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Showing 731 results for Types of Manuscript: Original Research

Leila Hosseinmardi, Abdolhossein Shiravi, Gholam Hossein Meftahi, Mohammad Reza Afarinesh,
Volume 0, Issue 0 (7-2019)
Abstract

Introduction: The basolateral amygdala (BLA) is implicated in stress-related disorders such as anxiety-like behavior. Substantial data exist demonstrating a close relationship between anxiety and adrenergic receptor function in patients with anxiety disorders, however, little is known about the effects of the β1 adrenergic receptor in the BLA on anxiety. These experiments examined the effects of the β1 adrenergic receptor in the BLA on anxiety-like behavior.
Methods: Male Wistar rats were exposed to foot-shock stress four consecutive days that were uncontrollable. The β1-adrenoreceptor agonist (Dobutamine; 0.5 µl/side) or antagonist (Atenolol; 0.25 µl/side) bilaterally infused into the BLA five minutes before foot-shock stress. Anxiety-like behaviors were assessed 24 h after four consecutive day’s uncontrollable stress using Elevated Plus-Maze (EPM) and Open Field Test (OFT).
: Findings of EMP revealed that foot-shock stress leads to effect with reduction the time spent and the number of entries into the open arms, and increased head-dipping. Intra-BLA infusions of Atenolol before stress affected animal behavior differently, such that it significantly (P<0.05) increased the time spent and the number of entries into the open arms and decreased head-dipping. Also, OFT results showed the intra-BLA infusion of Atenolol increased the time periods spent in the center, number of center entries and reduced the number of rearing as compared with the stress group.
Conclusion: These results suggest that the anxiety-like behavior observed after the foot-shock stress is mediated, in part, by exaggerated β1 adrenergic receptor acting at the BLA.

 
Maryam Moosavi, Roksana Soukhaklari, Rasoul Ghasemi,
Volume 0, Issue 0 (7-2019)
Abstract

Introduction: Human neuroblastoma cell line is used in studying Parkinson’s disease (PD) due to its similarities to dopaminergic neurons. 6-hydroxydopamine (6-OHDA), a catecholaminergic neurotoxin, has been widely used to induce cell death in cellular models of PD. Although the brain glucose entry is not dependent on insulin, this peptide has been reported to have a role in PD, in which insulin signaling disruption is reported. This study aimed to evaluate, if insulin is efficient in preventing 6-OHDA induced cell death in human neuroblastoma cells as well as its effect on Phoshorylated Akt (p-Akt)/total Akt (t-Akt) ratio. Methods: The cells -grown in DMEM/F12 media supplemented with 10% fetal bovine serum- were exposed to 6-OHDA with/without insulin for 24 h, and then MTT assay was done to examine their viability. A pilot study was performed to assess the protective doses of insulin, and accordingly the doses 0.9 and 1 mM were selected. Western blot assay was done to evaluate the effect of 6-OHDA or insulin on p-Akt and t-Akt level. Results: The results indicated that insulin has potency to prevent SH-SY5Y cell death, and p-Akt/t-Akt decline induced by 6-OHDA. Conclusion: The results suggested insulin as a protective agent in dopaminergic cells.
Shiva Roshankhah, Cyrus Jalili, Mohammadreza Salahshoor,
Volume 0, Issue 0 (7-2019)
Abstract

Introduction: Petroselinum crispum (P. Crispum) is an associate of Umbelliferae family that has several therapeutic attributes. Ischemia/reperfusion (I/R) is one of the main challenges in acute kidney damage. This study was designed to assess the anti-inflammatory and protective effects of P. Crispum extract against I/R-induced renal disorders.
Methods: Forty male rats were randomly divided into five groups (n = 8) namely normal control (saline) and I/R control group, and three groups of I/R intraperitoneally pretreated with various doses of P. Crispum (100, 150, and 200 mg/kg). The I/R-induced renal inflammation was evaluated by determining leukocyte infiltration and mRNA expression level of intercellular adhesion molecule-1 and tumor necrotic factor-alpha. Antioxidant capacity of kidneys and thiobarbituric acid reactive species were measured in kidneys for the evaluation of oxidative stress. In addition, the diameters of renal glomeruli, kidney function indicators, and serum nitrite oxide levels were respectively determined by morphometric analysis, autoanalyzer device and Griess technique. Data were analyzed by one-way ANOVA test.
 Results: The I/R increased all measured parameters except for the tissue Ferric reducing/antioxidant power (FRAP) level, which was decreased compared to the normal control group (P < 0.001). However, pretreatment with P. Crispum extract in all doses significantly reduced blood urea nitrogen (BUN), kidney malondialdehyde (MDA), creatinine, glomerular diameter, leukocyte infiltration, levels of tumor necrotic factor-alpha, adhesion molecule-1 expression, and nitrite oxide and increased tissue FRAP compared to the I/R control group (P < 0.001).
Conclusion: It seems that P. Crispum administration improves I/R-induced acute kidney injury.

