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Hreday N. Sapru - One of the best experts on this subject based on the ideXlab platform.
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Mechanism of heart rate responses elicited by Chemical Stimulation of the hypothalamic paraventricular nucleus in the rat.
Brain Research, 2009Co-Authors: Tetsuya Kawabe, Vineet C. Chitravanshi, Takeshi Nakamura, Kazumi Kawabe, Hreday N. SapruAbstract:Abstract This study was designed to examine the mechanism of heart rate (HR) responses elicited by the Stimulation of hypothalamic paraventricular nucleus (PVN). Experiments were done in urethane-anesthetized, barodenervated, adult, male Wistar rats. Chemical Stimulation of the PVN by unilateral microinjections of N-methyl- d -aspartic acid (NMDA) elicited increases in HR which were attenuated by bilateral vagotomy. PVN-induced tachycardia was also attenuated by the blockade of the spinal ionotropic glutamate receptors (iGLURs) which was accomplished by intrathecal injections at T9–T10 or direct application at T1–T4 of iGLUR antagonists. The blockade of spinal iGLURs combined with bilateral vagotomy completely blocked PVN-induced tachycardia. Blockade of GABA receptors in the medial nucleus tractus solitarius (mNTS) also attenuated the PVN-induced tachycardia. Complete blockade of PVN-induced tachycardia was also observed after the blockade of iGLURs in both the spinal cord and mNTS. Combination of the blockade of mNTS GABA receptors and spinal iGLURs also abolished PVN-induced tachycardia. PVN-induced tachycardia was not altered by the blockade of spinal vasopressin or oxytocin receptors at T1–T4. These results suggested that in barodenervated rats: 1) tachycardia elicited by the Chemical Stimulation of the PVN was mediated via both inhibition of vagal and activation of sympathetic outflows to the heart, 2) the vagal inhibition contributing to the PVN-induced tachycardia was mediated by the iGLURs and GABARs in the mNTS, 3) sympathetic activation contributing to the PVN-induced tachycardia was mediated via spinal iGLURs, and 4) spinal vasopressin and oxytocin receptors were not involved in the mediation of PVN-induced tachycardia.
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cardiovascular responses to Chemical Stimulation of the lateral tegmental field and adjacent medullary reticular formation in the rat
Brain Research, 2003Co-Authors: Vitaliy Marchenko, Hreday N. SapruAbstract:Abstract Relatively few studies have been done to characterize cardiovascular responses to the Chemical Stimulation of sites located in the medullary lateral tegmental field (LTF) and most of them have been carried out in anesthetized animals. Our experiments were carried out in decerebrated, artificially ventilated, adult male Wistar rats. In the LTF, two types of cardiovascular responses were elicited. One type consisted of pressor responses accompanied by bradycardia. Such responses were elicited from a region 0.4 mm caudal to 0.8 mm rostral to the calamus scriptorius (CS); maximum responses were elicited from a site 0.6 mm rostral to the CS, 1.2 mm lateral to the midline and 1.2 mm deep from the dorsal medullary surface. Another type consisted of pressor responses without any change in heart rate; such responses were elicited from a region 1–1.6 mm rostral to the CS. Nucleus ambiguus (nAmb) and dorsal motor nucleus of the vagus (nDMX) and the reticular formation surrounding these areas were the main sites from which bradycardia (accompanied by either no or small changes in BP) was elicited. In the nAmb, maximum bradycardia was elicited from a site 0.6 mm rostral to the CS, 1.8 mm lateral to the midline and 2.4 mm deep from the dorsal medullary surface. In the nDMX, most prominent bradycardic responses were elicited at 0–0.6 mm rostral to the CS, and 0.6 mm lateral to the midline and 1 mm deep from the dorsal medullary surface. Cardiovascular effects elicited from sites in other well-known areas, such as the rostral ventrolateral medullary pressor area (RVLM) and caudal ventrolateral medullary depressor area (CVLM), and the nucleus tractus solitarius (nTS) were also included for comparison of different responses. These results are expected to prove useful in studies in which the microinjection technique is used to characterize cardiovascular responses.
