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Masoumeh Jorjani - One of the best experts on this subject based on the ideXlab platform.

  • the demyelination and altered motor performance following Electrolytic Lesion in the ventrolateral white matter of spinal cord in male rats benefit of post injury administration of estradiol
    Physiology and Pharmacology, 2016
    Co-Authors: Mina Afhami, Kobra Naseri, Elham Saghaei, Fatemeh Abbaszadeh, Mohammad Javan, Masoumeh Jorjani
    Abstract:

    Abstract Introduction: Spinal cord injuries are accompanied with significant demyelination of axons and subsequent locomotor dysfunction. To identify the extent of damage following Electrolytic Lesion of ventrolateral white matter, essential area for initiation of locomotor activity, we assessed demyelination as well as alteration in motor performance. Moreover, the protective effect of estradiol as a candidate treatment for preservation of myelin and locomotor activity after injury was examined due to its antiapoptotic and anti-inflammatory activities. Methods: A unilateral Electrolytic Lesion positioned in the right ventrolateral funiculus (VLF) was applied following laminectomy at T8-T9. In the estradiol-treated injury group, animals received a pharmacological single dose of estradiol valerate (4 mg/kg) at 30min post injury. Locomotor function was assessed using rotarod and open field tasks during 4 weeks after injury. Results: Obtained results showed significant demyelination at the site of injury and caudal areas following Lesion as well as altered motor performance. Post-spinal cord injury administration of estradiol enhanced white matter maintenance at the site of Lesion, restored the level of myelin basic protein (MBP), decreased TUNEL positive cells and improved functional recovery. Conclusion: Taken together, these results indicate that demyelination after Lesion in VLF may be a contributing factor to limited motor performance, and suggest that pharmacological doses of estradiol may have an early protective effect through sparing of white matter

  • aromatase inhibition exacerbates pain and reactive gliosis in the dorsal horn of the spinal cord of female rats caused by spinothalamic tract injury
    Endocrinology, 2014
    Co-Authors: Samar Ghorbanpoor, Ali Haerirohani, Luis M Garciasegura, Fariba Khodagholi, Masoumeh Jorjani
    Abstract:

    Central pain syndrome is characterized by severe and excruciating pain resulting from a Lesion in the central nervous system. Previous studies have shown that estradiol decreases pain and that inhibitors of the enzyme aromatase, which synthesizes estradiol from aromatizable androgens, increases pain sensitivity. In this study we have assessed whether aromatase expression in the dorsal horns of the spinal cord is altered in a rat model of central pain syndrome, induced by the unilateral Electrolytic Lesion of the spinothalamic tract. Protein and mRNA levels of aromatase, as well as the protein and mRNA levels of estrogen receptors α and β, were increased in the dorsal horn of female rats after spinothalamic tract injury, suggesting that the injury increased estradiol synthesis and signaling in the dorsal horn. To determine whether the increased aromatase expression in this pain model may participate in the control of pain, mechanical allodynia thresholds were determined in both hind paws after the intrathe...

  • in vivo microdialysis of glutamate in ventroposterolateral nucleus of thalamus following Electrolytic Lesion of spinothalamic tract in rats
    Experimental Brain Research, 2014
    Co-Authors: Ali Ghanbari, Alireza Asgari, G R Kaka, H R Falahatpishe, Asieh Naderi, Masoumeh Jorjani
    Abstract:

    Central pain is one of the most important complications after spinal cord injury (SCI), and thereby, its treatment raises many challenges. After SCI, in a cascade of molecular events, a marked increase in glutamate at the injury site results in secondary changes which may impact on supraspinal regions, mainly ventroposterolateral (VPL). There is little information about the changes in glutamate metabolism in the VPL and whether it contributes to SCI-related central pain. The present study was performed to evaluate glutamate release in the VPL following Electrolytic Lesion of spinothalamic tract (STT). A laminectomy was performed at spinal segments of T9–T10 in male rats, and then, unilateral Electrolytic Lesions were made in the STT. Glutamate concentrations in ipsilateral VPL dialysate were measured by HPLC method at days 3, 7, 14, 21 and 28 post-injury. Tactile pain and motor activity were also examined. Glutamate levels were significantly increased in ipsilateral VPL of spinal-cord-injured rats 2 weeks after SCI and remained high up to day 28 post-surgery. The STT Lesions had no marked effect on our measures of motor activity, but there was a significant decrease in paw withdrawal threshold in the hind paws at day 14 post-SCI. These findings suggest that an increased release of glutamate in VPL plays a role in secondary pathologic changes, leading to neuronal hyperexcitation and neuropathic pain after SCI.