 
Mojtaba Salamtian, Vahid Mohammadi, Seyyed Meysam Abtahi Froushani,
Volume 0, Issue 0 (7-2019)
Abstract

This study was designed to evaluate the effects of cinnamon extract on the treatment and control of inflammation in acetic acid-induced ulcerative colitis in Rats. Thirty-two male Wistar rats were divided into four groups: untreated control, positive control group (acetic acid-induced ulcerative colitis), cinnamon extract treated group (150 mg/kg BW; P.O.daily) and treated group with prednisolone (4 mg/kg BW; P.O.daily). After 10 consecutive days, the rats were euthanized and examined for the production of inflammatory mediators and oxidative stress indices in the intestinal tissue. Obtained data showed that both therapies could reduce the cumulative disease score. The results also indicated that treatment with Cinnamon caused a more benefit in restoring the total antioxidant capacity of the colonic specimens of the colitis induced rats compared to treatment with Prednisolone. The levels of MPO and NO were down-regulated in the guts of Cinnamon treated rats more than Prednisolone groups. Prednisolone significantly decreased the levels of TNF- α and IL-6 cytokines more than colitis rats treated with Cinnamon extract. The levels of COX-2 were decreased and conversely, the total protein content of colonic homogenates was increased in the guts of both treatment groups in a non-significant manner, compared to untreated colitis rats. These results demonstrated treatment with Cinnamon as herbal medicine is a promising strategy to improve the inflammation in a rat model of ulcerative colitis. It is logical to consider some of the beneficial effects of cinnamon extract associated with its direct antioxidant benefits, along with its direct anti-inflammatory benefits.
Firouzeh Gholampour, Sareh Mansouri,
Volume 0, Issue 0 (7-2019)
Abstract

Background: Renal ischemia/reperfusion (IR) is considered as one of the most prevalent reasons of acute renal failure (ARF). As renal failure is progressed, renal gluconeogenesis and insulin clearance are decreased. Berberine is the most important alkaloid of Berberis vulgaris. It has anti-diabetic, anti-inflammatory, and anti-microbial properties. The goal of this study was to assign the effect of RIR on the pancreas and to define the effect of berberine on the pancreatic damages induced by RIR. Methods: Male rats were allocated into four groups (n=7): Sham (no intervention), Ber (Berberine, 15 mg/kg/day), I/R (subjected to 45 min bilateral renal artery occlusion), Ber + I/R (Berberine, 15 mg/kg/day). After 24 hr, blood samples were gathered for biochemical analysis, and eventually pancreas tissue samples were kept for subsequent histological examination. Results: The ischemic challenge of kidneys resulted in pancreatic vascular congestion, which was associated with decreased plasma level of glucose as well as increased plasma insulin, creatinine, and blood urea nitrogen levels at the termination of reperfusion period. In Ber + I/R group, pancreatic vascular congestion and decreased plasma level of insulin were improved concomitant to increase in plasma creatinine and urea nitrogen being smaller than those of the non-treated rats. Berberine exhibited an ameliorative effect on the pancreas against RIR-induced damages. Conclusion: RIR injury has some roles in the development of tissue damages and probably functional disorders of the pancreas in rats. Furthermore, berberine has an ameliorative effect against organ injury induced by RIR in rat.
Hamid Reza Akbari, Farimah Beheshti, Hamid Reza Sadeghnia, Yousef Baghcheghi, Mahmoud Hosseini,
Volume 0, Issue 0 (7-2019)
Abstract