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Spinal cord lactate concentration during Chemical Stimulation of the nucleus tractus solitarii in anesthetized rats.
Neuroscience Research, 1996Co-Authors: Yoh Ikegami, Masanobu Maeda, Hreday N. Sapru, M Nakai, Akira Yokota, Yoshiaki HayashidaAbstract:This study was conducted to determine the mechanism of spinal cord blood flow (SCBF) decrease following the nucleus tractus solitarii (NTS) activation. In urethane-anesthetized, paralyzed and artificially ventilated rats, neurons in the NTS were Chemically stimulated by microinjection of l-glutamate (1.7 nmol; 50 nl) and the lactate concentration, one of indicators of local neuronal metabolism, in the spinal cord was monitored in real time using an enzyme electrode. Before the Chemical Stimulation study, the responses of the enzyme electrode and its specificity were tested in vitro and in vivo. The electrode responded to step changes in lactate concentration and a calibration plot and regression line were obtained in vitro. The lactate concentration was significantly (P < 0.01) increased during induced apnea in vivo (n = 8). The lactate concentration in the spinal cord was not significantly changed by Chemical Stimulation of the NTS when arterial blood pressure (ABP) remained above the lower limit of spinal cord autoregulation (n = 21). When Chemical Stimulation of the NTS decreased ABP to below the lower limit of autoregulation (n = 18), the lactate concentration in the spinal cord was significantly (P < 0.01) increased. This may only be due to hypotensive effects because the lactate concentration was also significantly (P < 0.01) increased when the ABP was passively decreased below the lower limit of autoregulation by controlled hemorrhage in intact (n = 11) and sinoaortic denervated rats (n = 10). Intravenous lactate injection produced no significant increase in the current from the enzyme electrode in the spinal cord (n = 4). Using the electrode with inactivated enzyme solution, the current from the electrode did not change with the increase in lactate in the spinal cord. These findings indicate that the enzyme electrode can detect rapid changes of lactate, a product of anaerobic metabolism. These results also indicate that the spinal cord vasoconstrictor response elicited by Chemical Stimulation of the NTS, which was performed above the lower limit of spinal cord autoregulation in our previous study, may be due to neurogenic regulatory mechanism, but not to the secondary effects of changes in metabolism.
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Chemical Stimulation of the nucleus tractus solitarii decreases spinal cord blood flow in anesthetized rats
Neuroscience Letters, 1995Co-Authors: Masanobu Maeda, A. J. Krieger, Hreday N. Sapru, M Nakai, Yoh Ikegami, Masaiwa Inoueaa, Seiji Takao, Yoshiaki HayashidaaAbstract:L-Glutamate was microinjected into the nucleus tractus solitarii (NTS) in anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, and spinal cord blood flow (SCBF) was determined using a combination of labeled microspheres. Unilateral Chemical Stimulation of the NTS (n = 13) significantly decreased SCBF in the cervical cord from 43 ± 6 (mean ± SEM) to 28 ± 4 (P < 0.05), in the thoracic cord from 35 ± 3 to 24 ± 4 (P < 0.01), and in the lumbar cord from 49 ± 3 to 40 ± 3 ml min− (100 g)− (P < 0.05). The decrease in SCBF was not due to the decrease in arterial blood pressure (ABP) because the SCBF during the Chemical Stimulation of the NTS was significantly smaller (P < 0.05) than the SCBF during controlled hemorrhagic hypotension (n = 11). Chemical Stimulation of the NTS did not affect the reactivity of the spinal cord vessels to hypercapnia (n = 5). Microinjection of the vehicle solution into the NTS had no effects on spinal cord circulation (n = 9). These results suggest that the cell bodies within the NTS may play a role in the control of spinal cord circulation.
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Spinal cord blood flow decreases following Chemical Stimulation of the rostral ventrolateral medullary pressor area in anesthetized rats.