  • in vivo microdialysis of glutamate in ventroposterolateral nucleus of thalamus following Electrolytic Lesion of spinothalamic tract in rats
    Experimental Brain Research, 2014
    Co-Authors: Ali Ghanbari, Alireza Asgari, G R Kaka, H R Falahatpishe, Asieh Naderi, Masoumeh Jorjani
    Abstract:

    central pain is one of the most important com- plications after spinal cord injury (scI), and thereby, its treatment raises many challenges. after scI, in a cascade of molecular events, a marked increase in glutamate at the injury site results in secondary changes which may impact on supraspinal regions, mainly ventroposterolateral (VPl). there is little information about the changes in glutamate metabolism in the VPl and whether it contributes to scI- related central pain. the present study was performed to evaluate glutamate release in the VPl following electro- lytic Lesion of spinothalamic tract (stt). a laminectomy was performed at spinal segments of t9-t10 in male rats, and then, unilateral Electrolytic Lesions were made in the stt. Glutamate concentrations in ipsilateral VPl dialysate were measured by hPlc method at days 3, 7, 14, 21 and 28 post-injury. tactile pain and motor activity were also examined. Glutamate levels were significantly increased

  • role of microglia and astrocyte in central pain syndrome following Electrolytic Lesion at the spinothalamic tract in rats
    Journal of Molecular Neuroscience, 2013
    Co-Authors: Kobra Naseri, Elham Saghaei, Fatemeh Abbaszadeh, Mina Afhami, Ali Haeri, Farzaneh Rahimi, Masoumeh Jorjani
    Abstract:

    Central pain syndrome (CPS) is a debilitating state and one of the consequences of spinal cord injury in patients. Many pathophysiological aspects of CPS are not well documented. Spinal glia activation has been identified as a key factor in the sensory component of chronic pain. In this study, the role of glial subtypes in the process of CPS induced by unilateral Electrolytic Lesion of spinothalamic tract (STT) is investigated. Male rats received a laminectomy at T8–T9 and then unilateral Electrolytic Lesion centered on the STT. Thermal and mechanical thresholds as well as locomotor function were measured on days 0, 3, 7, 14, 21, and 28 post-injuries by tail flick, von Frey filament, and open field tests, respectively. To investigate the spinal glial activation following denervation in STT-Lesioned groups, Iba1 and GFAP were detected by immunohistochemistry and Western blotting at the same time points. Data showed that STT Lesion significantly decreased thermal pain at day 3 in comparison with sham groups. Significant bilateral allodynia appeared in hind paws at day 14 after spinal cord injury and continued to day 28 (P < 0.05). Additionally, Electrolytic spinal Lesion attenuated locomotor function of injured animals after 7 days (P < 0.05). In both histological assessments and Western blotting, Iba1 increased at days 3 and 7 while increased GFAP occurred from day 14 to 28 after Lesion. It appears that microglial activation is important in the early stages of pain development and astrocytic activation occurs later. These events may lead to behavioral outcomes especially central neuropathic pain.

Abbas Haghparast - One of the best experts on this subject based on the ideXlab platform.

  • analgesic effect of morphine microinjected into the nucleus raphe magnus after Electrolytic Lesion of nucleus cuneiformis in tail flick and formalin tests in rat
    Physiology and Pharmacology, 2011
    Co-Authors: Leila Ahmadmolaei, Mehdi Ordikhaniseyedlar, Maryam Ziaei, Raha Khademi, Pegah Rouzmeh, Abbas Haghparast
    Abstract:

