Physiology
Fereshteh Anbarian; Esmaeal Tamaddonfard; Amir Erfanparast; Farhad Soltanalinejad-Taghiabad
Volume 14, Issue 10 , October 2023, , Pages 549-557
Abstract
The cerebellum and its deep nuclei contribute to the regulation of important functions including motor coordination and pain. Histamine modulates some functions of the fastigial nucleus (FN) such as motor coordination. In this study, by application of histamine and activation of its H1 and H2 receptors, ...
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The cerebellum and its deep nuclei contribute to the regulation of important functions including motor coordination and pain. Histamine modulates some functions of the fastigial nucleus (FN) such as motor coordination. In this study, by application of histamine and activation of its H1 and H2 receptors, the FN processing of visceral pain, general locomotor activity and motor coordination were targeted. The possible mechanism of action was followed by the inhibition of opioid receptors. The right and left sides of the FN were surgically implanted with guide cannulas. Immediately after an intraperitoneal injection of acetic acid (1.00 mL, 1.00%), the first writhing onset latency and the writhing number over 60 min were recorded. Open-field and rotarod tests were applied for general locomotor and motor coordination assessment, respectively. Histamine and dimaprit (H2 receptor agonist) increased first writhing onset latency, decreased the writhing number and increased falling time from the rod. These effects were prevented by ranitidine (H2 receptor antagonist) pre-treatment. Significant alterations were not observed by histamine H1 receptor agonist (2-pyridylethylamine) and antagonist (mepyramine). Naloxone, with no effect on falling time from the rod, inhibited the antinociceptive effects of histamine and dimaprit. Beam break number was not affected by the above-mentioned treatments. Based on the results, it can be suggested that histamine H2, but not H1 receptors at the FN might have had an inhibitory role on acetic acid-induced visceral pain and improved motor coordination. The antinociception, but not motor coordination might be mediated by FN opioid receptors.
Sara Salimi; Esmaeal Tamaddonfard; Farhad Soltanalinejad-Taghiabad
Volume 12, Issue 4 , December 2021, , Pages 429-436
Abstract
The aim of the present study was to investigate the effects of intra-ventrolateral periaqueductal gray (vlPAG) microinjection of histamine and thioperamide (a histamine H3 receptor antagonist/inverse agonist) on neuropathic pain. To explore the possible mechanism, naloxone was microinjected alone or ...
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The aim of the present study was to investigate the effects of intra-ventrolateral periaqueductal gray (vlPAG) microinjection of histamine and thioperamide (a histamine H3 receptor antagonist/inverse agonist) on neuropathic pain. To explore the possible mechanism, naloxone was microinjected alone or in combination with histamine and thioperamide. Neuropathic pain was induced by the left sciatic nerve chronic constriction injury. Both the right and left sides of vlPAG of the brain were surgically cannulated. Cold allodynia and mechanical hyperalgesia were recorded by acetone evaporation and von Frey filament tests. Areas under curve of allodynia and hyperalgesia were calculated. Histamine (0.50 and 2.00 µg per site), thioperamide (4.00 µg per site) and thioperamide (4.00 µg per site) before histamine (2.00 µg per site) suppressed cold allodynia and mechanical hyperalgesia after microinjection into the vlPAG. Microinjection of naloxone (0.25 and 1.00 µg per site) into the vlPAG had no effect on cold allodynia and mechanical hyperalgesia. The anti-allodynic and anti-hyperalgesic effects induced by microinjection of histamine (2.00 µg per site) and thioperamide (4.00 µg per site) into the vlPAG were inhibited by prior microinjection of naloxone (1.00 µg per site) into the same site. The above-mentioned agents did not alter locomotor activity. Based on our present results, it was concluded that exogenous (by histamine microinjection) and endogenous (by thioperamide microinjection) histamine of the vlPAG might contribute to the descending pain control mechanisms through a naloxone-sensitive mechanism.
Farshad Safaei; Esmaeal Tamaddonfard; Saeed Nafisi; Mehdi Imani
Volume 12, Issue 2 , June 2021, , Pages 149-156
Abstract
This study was designed to investigate the effects of peripheral [intraperitoneal (IP)] and central [intracerebroventricular (ICV)] administration of cinnamaldehyde on concentrations of blood glucose and serum insulin in the acute hyperglycemia induced by ketamine/xylazine. Yohimbine (a α2-adrenoceptor ...