Journal of the Autonomic Nervous System, 1992Co-Authors: Masanobu Maeda, A. J. Krieger, M Nakai, Hreday N. SapruAbstract:Abstract In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral medullary pressore area (VLPA) were Chemically stimulated by microinjections of l -glutamate (1.7–5.0 nmol in 100 nl of 0.9% sodium chloride solution) and the spinal cord blood flow (SCBF) was determined using a combination of labeled microspheres ( 57 Co, 113 Sn and 46 Sc). In order to measure SCBF at normotension, moderate hypotension within the lower limit of spinal cord autoregulation was induced by controlled hemorrhage ( n = 12). Unilateral Chemical Stimulation of the VLPA in these rats increased arterial blood pressure (ABP) but it remained within normotensive range. The SCBFs of cervical, thoracic and lumbar cord decreased significantly from 27 ± 3 (mean ± S.E.M.) to 20 ± 2 ( P P P −1 · (100 g) −1 , respectively. The spinal cord vascular resistances (SCVRs) of cervical, thoracic and lumbar cord increased significantly from 3.7 ± 0.4 to 5.0 ± 0.6 ( P P P −1 · (100 g) −1 ], respectively. During the Chemical Stimulation of the VLPA, SCBF increased in response to the changes in arterial PaCO 2 indicating that the reactivity of spinal cord vasculature was intact ( n = 5). Microinjections of l -glutamate into an area adjacent to the VLPA had no effect on spinal cord circulation ( n = 5). These results suggest that the neurons within the VLPA may play a role in the control of spinal cord circulation.
Abbas Haghparast - One of the best experts on this subject based on the ideXlab platform.
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Modulatory role of hippocampal dopamine receptors in antinociceptive responses induced by Chemical Stimulation of the lateral hypothalamus in an animal model of persistent inflammatory pain
Brain Research Bulletin, 2020Co-Authors: Masoud Zakeri, Saeed Soltanizadeh, Saeideh Karimi-haghighi, Abbas HaghparastAbstract:Abstract The lateral hypothalamus (LH) plays a complicated role in the modulation of inflammatory pain. There are a number of connections between the LH and the hippocampus. This study evaluated the pain modulatory role of intra-CA1 dopamine receptors in LH Chemical Stimulation-induced antinociception in the formalin test (persistent inflammatory pain model). Vehicle control groups received saline or DMSO into the CA1 and saline into the LH. Carbachol control groups received carbachol (250 nM) into the LH 5 min after saline or DMSO injections into the CA1. In the treatment groups, intra-CA1 administration of SCH-23,390 or Sulpiride (D1- or D2-like dopamine receptor antagonists, respectively) was performed 5 min before carbachol injection. Formalin tests were done in all rats 5 min after the second injection. LH Chemical Stimulation-induced antinociception during both phases of the formalin test was alleviated by the intra-CA1 administration of dopamine receptor antagonists. The inhibitory effects of the D1 or D2-like dopamine receptor antagonist on LH Chemical Stimulation-induced analgesia was nearly the same in the both phases of formalin‐induced pain-related behaviors. The findings show that the LH-CA1 pathway contributes to the modulation of formalin-induced pain. Moreover, the results indicate that D1- and D2-like dopamine receptors in the CA1 participate in the LH Chemical Stimulation-induced antinociception.
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Chemical Stimulation of the lateral hypothalamus induced seeking behaviors in rats: Involvement of orexin receptors in the ventral tegmental area
European Journal of Pharmacology, 2020Co-Authors: Maedeh Mahmoudi, Saeideh Karimi-haghighi, Mehrdad Maleki-roveshti, Abbas HaghparastAbstract:Abstract Orexinergic projections originated from the lateral hypothalamus (LH) to the ventral tegmental area (VTA) play essential role in reward-related behaviors. Our previous studies show that intra-LH injection of carbachol, as a cholinergic agonist, induces conditioned place preference (CPP) in rats. This study aimed to determine whether Chemical Stimulation of the LH alone can induce reinstatement or not, and whether intra-VTA orexin receptors are involved in the reinstatement of intra-LH carbachol-induced CPP in the rats. The animals were unilaterally treated by carbachol (250 nM) in the LH during 3-day conditioning phase. Then, they underwent an extinction phase without receiving carbachol, and on the reinstatement day, animals received a different priming dose of carbachol in the separate groups. Extinguished animals unilaterally received intra-VTA administration of SB334867 or TCS OX2 29 as orexin-1 or orexin-2 receptor antagonists to evaluate the role of orexin receptors before effective priming dose of carbachol on the reinstatement day. Findings showed that intra-LH microinjection of a priming dose of carbachol (25 and 50 nM) induced the reinstatement of LH Chemical Stimulation-induced CPP. Moreover, it was indicated that, intra-VTA administration of either SB334867 or TCS OX2 29 (10 and 30 nM) before to intra-LH injection of the priming dose of carbachol (50 nM) dose-dependently inhibited the reinstatement of intra-LH carbachol-induced CPP. Also, the orexin-2 receptor antagonist was a little more effective than orexin-1 receptor antagonist for inhibiting the reinstatement of LH Chemical Stimulation-induced CPP. The consequences propose that both orexin receptors in the VTA play roles in the reinstatement of intra-LH carbachol-induced CPP.