    Introduction: The antinociceptive effect of morphine is, in part, mediated through the activation of a descending pathway. One of the major components of this pathway is the nucleus raphe magnus (NRM). Our previous study demonstrated the involvement of NRM in the analgesic effect of morphine microinjected into the nucleus cuneiformis (NCF) in a descending manner. The aim of the current study was to investigate another aspect of the interaction between these two nuclei in both acute and chronic inflammatory pain models. Methods: In order to calculate 50% effective dose (ED50) of morphine, animals received bilateral morphine injections (1, 2.5, 5 and 10 μg/0.5 μl saline) into the NRM. The obtained ED50 of morphine was applied into the NRM with/without bilateral Electrolytic Lesion (500 μA, 30 sec) of the NCF. Tail-flick and formalin tests were applied as behavioral analgesic tests in this study. Results: Results interestingly showed that the intra-NRM morphine injection (ED50; 1 μg/0.5 μl saline) resulted in an increase in tail flick latencies (morphine-induced antinociception) at 30-min intervals, while bilateral Electrolytic Lesions in the NCF could notably decreased the morphine-induced antinociception during 30-90 min after the injection of morphine. Data also showed that bilateral morphine microinjected into the NRM, dose-dependently increases the antinociceptive responses during both early and late phases of formalin test. The antinociceptive effect of morphine microinjected into the NRM was significantly attenuated at the late phase but not early phase following the bilateral destruction of NCF in formalin test. Conclusion: It could be concluded that there is a reciprocal interaction between NRM and NCF during morphine induced antinociception in both acute and chronic inflammatory pain models in rat.

  • Contribution of the Nucleus Cuneiformis to the Antinociceptive Effects of Systemic Morphine on Inflammatory Pain in Rats
    Iran University of Medical Sciences, 2011
    Co-Authors: Abdolaziz Ronaghi, Mohammad Ebrahimzadeh, Abbas Haghparast
    Abstract:

    Introduction: The role of midbrain reticular formation, which includes the nucleus cuneiformis (NCF), as a crucial antinociceptive region in descending pain modulation has long been investigated. In this study, we tried to highlight the role of NCF in morphine-induced antinociception in formalin-induced pain model in rats. Methods: A total of 201 male Wistar rats weighing 260-310 g were used in this study. The effective dose of morphine in systemic administration (intraperitoneal i.p.) was determined after a dose- and time-response protocol. In consequent groups, bilateral Electrolytic Lesion (500 μA, 30 sec) or reversible inactivation (lidocaine 2%) were used in the NCF before systemic administration of morphine, and then, the nociceptive test was immediately carried out. Results: The results showed that administration of 6 mg/kg morphine, 30 min before the formalin test, is the best dose- and time-response set in these experiments. The obtained data also indicated that bilateral electrical destruction or reversible inactivation of the NCF significantly decreased antinociceptive responses of systemic morphine (6 mg/kg i.p.) during the second phase of formalin test (P

  • effects of Electrolytic Lesion of dorsolateral periaqueductal gray on analgesic response of morphine microinjected into the nucleus cuneiformis in rat
    Neuroscience Letters, 2009
    Co-Authors: Abbas Haghparast, Leila Ahmadmolaei
    Abstract:

    Abstract The periaqueductal gray (PAG) and nucleus cuneiformis (CnF), like the rostral ventromedial medulla, have functional roles in descending pain-inhibitory pathway related to morphine antinociception. There is not any evidence concerning the role of different regions of the PAG on antinociceptive effect of morphine administered into the CnF in pain modulatory system. In the present study, we investigate whether Electrolytic Lesion of dorsolateral periaqueductal gray (dl-PAG) influence the analgesic effect of morphine microinjected into the CnF. 71 adult male Wistar rats weighting 230–280 g cannulated bilaterally into the CnF, concurrently Lesion of dl-PAG was done. The tail-flick and formalin tests were performed to measure pain and antinociceptive effect of morphine microinjected into the CnF (2.5 μg/0.3 μl saline per side). The tail-flick latency was measured at 15, 30, 45, 60 and 75 min following morphine microinjection. In formalin test, pain behavior was recorded for 60 min in early (0–5 min) and late (15–60 min) phases after formalin injection. Each rat was given a subcutaneous 50-μl injection of formalin 2.5% into plantar surface of hind paw following morphine administration. The results showed that dl-PAG Lesion attenuated the effect of morphine microinjected into the CnF both in tail-flick and formalin tests while dl-PAG Lesion solely did not alter basal pain behavior as compared to control group. In conclusion, our results suggest the existence of a direct or indirect projection from CnF to the dl-PAG at least at the level of the morphine antinociception in pain modulation.