Introduction: Angiotensin converting enzyme (ACE) inhibitors are suggested to have some beneficial effects on the brain. In the present study the protective effects against brain tissues oxidative damage as possible mechanism for learning and memory improving effects of captopril was investigated in scopolamine treated rats.
Material and methods: Fifty male Wistar rats were divided into seven groups and treated: saline as a control group, Sco (scopolamine) and Sco-Capto10, 50 and 100 (captopril 10, 50 and 100 mg/ kg before scopolamine). Treatment was passive avoidance test and then the cortical tissues were collected to measure malondialdehyde (MDA), nitric oxide(NO) metabolites , thiol, super oxide dismutase (SOD) and catalase (CAT).
 Results: Scopolamine decreased the latency to enter the dark in passive avoidance test compared to control group (P<0.01- P<0.001). It also increased MDA and NO metabolites (P<0.001) while decreased thiol, SOD and CAT in comparison with control group (P<0.001). Captopril increased the latency to enter the dark (P<0.05- P<0.001). It also decreased MDA and NO metabolites (P<0.01 P<0.001) while, increased thiol, SOD and CAT (P<0.05- P<0.001).
 Conclusion: Captopril protected from the brain tissues oxidative damage to improve learning and memory impairment induced by scopolamine. 
Miss Zeinab Hamidizad, Shima Ababzadeh, Fatemeh Heidari, Narges-Al-Sadat Haeri, Mohsen Eslami Farsani, Mehdi Sadegh,
Volume 0, Issue 0 (7-2019)
Abstract

Introduction: Cobalamin (vitamin B12) is essential for metabolism of the nervous system and its supplementation attenuate neuropathic and neuroinflammatory diseases. We designed to investigate the neuroprotective effects of Cobalamin against the trimethyltin chloride (TMT) induced structural and functional damages in the hippocampus.
Methods: Adult male Wistar rats were divided into four groups: 1) control: received saline; 2) TMT: received a single dose of TMT (8 mg/kg; i.p) to induce hippocampal damages; 3) Cobalamin: received cobalamin (18 mg/kg; i.p) for five consecutive days; 4) TMT + cobalamin: received single i.p injection of TMT then were treated with cobalamin for five consecutive days. In day six of the experiments, behavioral effects of TMT and Cobalamin were evaluated through shuttle box and novel object recognition task. After the behavioral tests, animals were perfused transcardially and Nissl staining was used on hippocampus to assess neural cell damages.
Results: Novel object exploring time was significantly decreased in TMT treated rats (p< 0.05) and treatment with cobalamin after TMT injection significantly recompensed this effect of TMT (p< 0.05). In passive avoidance TMT significantly decreased latency to enter the dark box (p< 0.001), while cobalamin administration after the TMT injection significantly abolished this effect of TMT (p<0.05). Neural cell counted in the areas of hippocampus was significantly decreased in the TMT group (p< 0.05) and cobalamin treatment after the TMT injection significantly prevented neural cell loss (p< 0.05). Conclusion: These results indicate a neuroprotective role for Cobalamin against the TMT induced memory impairment and hippocampal neuronal loss.
Ali Rashidipour,
Volume 1, Issue 1 (4-1997)
Abstract

Ketamine (KET) induced blockade of cortical spreading depression (CSD) declines with repeated KET applications in a way suggesting the development of tolerance. Possible mechanism of this process was studied in 31 rats anestheized with pentobarbital. CSD was elicited by injection of 1µl of 5% KCl into cortex at 15 min intervals and monitored by recording the accompanying slow potential waves. After control recording, five injections of KET (50 mg/kg) were applied at 75 min intervals. The first KET injection elicited CSD blockade lasting for 30-45 min at the near and for 60- 75 min at the far electrode. The CSD blocking effect of subsequent injections gradually declined and was not recognizable after the fifth KET injection. MK-801 (2 & 5 mg/kg) injected to rats with marked KET tolerance 30 min after the last KET dose, failed to block CSD. Without KET pretreatment the same dosage of MK-801 induced CSD blockade lasting more than 1 h. KET tolerance did not prevent local CSD blockade in cortical area superfused with 10 mol/l AP5. It is concluded that repeated applications of KET may induce some conformational changes at binding site(s) in the N-methyl-D-aspartate (NMDA) controlled channels shared by both KET and MK-801