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role of intra hippocampal orexin 1 and orexin 2 receptors in conditioned place preference induced by Chemical Stimulation of the lateral hypothalamus
Behavioural Brain Research, 2015Co-Authors: Ali Rashidypour, Abbas Haghparast, Marzieh Moradi, Zahra FatahiAbstract:Abstract Evidence from animal models suggests a role for orexinergic system in reward processing and drug addiction. The lateral hypothalamus (LH) orexin neurons send projections to the dorsal hippocampus (CA1 region) which plays a pivotal role in reward processes. Moreover, it has been shown that orexin containing terminals and orexin receptors are distributed in the hippocampal formation. In this study, we assessed the role of orexin 1 (OX1r) and orexin2 (OX2r) receptors in the CA1 on the development of LH Stimulation-induced conditioned place preference (CPP). Animals weighing 230–280 g were unilaterally implanted by two separate cannulae into the LH and CA1. The CPP paradigm was done; SB334867 and TCSOX229, as selective OX1r and OX2r antagonists (1, 3, 10 and 30 nM/0.5 μl DMSO) administrated into the CA1 prior to intra-LH carbachol microinjection (250 nM; the most effective dose) during the 3-days conditioning phase, respectively. Conditioning scores and locomotor activities were recorded by Ethovision software on the test day. The results showed that the administration of OX1r and OX2r antagonists into the CA1 attenuated the development of CPP induced by Chemical Stimulation of the LH. However, this decrease in OX1r antagonist treated groups was more significant than that in OX2r antagonist treated animals. Our findings suggest that OX1 and OX2 receptors in the CA1 region of the hippocampus were involved in the development of CPP induced by Chemical Stimulation of the LH and the efficiency of OX1 receptors in this phenomenon was more considerable than OX2 receptors in rats.
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Chemical Stimulation of the lateral hypothalamus by carbachol attenuated the formalin induced pain behaviors in rats
Pharmacology Biochemistry and Behavior, 2015Co-Authors: Somayeh Ezzatpanah, Vahab Babapour, Bahman Sadeghi, Abbas HaghparastAbstract:Abstract Electrical and Chemical Stimulation of the lateral hypothalamus (LH) produces analgesia. Previous studies emphasized the importance of LH in the modulation of nociceptive behaviors in the acute pain models. In the current study, for the first time, we examined the effect of direct Chemical Stimulation of the LH with cholinergic receptor agonist, carbachol, on pain-related behaviors in the formalin test as a model of persistent inflammatory pain. Forty-eight adult male Wistar rats were implanted unilaterally with cannula into the LH. Four doses of carbachol (62.5, 125, 250 and 500 nM / 0.5 μl saline) were microinjected into the LH just 5 min before the formalin test. Vehicle group received 0.5 μl saline into the LH. Pain-related behaviors were quantified and monitored in 5-min blocks for 60 min test period. Average nociceptive scores and area under the curve (AUC) as raw pain scores × time by the linear trapezoidal method were used for the statistical analyses. One important finding of our study was that carbachol blocks the nociceptive responses in both phases of formalin-induced nociception in a dose-dependent manner. Altogether, the percentage decrease of AUC values calculated for treatment groups, compared to the control group, was more significant in the late phase than the early phase. These findings suggest that LH modulates formalin-induced nociception through spinal and/or supraspinal sites.