  • Electrolytic Lesion of the nucleus raphe magnus reduced the antinociceptive effects of bilateral morphine microinjected into the nucleus cuneiformis in rats
    Neuroscience Letters, 2008
    Co-Authors: Abbas Haghparast, Mehdi Ordikhaniseyedlar, Maryam Ziaei
    Abstract:

    Abstract Several lines of investigation show that the rostral ventromedial medulla is a critical relay for midbrain regions, including the nucleus cuneiformis (CnF), which control nociception at the spinal cord. There is some evidence that local stimulation or morphine administration into the CnF produces the effective analgesia through the nucleus raphe magnus (NRM). The present study tries to determine the effect of morphine-induced analgesia following microinjection into the CnF in the absence of NRM. Seven days after the cannulae implantation, morphine was microinjected bilaterally into the CnF at the doses of 0.25, 1, 2.5, 5, 7.5 and 10 μg/0.3 μl saline per side. The morphine-induced antinociceptive effect measured by tail-flick test at 30, 60, 90 and 120 min after microinjection. The results showed that bilateral microinjection of morphine into the CnF dose-dependently causes increase in tail-flick latency (TFL). The 50% effective dose of morphine was determined and microinjected into the CnF (2.5 μg/0.3 μl saline per side) in rats after NRM Electrolytic Lesion (1 mA, 30 s). Lesion of the NRM significantly decreased TFLs, 30 ( P P

  • Electrolytic Lesion of the nucleus raphe magnus reduced the antinociceptive effects of bilateral morphine microinjected into the nucleus cuneiformis in rats
    Neuroscience Letters, 2008
    Co-Authors: Abbas Haghparast, Mehdi Ordikhaniseyedlar, Maryam Ziaei
    Abstract:

    Several lines of investigation show that the rostral ventromedial medulla is a critical relay for midbrain regions, including the nucleus cuneiformis (CnF), which control nociception at the spinal cord. There is some evidence that local stimulation or morphine administration into the CnF produces the effective analgesia through the nucleus raphe magnus (NRM). The present study tries to determine the effect of morphine-induced analgesia following microinjection into the CnF in the absence of NRM. Seven days after the cannulae implantation, morphine was microinjected bilaterally into the CnF at the doses of 0.25, 1, 2.5, 5, 7.5 and 10 microg/0.3 microl saline per side. The morphine-induced antinociceptive effect measured by tail-flick test at 30, 60, 90 and 120 min after microinjection. The results showed that bilateral microinjection of morphine into the CnF dose-dependently causes increase in tail-flick latency (TFL). The 50% effective dose of morphine was determined and microinjected into the CnF (2.5 microg/0.3 microl saline per side) in rats after NRM Electrolytic Lesion (1 mA, 30 s). Lesion of the NRM significantly decreased TFLs, 30 (P<0.01) and 60 (P<0.05) but not 90-120 min after morphine microinjection into the CnF, compared with sham-Lesion group. We concluded that morphine induces the analgesic effects through the opioid receptors in the CnF. It is also appeared that morphine-induced antinociception decreases following the NRM Lesion but it seems that there are some other descending pain modulatory pathways that activate in the absence of NRM.

Maryam Ziaei - One of the best experts on this subject based on the ideXlab platform.

  • analgesic effect of morphine microinjected into the nucleus raphe magnus after Electrolytic Lesion of nucleus cuneiformis in tail flick and formalin tests in rat
    Physiology and Pharmacology, 2011
    Co-Authors: Leila Ahmadmolaei, Mehdi Ordikhaniseyedlar, Maryam Ziaei, Raha Khademi, Pegah Rouzmeh, Abbas Haghparast
    Abstract:

