Iranian Society of Physiology and Pharmacology
Physiology and Pharmacology
24765236
24765244
11
4
2008
1
1
Effect of Norepinephrine depletion on induction of experience dependent plasticity in male rat barrel cortex
244
251
EN
Vahid
Sheibani
Neuroscience research center,Kerman university of Medical Sciences
Vsheibani2@yahoo.com
Y
Somaye
Arabzadeh
Neuroscience research center,Kerman university of Medical Sciences
N
Mohamadreza
Afarineshkhaki
Neuroscience research center,Kerman university of Medical Sciences
reza.afarinesh@gmail.com
N
Ali
Shamsizadeh
Neuroscience research center,Kerman university of Medical Sciences
alishamsy@yahoo.com
N
Hossein
Aminizadeh
Neuroscience research center,Sheed Beheshti university of Medical Sciences
N
Saeed
Azizolahi
Neuroscience research center,Kerman university of Medical Sciences
N
Introduction: Barrel cortex of rats is a part of somatosensory cortex, which receives information from facial whiskers. Vibrisectomy by sensory deprivation leads to some changes in the barrel cortex, which have been known as experience dependent plasticity. On the other hand, Norepinephrine (NE) and locus coeruleus, which is the main source of NE, influenced response properties of cortical barrel neurons. In this study, the effect of NE depleted and sensory deprivation on induction of experience dependent plasticity was investigated.
Materials and methods: In this study sixty wistar rats (250±25gr) were used. Rats were divided into four groups: 1.Control group (Intact). 2. NE depleted group in which Norepinephrine was selectively depleted by IP injection of DSP4. 3. Sensory deprivation group that all whiskers (except the whisker D2) on the left side were trimmed every other day. 4. NE depleted + sensory deprivation group.
By using extracellular single unit recordings, the excitatory (magnitude and latency) and initiatory (Conditioning Test Ratio, CTR index) receptive fields of barrel cortical neurons were calculated.
Results: Sensory deprivation led to an increase both in the response magnitude to principle whisker deflection (spared whisker) and in the CTR. In NE depleted + sensory deprivation group, the response magnitude and CTR index were the same as control group.
Conclusion: The result showed that experience dependent plasticity has a facilitating effect on excitatory receptive field while decreasing the inhibitory circuits in the brain. When NE content of the brain was depleted before sensory deprivation, these changes were not seen. We conclude that NE depletion inhibits the plastic changes in the response properties of neurons following sensory deprivation.
Barrel Cortex, Norepinephrine, Rat, Sensory Deprivation
http://ppj.phypha.ir/article-1-370-en.html
http://ppj.phypha.ir/article-1-370-en.pdf
Iranian Society of Physiology and Pharmacology
Physiology and Pharmacology
24765236
24765244
11
4
2008
1
1
Assessment of the effect of nitric oxide within hippocampal CA1 area on spatial learning and memory in morphine dependent rats
252
260
EN
Ali
Pourmotabbed
apourmotabbed@yahoo.com
Y
Parychehr
Yaghmaei
N
Parviz
Imani
N
Seyed Ershad
Nedaei
N
Atefeh
Touhidi
N
Introduction: There are evidences showing the role of nitric oxide in the opiate reward properties. The role of nitric
oxide signaling pathway as an intracellular mechanism on augmentation of long term potentiation in hippocampal CA1
area of rats is also confirmed. It has been also reported that oral morphine dependence facilitates formation of spatial
learning and memory via activation of NMDA receptors located in hippocampal CA1 area of rats. The effect of nitric
oxide within hippocampal CA1 area on the spatial learning and memory processes in morphine dependent rats is
unclear.
Methods: 33 N-MRI male rats (250-350 g) were divided into 4 experimental groups. Two cannulae were
stereotaxically implanted bilaterally into hippocampal CA1 area. After 5 days recovery, animals received morphine
sulfate or sucrose for 30 consecutive days in drinking water. Morris water maze (MWM) studies were performed from
day 26 to 30. In this period animals received bilateral intra-hippocampal CA1 injection of 3μg/ 2 μl L-NAME (NOS
inhibitor) or 2 μl saline (1 μl/site), 1 min before daily experimentation. Spatial learning and memory parameters were
subjected to analysis of variance (ANOVA).
Results: Morphine dependence facilitated spatial learning and memory in rats. This effect was inhibited with local
administration of L-NAME in hippocampal CA1 area.
Conclusion: Activation of intracellular NO signaling pathway in the pyramidal cells of hippocampal CA1 area may
involve in facilitating spatial learning and memory in morphine dependent rats.