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This study was designed to investigate the effects of peripheral [intraperitoneal (IP)] and central [intracerebroventricular (ICV)] administration of cinnamaldehyde on concentrations of blood glucose and serum insulin in the acute hyperglycemia induced by ketamine/xylazine. Yohimbine (a α2-adrenoceptor antagonist) was used alone and in combination with cinnamaldehyde to explore the α2-adrenergic receptor contribution. A total of 48 rats were divided into eight groups with six rats in each for IP administration of normal saline, vehicle, cinnamaldehyde (25.00, 50.00 and 100 mg kg-1), yohimbine (0.50 and 2.00 mg kg-1) and cinnamaldehyde plus yohimbine. These rats were used again for ICV administration 15 days after the completion of IP experiment. During this 15 days period, the lateral ventricle of the brain was surgically cannulated for ICV administration of normal saline, vehicle, cinna-maldehyde (25.00, 50.00 and 100 µg per rat), yohimbine (5.00 and 20.00 µg per rat) and cinnamaldehyde plus yohimbine. Blood glucose levels were measured from tail blood using a glucometer and serum insulin concentrations were determined via enzyme-linked immune-sorbent assay kit. The increased levels of blood glucose and the decreased concentrations of serum insulin were significantly decreased and increased, respectively, by separate and combined IP and ICV administrations of cinnamaldehyde and yohimbine. The systemic effects of these chemical compounds were significantly greater than the central ones. Based on the results, it can be argued that cinnamaldehyde has a potential to induce anti-hyperglycemic and antihypoinsulinemic effects. Peripheral and central α2-adrenegic receptors might be involved in these effects of cinnamaldehyde.
Pathology
Masoumeh Moradi-Arzeloo; Amir Abbas Farshid; Esmaeal Tamaddonfard; Siamak Asri-Rezaei
Volume 7, Issue 1 , March 2016, , Pages 47-54
Abstract
In the present study, we investigated the effects of histidine and vitamin C (alone or in combination) treatments against isoproterenol (a β-adrenergic receptor agonist)-induced acute myocardial infarction in rats. We used propranolol (a β-adrenergic receptor blocker) to compare the results. ...
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In the present study, we investigated the effects of histidine and vitamin C (alone or in combination) treatments against isoproterenol (a β-adrenergic receptor agonist)-induced acute myocardial infarction in rats. We used propranolol (a β-adrenergic receptor blocker) to compare the results. Rats were given intraperitoneal injections of histidine (40 mg kg-1) and vitamin C (40 mg kg-1) alone and combined daily for 21 days. Propranolol (10 mg kg-1) was orally administered daily for 10 days (from day 11 to day 21). Myocardial infarction was induced by subcutaneous injections of 150 mg kg-1 of isoproterenol at an interval of 24 hr on days 20 and 21. Blood and tissue samples were taken for histopathological and biochemical evaluations following electrocardiography recording on day 21. Isoproterenol elevated ST segment, increased heart weight, heart rate, serum activities of aspartate transaminase, lactate dehydrogenase, creatine kinase-MB and heart tissue content of malondialdehyde, and decreased R wave amplitude and superoxide dismutase and catalase activities of heart tissue. Necrosis, edema and inflammatory cells infiltration were observed in myocardial tissue sections. Our results indicated that histidine and vitamin C alone, and especially in combination prevent isoproterenol-induced cardiotoxicity and have similar protective effects with propranolol. Cardioprotective effects of histidine and vitamin C may be associated with their ability to reduce free radical-induced toxic effects.
Physiology
Esmaeal Tamaddonfard; Amir Erfanparast; Mina Taati; Milad Dabbaghi
Volume 5, Issue 1 , March 2014, , Pages 49-54
Abstract
Calcium, through its various channels involves in local, spinal and supra-spinal transmission of pain. In the present study, we investigated the separate and combined treatment effects of verapamil (a calcium channel blocker), morphine (an opioid agonist) and naloxone (an opioid antagonist) on pain in ...
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Calcium, through its various channels involves in local, spinal and supra-spinal transmission of pain. In the present study, we investigated the separate and combined treatment effects of verapamil (a calcium channel blocker), morphine (an opioid agonist) and naloxone (an opioid antagonist) on pain in the orofacial region of rats. Orofacial pain was induced by subcutaneous (SC) injection of formalin (50 µL, 1.5%) into the left upper lip side, and the time durations spent face rubbing with epsilateral forepaw were recorded in three min blocks for a period of 45 min. Formalin induced a biphasic pattern (first phase: 0-3 min; second phase: 15-33 min) of pain. Intraperitoneal (IP) injections of verapamil (2 and 8 mg kg-1) and morphine (2 and 4 mg kg-1) suppressed orofacial pain. Co-administration of sub-analgesic doses of verapamil (0.5 mg kg-1) and morphine (1 mg kg-1) produced second phase analgesia. Both phases of formalin-induced pain were suppressed when an analgesic dose (2 mg kg-1) of verapamil co-administered with a sub-analgesic dose (1 mg kg-1) of morphine. The SC injection of naloxone (2 mg kg-1) alone with no effect on pain intensity, prevented the antinociceptive effects induced by morphine (2 mg kg-1), but not verapamil (2 mg kg-1). The obtained results showed antinociceptive effects for verapamli and morphine on orofacial pain. Co-administrations of verapamil and morphine produced antinociceptive effects. It seems that opioid analgesic system may not have a role in the verapamil-induced antinociception.