    Introduction: The antinociceptive effect of morphine is, in part, mediated through the activation of a descending pathway. One of the major components of this pathway is the nucleus raphe magnus (NRM). Our previous study demonstrated the involvement of NRM in the analgesic effect of morphine microinjected into the nucleus cuneiformis (NCF) in a descending manner. The aim of the current study was to investigate another aspect of the interaction between these two nuclei in both acute and chronic inflammatory pain models. Methods: In order to calculate 50% effective dose (ED50) of morphine, animals received bilateral morphine injections (1, 2.5, 5 and 10 μg/0.5 μl saline) into the NRM. The obtained ED50 of morphine was applied into the NRM with/without bilateral Electrolytic Lesion (500 μA, 30 sec) of the NCF. Tail-flick and formalin tests were applied as behavioral analgesic tests in this study. Results: Results interestingly showed that the intra-NRM morphine injection (ED50; 1 μg/0.5 μl saline) resulted in an increase in tail flick latencies (morphine-induced antinociception) at 30-min intervals, while bilateral Electrolytic Lesions in the NCF could notably decreased the morphine-induced antinociception during 30-90 min after the injection of morphine. Data also showed that bilateral morphine microinjected into the NRM, dose-dependently increases the antinociceptive responses during both early and late phases of formalin test. The antinociceptive effect of morphine microinjected into the NRM was significantly attenuated at the late phase but not early phase following the bilateral destruction of NCF in formalin test. Conclusion: It could be concluded that there is a reciprocal interaction between NRM and NCF during morphine induced antinociception in both acute and chronic inflammatory pain models in rat.

  • Electrolytic Lesion of the nucleus raphe magnus reduced the antinociceptive effects of bilateral morphine microinjected into the nucleus cuneiformis in rats
    Neuroscience Letters, 2008
    Co-Authors: Abbas Haghparast, Mehdi Ordikhaniseyedlar, Maryam Ziaei
    Abstract:

    Abstract Several lines of investigation show that the rostral ventromedial medulla is a critical relay for midbrain regions, including the nucleus cuneiformis (CnF), which control nociception at the spinal cord. There is some evidence that local stimulation or morphine administration into the CnF produces the effective analgesia through the nucleus raphe magnus (NRM). The present study tries to determine the effect of morphine-induced analgesia following microinjection into the CnF in the absence of NRM. Seven days after the cannulae implantation, morphine was microinjected bilaterally into the CnF at the doses of 0.25, 1, 2.5, 5, 7.5 and 10 μg/0.3 μl saline per side. The morphine-induced antinociceptive effect measured by tail-flick test at 30, 60, 90 and 120 min after microinjection. The results showed that bilateral microinjection of morphine into the CnF dose-dependently causes increase in tail-flick latency (TFL). The 50% effective dose of morphine was determined and microinjected into the CnF (2.5 μg/0.3 μl saline per side) in rats after NRM Electrolytic Lesion (1 mA, 30 s). Lesion of the NRM significantly decreased TFLs, 30 ( P P

  • Electrolytic Lesion of the nucleus raphe magnus reduced the antinociceptive effects of bilateral morphine microinjected into the nucleus cuneiformis in rats
    Neuroscience Letters, 2008
    Co-Authors: Abbas Haghparast, Mehdi Ordikhaniseyedlar, Maryam Ziaei
    Abstract:

    Several lines of investigation show that the rostral ventromedial medulla is a critical relay for midbrain regions, including the nucleus cuneiformis (CnF), which control nociception at the spinal cord. There is some evidence that local stimulation or morphine administration into the CnF produces the effective analgesia through the nucleus raphe magnus (NRM). The present study tries to determine the effect of morphine-induced analgesia following microinjection into the CnF in the absence of NRM. Seven days after the cannulae implantation, morphine was microinjected bilaterally into the CnF at the doses of 0.25, 1, 2.5, 5, 7.5 and 10 microg/0.3 microl saline per side. The morphine-induced antinociceptive effect measured by tail-flick test at 30, 60, 90 and 120 min after microinjection. The results showed that bilateral microinjection of morphine into the CnF dose-dependently causes increase in tail-flick latency (TFL). The 50% effective dose of morphine was determined and microinjected into the CnF (2.5 microg/0.3 microl saline per side) in rats after NRM Electrolytic Lesion (1 mA, 30 s). Lesion of the NRM significantly decreased TFLs, 30 (P<0.01) and 60 (P<0.05) but not 90-120 min after morphine microinjection into the CnF, compared with sham-Lesion group. We concluded that morphine induces the analgesic effects through the opioid receptors in the CnF. It is also appeared that morphine-induced antinociception decreases following the NRM Lesion but it seems that there are some other descending pain modulatory pathways that activate in the absence of NRM.