Nitric oxide, morphine, hippocampal CA1, spatial learning and memory, rat
http://ppj.phypha.ir/article-1-464-en.html
http://ppj.phypha.ir/article-1-464-en.pdf
Iranian Society of Physiology and Pharmacology
Physiology and Pharmacology
24765236
24765244
11
4
2008
1
1
The role of Na+-K+-ATPase in the basic and rate-dependent properties of isolated perfused rabbit Atrioventricular Node
261
269
EN
Khoori
Vahid
N
Nayebpour
Mohsen
m_nayeb_2000@yahoo.com
Y
Naseri
Mohsen
N
Hoseinkhalehjir
Seyedgholamreza
N
Salehi
Aref
N
Introduction: Ouabaine is a well-known atrioventricular (AV) node depressant agent, but its effects on functional
properties of the AV node have not been cleared. The aim of the present study was to determine how ouabaine
administration modifies the rate-dependent properties of the AV node.
Methods: Selective stimulation protocols were used to quantify independently electrophysiological properties of the
Node. Ouabaine was added directly to superfusion tyrods in a cumulative model (0.05, 0.1, 0.2, 0.25 μM) . The same
stimulation protocols were repeated before and after ouabaine addition. Comparisons among multiple groups were made
by two-way analysis of variance. P<0.05 was considered significant.
Results: Ouabaine decreased fatigue in low concentration (0.05μM), whereas at high concentrations increased the
magnitude of fatigue. Ouabaine (0.2, 0.25 μM) caused significant increase in basic properties of the AV-Node (AVCT,
WBCL, ERP, FRP). WBCL was prolonged by ouabaine (0.25 μM) from 147.5 ± 8.9 to 194 ± 13 msec. Also amount of
facilitating decreased by 0.2 μM ouabaine from 43.3 ± 5 to 38.8 ± 5 msec.
Conclusion: The paradoxical effects of ouabaine on the fatigue indicate potential role of Na+-K+-ATPase in the
protective mechanism of the AV-node.
Isolated heart, rabbit AV Nod ,Ouabaine, Na+-K+ ATPase
http://ppj.phypha.ir/article-1-463-en.html
http://ppj.phypha.ir/article-1-463-en.pdf
Iranian Society of Physiology and Pharmacology
Physiology and Pharmacology
24765236
24765244
11
4
2008
1
1
Investigation on the vasodilatory effect of insulin through KATP channels and NO pathway in the skin vessels of native and diabetic rats
270
275
EN
zahra
Barabadi
Tabiat Modares University
zbarabadi@yahoo.com
N
Sohrab
Hajizadeh
Tabiat Modares University
hajizads@modares.ac.ir
Y
mohammad
Javan
Tabiat Modares University
mjavan@modares.ac.ir
N
batool
Erfani
Tabiat Modares University
batoolerfani@yahoo.com
N
ali
Heidarian pour
Tabiat Modares University
hei
N
Introduction: Endothelium and smooth muscle dysfunction are the most important complications of diabetes. In type 1 diabetic patients, absence of insulin leads to vasoconstriction and lower skin blood perfusion. Release of some mediators by endothelium which is induced by insulin causes vasodilation, but the exact mechanism of insulin vasodilatory effect is not detected properly. At present study we investigated the role of NO as a vasodilator and KATP channels and their intraction in the vasodilatory effect of insulin on the skin vessles.
Methods: Male wistar rats (200-250 gr) were made diabetic by streptozocin (50mg/kg, s.c). After 40 days of diabetes induction, skin blood flow was measured by Laser Doppler Flowmetry technique (LDF). Insulin, LNNA (NO blocker) and Glibenclamide (KATP blocker) infusion were made by infusion pump subcutaneousely.
Results: 1- Insulin increases skin blood flow in both control and diabetic groups and this increase was significantly higher in diabetic group. 2- Insulin vasodilatory effect was decreased by LNNA. 3- The vasodilatory effect of insulin was decreased by Glibenclamide. 4- Simultaneous block of both NO and KATP was more effective.
Conclusion: Insulin induces vasodilation in part by NO release and partly by activation of K ATP channels. However some interaction has been seen between both routes. Although by block of both these routes, blood flow has not been completely inhibited. So it is supposed that other factors may be involved in this effect and yet to be illucidated.