Volume 1, Issue 1 (4-1997)
Abstract

The results of psychophysical studies suggest that displacement velocity may contribute significantly to the sensation of subcortical somatosensory neurons. The cortical correlates of these phenomena, however, are not known. In the present study the responses of rapidly adapting (RA) neurons in the forelimb region of cat primary somatosensory cortex (SI) to controlled displacement of skin and hair was studied. The cortical RA neurons were grouped according to their response patterns to constant-velocity ramp stimuli. Firing frequency, spontaneous activity, receptive field organization, and cortical laminar location of the RA neurons were studied and compared between the groups. There was a continuum in the response pattern of RA neurons to constant -velocity displacement. In one extent of the continuum, (G1IF1, n = 16) neurons typically responded to constant-velocity ramp stimuli with 1-3 impulses at the beginning of the ramp they had little or no spontaneous activity and responded only to fast stimuli. In the other extent of the continuum, (G2IF2, n = 15) neurons responded throughout the ramp and sometimes during the initial phase of sustained stimuli. These neurons usually had higher spontaneous activities than G1IF1 neurons and responded to relatively slower stimuli. Gint/Fint (n = 18) neurons fell between the two types: they had an initial brief response which was sometimes followed, after a period of low or no activity, by a discharge towards the end of the ramp. Nine neurons had response patterns suggesting the existence of either convergence between these types or input from other types of mechanoreceptors. The average and instantaneous firing frequency of the majority of RA neurons increased as the ramp velocity was increased. The variation in the firing frequency of G2IF2 RA neurons had the widest range of firing frequencies and, in average, generated higher firing frequencies to both low and high displacement velocities. Coefficients of regression lines for linear, logarithmic and power functions were not significantly different among RA types. No correlation was found between cortical laminar location and RA types.
Mohammad Reza Zarrindast, Abolghasemi, Masoumeh Sabetkasai,
Volume 1, Issue 1 (4-1997)
Abstract

In the present study, the effects of different doses of nicotine on immobility time in mice were tested. Intraperitioneal administration of low doses of nicotine (0.025 mg/kg) decreased, but higher doses (0.8 and 1 mg/kg) increased immobility time. The anti-immobility response induced by low doses of nicotine was inhibited by high doses of the D2 receptor antagonist sulpiride, the central nicotinic receptor antagonist mecamylamine, reserpine and propranolol. The D1 receptor antagonist SCH 23390, the peripheral D2 receptor antagonist domperidone, hexamethonium, phenoxybenzamine and atropine did not alter nicotine effect. It can be concluded that the anti-immobility effect induced by low doses of nicotine is mediated by D2 dopamine receptor mechanism and possibly through a central nicotinic receptor stimulation.

Volume 1, Issue 1 (4-1997)
Abstract

  Electrocochleography (ECoG) records the electrophysiologic activity of the most peripheral part of the auditory system, the inner ear cochlea and the 8th nerve. Auditory evoked potentials being recorded are Cochlear Microphonic (CM) and Summating Potential (AP). In order to provide the proper background for laboratory research and introducing an ECoG curve of a model animal, it was decided to record the ECoG from rabbit. Rabbits of either sex weighting about 2 kg (n=25) were experimented upon. Evoked auditory potentials to clicks of 75 and 85 dB were analyzed off-line and compared with human data obtained from a clinical audiometry laboratory. The results are as followed: -SP/AP amplitude and latency showed no significant difference in either intensities, in rabbit. -SP and AP amplitude and latency were significantly greater in rabbit. -The ratio of SP/AP amplitude and latency in rabbit and human indicated no differences. -AP amplitude in 75 dB intensity was greater in the right ear compared with the left (p ≤0.05) however, in other cases, amplitude of waves was greater in the left ear (p ≤0.05).