Wilson Abrão Saad - One of the best experts on this subject based on the ideXlab platform.

  • lateral hypothalamus Lesions influences water and salt intake and sodium and urine excretion and arterial blood pressure induced by l name and fk 409 injections into median preoptic nucleus in conscious rats
    Life Sciences, 2004
    Co-Authors: Wilson Abrão Saad, Luiz Antonio De Arruda Camargo, Ismael Francisco Motta Siqueira Guarda, William Abrao Saad, Gustavo Garcia, Laura Izabel Gutierrez, Sylvio Simoes, Renata Saad Guarda
    Abstract:

    Abstract Male Holtzman rats weighting 200–250 g were anesthetized with zoletil 50 mg/Kg (tiletamine chloridrate 125,0 mg and zolazepan chloridrate 125,0 mg) into quadriceps muscle and submitted an Electrolytic Lesion of the lateral hypothalamus (LH) and a stainless steel cannula was implanted into their median preoptic nucleus (MnPO). We investigated the effects of the injection into the (MnPO) of FK 409 (20 μg/0.5 μl), a nitric oxide (NO) donor, and N W -nitro-L-arginine methyl ester (L-NAME) 40 μg/0.5 μl, a nitric oxide synthase inhibitor (NOSI), on the water and sodium appetite and the natriuretic, diuretic and cardiovascular effects induced by injection of L-NAME and FK 409 injected into MnPO in rats with LH Lesions. Controls were injected with a similar volume of 0.15 M NaCl. L-NAME injected into MnPO produced an increase in water and sodium intake and in sodium and urine excretion and increase de mean arterial pressure (MAP). FK 409 injected into MnPO did not produce any change in the hydro Electrolytic and cardiovascular parameters in LH-sham and Lesioned rats. FK 409 injected before L-NAME attenuated its effects. These data show that Electrolytic Lesion of the LH reduces fluid and sodium intake as well as sodium and urine excretion, and the pressor effect induced by L-NAME. LH involvement with NO of the MnPO excitatory and inhibitory mechanisms related to water and sodium intake, sodium excretion and cardiovascular control is suggested.

  • Effect of Electrolytic and chemical Lesion by ibotenic acid of the septal area on water and salt intake
    Brain research bulletin, 1998
    Co-Authors: Wilson Abrão Saad, Luiz Antonio De Arruda Camargo, José Antunes-rodrigues, Silvio Simões
    Abstract:

    Water and sodium chloride intake was studied in male Holtzman rats weighing 250-300 g that had been subjected to Electrolytic and chemical Lesions of the septal area (SA). Water intake increased in animals with Electrolytic Lesion of the SA bilaterally from 169.37+/-8.55 (sham) to 214.87+/-23.10 ml/5 days (Lesioned). Water intake decreased after ibotenic acid Lesion of the SA from 229.33+/-27.60 to 127.33+/-22.84 ml/5 days. Sodium chloride intake (1.5%) increased in animals with Electrolytic Lesion of the SA from 10.0+/-1.73 to 15.5+/-1.95 ml/5 days after Lesion. Also sodium chloride (1.5%) intake increased after ibotenic acid injection into the SA to a greater extent (from 7.83+/-1.25 to 14.33+/-1.87 ml/5 days). The results indicate that the water intake response may be due to Lesions that involve cell bodies and fibers of passage and that the sodium intake response can also be induced by Lesions which involve only cell bodies. Finally, these results led us to conclude that the SA uses its cell bodies and afferent bodies and fibers for processing inputs mediating water intake and salt appetite and that the cells bodies of the SA are implicated in increased water intake.

