsorption at the distal nephron in NDI, which together elevated Na+ excretion and urinary osmolality but kept the urine volume unchanged in the first hour. Thereafter, the resultant sodium depletion led to the activation of neural reflexes that reduced distal fluid delivery to compensate for BFTZ-induced natriuresis-diuresis which, in cooperation with the direct distal BFTZ-antidiuretic effect, resulted in excretion of urine with a low volume, high osmolality, and normal sodium.
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http://dx.doi.org/10.1139/Y10-098DOI Listing
December 2010
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