Volume 1, Issue 1 (4-1997)
Abstract

On most adrenergic and cholinergic nerve terminals, prejunctional α-adrenoceptors belonging to the α2-subtype have been identified. Activation of these receptors will decrease the release of norepinephrine. It has been reported that several isolated tissue preparations contain prejunctional dopamine receptors, the stimulation of which inhibits neurotransmission. It has remained uncertain whether the inhibition of cholinergic transmission in the smooth muscle of different tissues is mediated by prejunctional α-adrenoceptors or prejunctional dopaminoceptors. On the basis of these findings we aimed to examine the effects of dopamine and α-adrenergic receptor agonists on twitch response evoked by electrical stimulation of guinea pig common bile duct (CBD). Effects of various doses of bromocriptine and apomorphine, dopamine receptor agonists, on electrically evoked contractile responses of guinea pig CBD were investigated in this study. Bromocriptine and apomorphine produced a concentration -dependent reduction of the twitch heights. IC50 values for bromocriptine and apomorphine were 2.75 ± 0.715 x 10-6 M and 1.69 ± 0.l1 x 10-5 M, respectively. Pretreatment with sulpride, 0.1 and 1.0 µM prevented bromocriptine and apomorphine induced inhibition. PA2 values of sulpiride against bromocriptine and apomorphine were 8.26 and 6.29, respectively. Clonidine, 0.1 -100 µM, produced 49.3 ± 2.5% inhibition of twitch responses. Its effect was partially antagonized by yohimbine (l µM). It is concluded that both dopamine D2 and adrenergic α2 prejunctional receptors are present on the guinea-pig CBD cholinergic nerve and it seems that the role of dopamine D2-receptors is dominant. D2-dopaminoreceptor and α2-adrenoceptor agonists may relieve the biliary spasm.
Farshad Alizadeh Mansouri, Fereshteh Motamedi, Fereshteh Fathollahi, Nafiseh Atapour, Saeed Semnanian,
Volume 1, Issue 1 (4-1997)
Abstract

The effects of chronic morphine administration on the development of long-term potentiation (LTP) were investigated at the Schaffer collateral-CA1 pyramidal cell synapses of the rat hippocampal slices using primed-bursts tetanic stimulation. Significant enhancement of orthodromic population spike (OPS) was found for all stimulus intensities after tetanic stimulation. OPS enhancement was greatest when tested with low to mid-range stimulus intensities (25, 50 and 100 µA). There was also significant decrease in OPS delay. These responses were similar in slices from both control and morphine dependent rats. At all delivered stimulus intensities, the amount of LTP of OPS in slices from dependent rats was larger than that of control slices. However, these differences in LTP of OPS were significant at low stimulus intensities. These findings suggest that chronic morphine administration had induced changes in CA1 neurocircuitry which modulated synaptic plasticity during high frequency stimulation and appeared as augmented LTP and also inhibition of LTP decay.
Farshad Alizadeh Mansouri, Fereshteh Motamedi, Fereshteh Fathollahi, Nafiseh Atapour, Saeed Semnanian,
Volume 1, Issue 1 (4-1997)
Abstract

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



Volume 1, Issue 1 (4-1997)
Abstract

  Iodine deficiency remains a major health problem in the world, including some parts of Iran. It has been recognized that there is usually a close and inverse relationship between iodine in the soil and water and presence of endemic goiter. Calcium has been suggested as one of goitrogens, though the definite role, extent and mechanism particularly in human have not been studied. Serum protein-bound iodine and urinary iodine excretion in male and female volunteers were investigated. To measure serum iodide concentration, blood samples were collected from 26 male and female subjects, with normal diet and two hours after consumption of calcium (10 mg/kg b.w.), iodine (5 µ g/kg b.w.) or iodine plus calcium. In another study carried out on 33 male and female volunteers, urinary iodine excretion during four different conditions was measured. The results indicate that high calcium intake with normal diet does not significantly effect serum protein-bound iodine concentrations, but high calcium intake plus iodine with normal diet can significantly increase serum protein-bound iodine concentrations. The result of this study, suggest that calcium significantly affects the iodine metabolism, when iodine intake is low.



Volume 1, Issue 1 (4-1997)
Abstract

  TBS (Theta Burst Stimulation) and PBs (Primed Bursts) are among effective tetanic stimulations for induction of LTP in hippocampus. Recent studies have indicated that TBS is effective in LTP induction in layer III synapses of neocortex, only if applied to layer IV. However, the possibility of neocortical LTP induction using PBs, has not yet been investigated. Sensory deprivation greatly influences the development of neocortex. Based on the effect of sensory deprivation on synaptic plasticity of developing neocortex, the induction of LTP by PBs in visual cortical slices of control and dark-reared rats, was studied. Results obtained show that application of PBs to layer IV, could effectively induce LTP. Field potential recordings consisted of two components pEPSPl and pEPSP2. In most cases PBs lead to selective potentiation of pEPSP2. Visual deprivation increased the incidence of LTP of pEPSP2 and also increased the incidence of LTD of pEPSP2. These findings show that PBs could be used as an effective tetanic stimulation to study the synaptic plasticity in neocortex. The effects of visual deprivation on LTP/LTD are consistent with its role on the development of NMDA system in neocortex.