Insulin, Diabetes, skin blood flow, NO, KATP channels.
http://ppj.phypha.ir/article-1-282-en.html
http://ppj.phypha.ir/article-1-282-en.pdf
Iranian Society of Physiology and Pharmacology
Physiology and Pharmacology
24765236
24765244
11
4
2008
1
1
Comparison of pain behavior responses in two peripheral neuropathic models (SNI, CCI) in rat
276
281
EN
Vahide
Mirzaei
Neuroscience research center
N
Homa
Manaheji
Neuroscience research center
hmanaheji@yahoo.com,
Y
Keivan
Keramati
Biology Department of Azad University of damghan
N
Nader
Maghsodi
Neuroscience research center
N
Jalal
Zaringhalam
Neuroscience research center
N
Introduction: Peripheral nerve injury leads to neuropathic pain syndromes and different sensation like allodynia
and hyperalgesia. Different animal models of neuropathic pain are used to study the neuropathic pain mechanisms. The
present study was performed on two models, (SNI). The purpose of this study was comparing the behavioral responses
of yhese two models and the role of saphenous and sural nerve in SNI model.
Methods: Male Wistar rats (180-220 g) were used. CCI models were made by 4 loose legations on common sciatic
nerve. In SNI models, 2 of 3 terminal branches of sciatic nerve were cut and the sural nerve was remained intact. Zero,
4, 7 and 14 days after the operation, thermal hyperalgesia and mechano allodynia were assessed with radiant heat with
von-frey filament.
Results: The results indicated mechano allodynia and thermal hyperalgesia at days 4th, 7th and 14th. In comparison
of SNI and CCI, there was no significant difference in pain behaviors however there was more sensitivity to allodynia
in the SNI model and more sensitivity to hyperalgesia in the CCI model. Saphenous territory showed less allodynia and
hyperalgesia than sural territory.
Conclusion: behavioral testes of CCI and SNI models demonstrated the hypersensitivity to both thermal and
mechanical stimuli. But there were different pain intensity between the sural and saphenous nerve territories in SNI
model. It seems different neuropathy models have different mechanisms and symptoms.
Thermal hyperalgesia, Mechano allodynia, CCI model, SNI model, Rat
http://ppj.phypha.ir/article-1-259-en.html
http://ppj.phypha.ir/article-1-259-en.pdf
Iranian Society of Physiology and Pharmacology
Physiology and Pharmacology
24765236
24765244
11
4
2008
1
1
Central mineralocorticoid receptors mediate impairing effects of corticosterone on memory retrieval in rats
282
292
EN
Mehdi
Khaksari
-
N
Ali
Rashidy-Pour
-
Rashidy-Pour@sem-ums.ac.ir
Y
Abbas Ali
Vafaei
-
aavaf43@yahoo.com
N
Introduction: Previous studies have indicated that stress levels of glucocorticoid hormones induce impairment of long term memory retrieval, but the underlying mechanisms (genomic or non-genomic) are not clear. To clarify this issue, we investigated the involvement of brain corticosteroid receptors and protein synthesis in the glucocorticoid-induced impairment of memory retrieval. Methods: 140 young rats were trained in the water maze (WM) task with six trials per day for six consecutive days. Retention of the spatial training was assessed 24 h after the last training session with a 60-s probe trial. Experiments included intraventricular injections of anisomycin ( 187.5 or 450 µg/5µl) , a specific protein synthesis inhibitor or specific antagonists for mineralocorticoid receptors (MR, 37.5, 75, 150 µg/5ul) or glucocorticoids receptors (GR, 75 or 150 µg/5ul) before corticosterone administration (1 mg/kg) shortly before retention testing. Results: The results showed that administration of anisomycin did not change the corticosterone response. Administration of the MR, but not GR, antagonist blocked the corticosterone-induced response. Conclusion: These findings provide evidence for the view that glucocorticoids impair memory retrieval through non-genomic mechanisms involving an interaction with central MRs.
Glucocorticoids, Mineralocorticoid receptor, Glucocorticoid receptor, Spironolactone, RU 38486, Anisomycin, Memory retrieval, Water Maze
http://ppj.phypha.ir/article-1-384-en.html
http://ppj.phypha.ir/article-1-384-en.pdf
Iranian Society of Physiology and Pharmacology
Physiology and Pharmacology
24765236
24765244
11
4
2008
1
1
Effect of coadministeration of NO and morphine in CA3 of hippocampus on learning and spatial memory in morphine dependent male rats
293
299
EN
Mahshid
Hoseinzadeh
Hosseinzadehmahshid@yahoo.com
N
Iran
Pouraboli
pouraboli_i@mail.uk.ac.ir
Y
Mehdi
Abbasnejad
mabbas@mail.uk.ac.ir
N
Batool
Pouraboli
N
Abstract:
ِIntroduction: The effect of morphine dependency on learning and spatial memory is controversial. So in this study effect of co-administeration of nitric oxide (NO) and morphine in CA3 of hippocampus on learning and spatial memory in morphine dependent rats was investigated.