  • Effect of lateral hypothalamus Lesions on the water and salt intake, and sodium and urine excretion induced by activation of the median preoptic nucleus in conscious rats
    Journal of the autonomic nervous system, 1995
    Co-Authors: Renata Kelli Pereira Da Silva, Wilson Abrão Saad, Antonio Renzi, José Vanderlei Menani, Luiz Antonio De Arruda Camargo
    Abstract:

    Abstract In this study we investigated the influence of Electrolytic Lesion of the lateral hypothalamus (LH) on the water and salt appetite, and the natriuretic, diuretic and cardiovascular effects induced by angiotensinergic, cholinergic and noradrenergic stimulation of the median preoptic nucleus (MnPO) in rats. Male Holtzman rats were implanted with a cannula into the MnPO. Other groups of sham- and LH-Lesioned rats received a stainless steel cannula implanted into the MnPO. ANGII injection into the MnPO induced water and sodium intake, and natriuretic, diuretic, pressor and tachycardic responses. Carbachol induced water intake, and natriuretic, pressor and bradycardic responses, whereas noradrenaline increased urine, sodium excretion and blood pressure, and induced bradycardia. In rats submitted to LH-Lesion only, water and sodium ixcretion bradycardia. In rats submitted to LH-Lesion only, water and sodium intake was reduced compared with sham rats. LH Lesion also reduced the sodium ingestion induced by ANGII (12 ng) into the MnPO. In LH-Lesioned rats, the dipsogenic, diuretic and pressor responses induced by ANGII (12 ng), carbachol (2 nmol) and noradrenaline (20 nmol) injection into the MnPO were reduced. The same occurred with sodium excretion when carbachol (2 nmol) and noradrenaline (20 nmol) were injected into the MnPO of LH-Lesioned rats, whereas ANGII (12 ng) induced an increase in sodium excretion. These data show that Electrolytic Lesion of the LH reduces fluid and sodium intake, and pressor responses to angiotensinergic, cholinergic and noradrenergic activation of the MnPO. LH involvement with MnPO excitatory and inhibitory mechanisms related to water and sodium intake, sodium excretion and cardiovascular control is suggested.

  • EFFECT OF Electrolytic AND CHEMICAL Lesion BY IBOTENIC ACID OF THE AMYGDALA ON SALT INTAKE
    Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas, 1994
    Co-Authors: Wilson Abrão Saad, M. A. Paulino, Laa Camargo, Antonio Renzi, José Vanderlei Menani, W. Abraosaad
    Abstract:

    Sodium chloride intake was studied in male Holtzman rats weighing 250-300 g submitted to Electrolytic and chemical Lesion of the cell bodies, not fibers of the amygdaloid complex. Sodium chloride (1.5%) intake increased in animals with Electrolytic Lesion of the corticomedial nucleus of the amygdala. Sodium chloride (1.5%) intake increased after ibotenic acid injection into the corticomedial nucleus of the amygdala to a larger extent (26.6 +/- 9.2 to 147.6 +/- 34.6 ml/5 days). The results indicate that sodium intake response can be induced by Lesions, which involved only cell bodies. The fibers of passage of the corticomedial nucleus of the amygdala produce a water intake less consistent than that induced by ibotenic acid, which is more acute. The results show that cell bodies of this region of the amygdala are involved in the control of sodium chloride intake.

Fernanda Augustini Pezzato - One of the best experts on this subject based on the ideXlab platform.

  • effect of lithium on behavioral disinhibition induced by Electrolytic Lesion of the median raphe nucleus
    Psychopharmacology, 2015
    Co-Authors: Fernanda Augustini Pezzato, Katsumasa Hoshino, Junior Jose De Anchieta C Horta, Miriam Garcia Mijares, Todd D. Gould
    Abstract:

    Rationale Alterations in brainstem circuits have been proposed as a possible mechanism underlying the etiology of mood disorders. Projections from the median raphe nucleus (MnR) modulate dopaminergic activity in the forebrain and are also part of a behavioral disinhibition/inhibition system that produces phenotypes resembling behavioral variations manifested during manic and depressive phases of bipolar disorder.