Saeed Semnanian, Ghasem Attarzadeh, Mohammad Hossein Pourgholami,
Volume 1, Issue 1 (4-1997)
Abstract

Recently, vast studies have been focused on the antinociceptive and anesthetic effects of α2 adrenergic receptors, using specific drugs such as medetomidine and dexmedetomidine. In the present study, we tried to assess the peripheral and central effects of dexmedetomidine in phasic and tonic pain, on rats, using tail flick and formalin tests. Dexmedetomidine, administered intraperitoneally (25, 50 and 100 µg/kg, i.p.) or intracerebroventrically (7.5, 10 and 20 µg, i.c.v.) induced total anesthesia. This effect could be seen by 10 and 20 µg, i.c.v. doses of the drug in spinal animals, too, which was reversed by 5 µg, i.c.v. of yohimbine. Dexmedetomidine (6.5 µg, i.c.v. or 20 µg, i.p.) showed antinociceptive effects in formalin test which was reversed by yohimbine (5 µg, i.c.v.). Dexmedetomidine (5, 6.5, 7.5, 10 and 20 µg, i.c.v. or 20, 25, 50 and 100 µg/kg, i.p.) had significant antinociceptive effects in tail flick test, which could be reversed by 5 µg, i.c.v. administration of yohimbine. The results of tail flick test in the spinal animals, shows that dexmedetomidine (6 µg, i.c.v.) in these animals induces antinociception, which was reversed by yohimbine pretreatment (1 mg/kg, i.p.). These results indicate that, dexmedetomidine probably exerts, its antinociceptive effect, through spinal α2 adrenergic receptors.
Fereshteh Motamedi, Ali Pourmotabbed, Yaghub Fathollahi, Farshad Alizadeh Mansouri, Saeed Semnanian,
Volume 1, Issue 2 (11-1997)
Abstract

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



Volume 1, Issue 2 (11-1997)
Abstract

  The effect of different doses (1-50 µ M) of imipramine (IMI) and desipramine (DES) on the rate and force of contraction of isolated rat atria was studied. IMI and DES produced a dose-dependent increase in force of contraction (31- 94% for IMI and 35-118% for DES). Pretreatment of rats with reserpine (5 mg/kg) on the isolated atria with propranolol (1 µ g) inhibited the positive ionotropic effect of both drugs. The two antidepressants IMI and DES showed a dose-dependent decrease in rate of contractions (19-87% and 16-88%, respectively). The positive ionotropic and negative chronotropic effects induced by these drugs was significantly prevented by a selective A1 antagonist (DPCPX, 3 µ M). The effects of IMI (5 µ M) and DES (5 µ M) the rate and contractile force was inhibited by atropine (10 nM). The selective A2 antagonist (DMPX, 1.5 µ M) prevented the ionotropic effect produced by IMI and DES. We conclude that in rat atria, the positive ionotropic action of IMI and DES is due to their action on adrenergic, muscarinic, adenosine A1 and A2 receptors, and Ca2+ influx or release from intracellular storages of the rat myocytes. The negative chronotropic action of these two drugs is probably due to the involvement of adenosine A1 receptors and cholinergic mechanisms.



Volume 1, Issue 2 (11-1997)
Abstract

In this study the effect of adrenergic receptor agonists and antagonists on physostigmine induced yawning was investigated. Intraperitoneal injection of different doses of physostigmine (0.03, 0.05, 0.1 and 0.2 mg/kg) caused yawning in white rats. The greatest response was seen at a dose of 0.2 mg/kg physostigmine. Phenylephrine, an α1 agonist, and clonidine, an α2 agonist, led to a decrease in physostigmine-induced yawning. Prazosine and high-dose phenoxybenzamine decreased the inhibitory effect of phenylephrine. Also, high doses of yohimbine decreased the effect of clonidine. Adrenergic receptor antagonists phenoxybenzamine, prazosine and propranolol had no significant effect on the physostigmine-induced response, while the α2 antagonist (yohimbine) and low-dose prazosine decreased physostigmine's effect. Based on these results, we may conclude that activation of α1 and α2 receptors leads to a decrease in physostigmine-induced yawning in rats.

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