Methods: After anaesthetization of male rats, cannulae implanted bilaterally in CA3 of hippocampus. After recovery period (7 days), morphine dependency induced then animals divided in 6 groups that received 1μl saline (Sham), L-Arginine, L-Name and morphine individually and L-Arginine with morphine or L-Name with morphine individually. Morphine dependency was induced by subcutaneous injection of morphine(10mg/kg first day and 20mg/kg for four days). Last dose of morphine(20mg/kg) was injected daily to maintain morphine dependency during test period (5 days) in morris water maze
Results: Results showed that L-Name decreased learning in morphine dependent rats although was ineffective on retention of memory. Morphine did not affect learning and spatial memory. Co-administeration of L-Arginine and morphine not only improved the effect of morphine on learning and memory but also promote the effect of L-Arginine on learning and spatial memory.
Conclusion: Thus co-administeration of NO and morphine in morphine dependent rats can improve learning and spatial memory differently from using them individually.
Keywords:Learning,SpatialMemory,Morphinedependency,Hippocampus,NO
http://ppj.phypha.ir/article-1-239-en.html
http://ppj.phypha.ir/article-1-239-en.pdf
Iranian Society of Physiology and Pharmacology
Physiology and Pharmacology
24765236
24765244
11
4
2008
1
1
Central administration of Peganum harmala seeds methanolic extract increases fear behavior in rats
300
305
EN
Vaezi
Gholamhassan
N
Masoud
Fereidoni
N
Leila
Etemadi
ll_etemadi@yahoo.com
Y
Maryam
Sabzali
N
Traditionally, Peganum harmala seeds (P.h) have been extensively used in the Asia region. We have
previously reported the increase of fear behavior by systemic administration of P.h extract. Here, we evaluated the
effect of central administration of the extract on the fear behavior.
Method: Methanolic extract of the plant's seeds (37% humidity) was prepared for the investigation. Elevated plusmaze
apparatus was used for evaluating the fear behavior. Adult male rats were categorized in 7 main groups (n=6). 1)
Sham control (saline 1 ul/rat, i.c.v) 2) Harmaline treated group (50 ug/rat, i.c.v). 3) Extract treated groups (10, 20, 25,
50, 100 ug/rat i.c.v respectively).
Results: All the doses of the P.h Methanolic extract as like as harmaline caused fear behavior (p<0.05). There was
no significant difference between the effects of harmaline and the doses of the plant extract.
Discusion: Overall, it is possible that the main alkaloid of the P.h (harmaline) is responsible for the increasing of
fear behavior. The effect seems to be done trough the central nervous system neurochemical mechanisms.
Peganum harmala , i.c.v, plus-maze, ethanolic extract, rat.
http://ppj.phypha.ir/article-1-69-en.html
http://ppj.phypha.ir/article-1-69-en.pdf
Iranian Society of Physiology and Pharmacology
Physiology and Pharmacology
24765236
24765244
11
4
2008
1
1
Effect of Dexamethasone on Preventing Tibial Nerve Conduction Velocity Loss in Tourniquet Neurepathic Rat
306
311
EN
Morteza
Jarrahi
jarrahi44@yahoo.com
Y
Ali
Rashidipour
N
Introduction: Ischaemic-reperfusion nerve injury has been suggested as the mechanism for post-tourniquet limb paralysis. As dexamethasone (Dex) has been shown to Prevent ischaemic-reperfusion process in some tissues, we tested the hypothesis that this drug would reduce tourniquet induced nerve injury.
Methods: 36 male Wistar rats (200-250 gr) were chosen and divided randomly into 6 equal groups as Sham Operated, Vehicle, Control and treatments (Dex1, Dex2 and Dex3). Tourniquet was applied to the right hind limb of all Animals except of Sham and Vehicle groups for 3 hours at the beginning of experiments. Animals of Control and Vehicle groups were injected by 1 cc vehicle (Normal saline containing 4% ethanol). Animals of Dex1, Dex2 and Dex3 groups were injected by 1mg/kg, 2mg/kg and 3mg/kg dexamethasone solution respectively 30 min before fastening tourniquet, 30 min after releasing tourniquet and daily during the week of experiment. Motor nerve conduction velocity (MNCV) was measured one week after releasing the tourniquet.
Results: MNCV of tibial nerve in response to nerve stimulation were measured at 1 week post-tourniquet release. Application of the tourniquet for 3 h decreased significantly (p<0.001) MNCV in all animals. Dexamethasone administration in doses of 2mg/kg and 3mg/kg (Dex2 and Dex3 groups) resulted in a significant improvement of MNCV (p<0.001) in comparison to Control group.