  • Behavioral effects of the Electrolytic Lesion in the region of the median raphe nucleus as an experimental model of mania in the rat and in the mouse
    Universidade de São Paulo, 2014
    Co-Authors: Fernanda Augustini Pezzato
    Abstract:

    Déficits na regulação serotoninérgica dos circuitos catecolaminérgicos tem sido propostos como um mecanismo relacionado à etiologia dos transtornos de humor. Projeções do núcleo mediano da rafe (MnR) modulam a atividade dopaminérgica no prosencéfalo e são também parte de um sistema de inibição/desinibição comportamental que se assemelha às variações nos níveis de atividade apresentados durante os polos do transtorno bipolar. O objetivo do presente estudo foi avaliar se as alterações comportamentais induzidas pela inativação do MnR podem ser um modelo animal para estudo da mania humana. No Capítulo I, o procedimento de lesão eletrolítica do MnR foi realizado em ratos Wistar machos, tendo como controles os grupos lesão fictícia e intacto. Os resultados confirmaram a capacidade desta manipulação experimental em reproduzir hiperatividade e estereotipia crônicas, aumento na frequência de respostas positivamente reforçadas por solução de sacarose e padrão comportamental de dominância social. Ainda, foi demonstrada a potencialidade do tratamento crônico com lítio em reduzir a hiperatividade. No Capítulo II foram realizadas lesões eletrolíticas do MnR em camundongos C57BL/6J machos, tendo novamente como controles os grupos lesão fictícia e intacto. Os resultados demonstraram desenvolvimento de hiperatividade, estereotipia e maior frequência de exposição a situações aversivas/de risco nos testes do labirinto em cruz elevado e do claro/escuro. O tratamento crônico com lítio atenuou ou reverteu parte destas alterações comportamentais. Análises do tecido encefálico demonstraram níveis terapêuticos equivalentes de LiCl em todos os grupos submetidos ao tratamento e a histologia confirmou o sítio de lesão. O conjunto dos dados obtidos sugere a adequação do modelo proposto pelo atendimento aos critérios de validade de face e preditiva apresentando como vantagens a mimetização de diversos sintomas do transtorno e a cronicidade destes. Ainda, a reprodutibilidade dos efeitos da lesão em diferentes espécies sugere a existência de homologia evolutiva, acrescentando fundamentos à validade de constructo hipotetizada. Por fim, destaca-se que este modelo de mania parece ser heurístico pela possibilidade de contribuir para a investigação dos mecanismos de ação do lítio e para a compreensão das relações de oposição entre os sistemas neurotransmissores excitatórios e inibitórios como parte da neurobiologia dos transtornos de humorDeficits in serotoninergic regulation of catecholaminergic circuits have been proposed as a mechanism related to the etiology of mood disorders. Projections from the median raphe nucleus (MnR) modulate the dopaminergic activity in the forebrain and are also part of a behavioral disinhibition/inhibition system that resembles the variations in activity levels shown during the poles of bipolar disorder. The aim of the present study was to evaluate if the behavioral effects induced by the inactivation of the MnR can be considered an animal model for studying the human mania. In Chapter I, the MnR Electrolytic Lesion was performed in male Wistar rats, having as control groups sham operated and intact animals. The results confirmed the capacity of this experimental manipulation to reproduce chronic hyperactivity and stereotypy, increased response frequency positively reinforced by sucrose solution and a social dominant behavioral pattern. Furthermore, it was shown the potentiality of the lithium treatment in reducing the hyperactivity. In Chapter II MnR Electrolytic Lesions were performed in C57BL/6J mice, having as control groups sham operated and intact animals. The results demonstrated the development of hyperactivity, stereotypy and increased frequency of exposure to aversive situations/\"risk taking\" in the elevated plus maze and light/dark box tests. Chronic treatment with lithium attenuated or reversed some of these behavioral alterations. Encephalic tissue analysis showed equivalent lithium therapeutic levels in all treated groups and the histology confirmed the Lesion site. The set of data obtained suggests the suitability of the proposed model for attending criteria for face and predictive validities presenting advantages such as the mimicking of several disorder symptoms and the chronicity of them. Also, the reproducibility of the effects of the Lesion in different species suggests the existence of evolutionary homology and adds basis to the construct validity hypothesized. Finally, it is emphasized that this model of mania seems to be heuristic by the possibility to contribute to the investigation of lithium mechanisms of action and for understanding the opposite relations between excitatory and inhibitory neurotransmitter systems as part of the neurobiology of mood disorder