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Potentiation of rewarding properties of morphine by concurrent Chemical Stimulation of lateral hypothalamus in rats.
Pharmacology Biochemistry and Behavior, 2013Co-Authors: Leila Zarepour, Alireza Komaki, Siamak Shahidi, Abdolrahman Sarihi, Abbas HaghparastAbstract:Orexinergic projections from the lateral hypothalamus (LH) have an important role in acquisition of morphine conditioned place preference (CPP). However, little is known about the functional interaction between orexinergic and opioidergic systems in the reward circuitry in the rats. In the present study, we investigated the effects of different doses of carbachol, for Chemical Stimulation of LH, on rewarding properties of morphine in the rats. 132 adult male albino Wistar rats weighing 220-320 g were unilaterally implanted by a cannula into the LH. The CPP paradigm was done; conditioning score and locomotor activity were recorded by Ethovision software. In this paradigm, we used different doses of carbachol (31.25, 62.5, 125 and 250 nmol/0.5 μl saline), as a cholinergic agonist, in the LH. In the next set of experiment, we concurrently administered the ineffective doses of carbachol (31.25 and 62.5 nmol) and morphine (1mg/kg; a dose that produced no appreciable effect when given alone) during 3-day conditioning (Acquisition) and post-conditioning (Expression) phases. Our results showed that unilateral intra-LH administration of both ineffective doses of carbachol during conditioning phase significantly (P
Masanobu Maeda - One of the best experts on this subject based on the ideXlab platform.
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Cerebral extracellular lactate concentration and blood flow during Chemical Stimulation of the nucleus tractus solitarii in anesthetized rats.
Brain Research, 1997Co-Authors: Yoh Ikegami, Masanobu Maeda, Akira Yokota, Yoshiaki HayashidaAbstract:The extracellular lactate concentration and blood flow in the cerebral cortex of urethane-anesthetized, paralyzed and artificially ventilated rats were monitored continuously and simultaneously using an enzyme electrode and a laser Doppler flowmeter (LDF), respectively, during Chemical Stimulation of the nucleus tractus solitarii (NTS) by microinjection of l-glutamate (1.7 nmol 50 nl). Chemical Stimulation of the NTS significantly decreased the arterial blood pressure (ABP) from 85 ± 17 to 68 ± 14 mmHg, heart rate from 418 ± 13 to 402 ± 19 beats · min−1 and cerebral blood flow (CBF) by 17.9 ± 6.2% (P < 0.001). However, Chemical Stimulation of the NTS significantly increased the lactate concentration by 58.9 ± 17.3 μM (P < 0.001). Barostat maneuver, which held systemic ABP constant during Chemical Stimulation of the NTS attenuated the responses in CBF and lactate concentration by 30 and 27%, respectively. The onset of the increase in lactate concentration was delayed about 19 s after that of the CBF decrease. Circulatory lactate produced no significant change in the cerebral extracellular lactate concentration. These results indicate that Chemical Stimulation of the NTS induces an increase in extracellular lactate concentration in the cerebral cortex through a decrease in CBF via cerebral vasoconstriction.
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Spinal cord lactate concentration during Chemical Stimulation of the nucleus tractus solitarii in anesthetized rats.