Conclusion: These data indicated that dexamethasone administration in doses of 2mg/kg and 3mg/kg could prevent nerve conduction velocity loss in tourniquet neurepathic rat.
Tourniquet Neuropathy-Ischaemic-Reperfusion Injury-Dexamethasone- Rat
http://ppj.phypha.ir/article-1-256-en.html
http://ppj.phypha.ir/article-1-256-en.pdf
Iranian Society of Physiology and Pharmacology
Physiology and Pharmacology
24765236
24765244
11
4
2008
1
1
The effect of amygdala lesion on anterior claustrum kindled seizures in rats
312
319
EN
Fariba
Zafari
Neuroscience research center.Cellular and malecular research center
N
Masome
Sabetkasaei
Neuroscience research center
kasai@sbmu.ac.ir
Y
Yousef
Sadeghi
Cellular and malecular research center
N
Mohammad
Mohammad-zade
Department od physiology,Tarbiat modares university.
N
Fateme
Deljo
Pasture institute
N
Introduction: The claustrum interconnects with the allocortical and neocortical regions and also projects to the hippocampus and the amygdala. .The role of claustrum in the complex partial seizure is not clear. Thus in this study the effect of amygdala lesion on anterior claustrum kindled seizures in rat were investigated.
Methods: Male Wistar rats, weighting 250-300 g, were received DC current via a bipolar electrode which is inserted in right basolateral amygdala. A tripolar electrode for stimulation and electroencephalography recording in the right anterior claustrum has been fixed. After a 10 days period of surgical recovery, animals were received kindling stimulation (60Hz, 2s, 1 ms pulse duration) daily, and kindling parameters were measured. In the control group animals did not receive DC current. In the lesion groups (2 groups) animals received DC current both before kindling stimulation and after full kindled statement respectively.
Results: Our result showed that amygdala lesion, were capable of delaying claustrum kindling. The delay in kindling was due to an increase in the stimulation trials required to kindle to seizure stages. Furthermore the effect of this lesion on established kindled seizures reduced the severity of claustrum by decrease the stage 5 duration and after discharge duration.
Conclusion: amygdale lesion had no effect on the expression of generalized seizures and claustrum play an important role in the propagation of epileptic seizure. Whereas the amygdala has a facilitators role in propagation claustrum kindled seizure.
Anterior claustrum, kindling, Amygdala lesion.
http://ppj.phypha.ir/article-1-258-en.html
http://ppj.phypha.ir/article-1-258-en.pdf
Iranian Society of Physiology and Pharmacology
Physiology and Pharmacology
24765236
24765244
11
4
2008
1
1
Study of the effects of maternal hypothyroidism and thyroxin therapy on the neuronal density of subiculum in rat newborns
320
326
EN
Zahra
Delshad
zahradelshad@myway.com
N
Morteza
Behnam Rasouli
behnam@ferdowsi.um.ac.ir
Y
Alireza
Fazel
N
Introduction: It is well established that thyroid hormones are essential for normal development of mammalian
brain. Thyroid hormone deficiency during critical period of brain development can exert devastative and irreversible
effects on neuronal functions as well as on learning abilities and memory. The aim of the present investigation was to
investigate the effects of maternal hypothyroidism on the neuronal structures of the subiculum in an experimental model
of cretinism.
Methods: Twenty five female Wistar rats were divided into experimental groups 1 and 2 and control. The
experimental groups were made hypothyroid (500 mg/L PTU in drinking water). The experimental group 2 received
PTU+Levothyroxin (1mg/L in drinking water). The controls only received drinking water. After two weeks the animals
were mated. During pregnancy and lactation, the treatment regime of all groups was continued as above. The brain of
20 days old newborns were dissected and fixed for histological preparation. The numerical density (NV) of subicular
neurons was estimated by applying a stereological technique "dissector".
Results: In addition to the effects of maternal hypothyroidism on the litter size and offspring weights, the results
showed significant increase of subicular neuronal density in experimental group 1 when compared with control
(p<0.001). There was also a significant difference (p<0.001) between the Nv of experimental groups 1 and 2.
Conclusion: The increased of neuronal Nv in hypothyroid rats was probably due to the retardation of the neuronal
normal growth and extension of their dendritic arborization. It seems that thyroxin therapy can improve the effects of
hypothyroidism on the neuronal structure of subiculum.
Maternal hypothyroidism, subiculum, PTU, rat
http://ppj.phypha.ir/article-1-72-en.html
http://ppj.phypha.ir/article-1-72-en.pdf