Neuroscience Research, 1996Co-Authors: Yoh Ikegami, Masanobu Maeda, Hreday N. Sapru, M Nakai, Akira Yokota, Yoshiaki HayashidaAbstract:This study was conducted to determine the mechanism of spinal cord blood flow (SCBF) decrease following the nucleus tractus solitarii (NTS) activation. In urethane-anesthetized, paralyzed and artificially ventilated rats, neurons in the NTS were Chemically stimulated by microinjection of l-glutamate (1.7 nmol; 50 nl) and the lactate concentration, one of indicators of local neuronal metabolism, in the spinal cord was monitored in real time using an enzyme electrode. Before the Chemical Stimulation study, the responses of the enzyme electrode and its specificity were tested in vitro and in vivo. The electrode responded to step changes in lactate concentration and a calibration plot and regression line were obtained in vitro. The lactate concentration was significantly (P < 0.01) increased during induced apnea in vivo (n = 8). The lactate concentration in the spinal cord was not significantly changed by Chemical Stimulation of the NTS when arterial blood pressure (ABP) remained above the lower limit of spinal cord autoregulation (n = 21). When Chemical Stimulation of the NTS decreased ABP to below the lower limit of autoregulation (n = 18), the lactate concentration in the spinal cord was significantly (P < 0.01) increased. This may only be due to hypotensive effects because the lactate concentration was also significantly (P < 0.01) increased when the ABP was passively decreased below the lower limit of autoregulation by controlled hemorrhage in intact (n = 11) and sinoaortic denervated rats (n = 10). Intravenous lactate injection produced no significant increase in the current from the enzyme electrode in the spinal cord (n = 4). Using the electrode with inactivated enzyme solution, the current from the electrode did not change with the increase in lactate in the spinal cord. These findings indicate that the enzyme electrode can detect rapid changes of lactate, a product of anaerobic metabolism. These results also indicate that the spinal cord vasoconstrictor response elicited by Chemical Stimulation of the NTS, which was performed above the lower limit of spinal cord autoregulation in our previous study, may be due to neurogenic regulatory mechanism, but not to the secondary effects of changes in metabolism.
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Chemical Stimulation of the nucleus tractus solitarii decreases spinal cord blood flow in anesthetized rats
Neuroscience Letters, 1995Co-Authors: Masanobu Maeda, A. J. Krieger, Hreday N. Sapru, M Nakai, Yoh Ikegami, Masaiwa Inoueaa, Seiji Takao, Yoshiaki HayashidaaAbstract:L-Glutamate was microinjected into the nucleus tractus solitarii (NTS) in anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, and spinal cord blood flow (SCBF) was determined using a combination of labeled microspheres. Unilateral Chemical Stimulation of the NTS (n = 13) significantly decreased SCBF in the cervical cord from 43 ± 6 (mean ± SEM) to 28 ± 4 (P < 0.05), in the thoracic cord from 35 ± 3 to 24 ± 4 (P < 0.01), and in the lumbar cord from 49 ± 3 to 40 ± 3 ml min− (100 g)− (P < 0.05). The decrease in SCBF was not due to the decrease in arterial blood pressure (ABP) because the SCBF during the Chemical Stimulation of the NTS was significantly smaller (P < 0.05) than the SCBF during controlled hemorrhagic hypotension (n = 11). Chemical Stimulation of the NTS did not affect the reactivity of the spinal cord vessels to hypercapnia (n = 5). Microinjection of the vehicle solution into the NTS had no effects on spinal cord circulation (n = 9). These results suggest that the cell bodies within the NTS may play a role in the control of spinal cord circulation.
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Spinal cord blood flow decreases following Chemical Stimulation of the rostral ventrolateral medullary pressor area in anesthetized rats.
Journal of the Autonomic Nervous System, 1992Co-Authors: Masanobu Maeda, A. J. Krieger, M Nakai, Hreday N. SapruAbstract:Abstract In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral medullary pressore area (VLPA) were Chemically stimulated by microinjections of l -glutamate (1.7–5.0 nmol in 100 nl of 0.9% sodium chloride solution) and the spinal cord blood flow (SCBF) was determined using a combination of labeled microspheres ( 57 Co, 113 Sn and 46 Sc). In order to measure SCBF at normotension, moderate hypotension within the lower limit of spinal cord autoregulation was induced by controlled hemorrhage ( n = 12). Unilateral Chemical Stimulation of the VLPA in these rats increased arterial blood pressure (ABP) but it remained within normotensive range. The SCBFs of cervical, thoracic and lumbar cord decreased significantly from 27 ± 3 (mean ± S.E.M.) to 20 ± 2 ( P P P −1 · (100 g) −1 , respectively. The spinal cord vascular resistances (SCVRs) of cervical, thoracic and lumbar cord increased significantly from 3.7 ± 0.4 to 5.0 ± 0.6 ( P P P −1 · (100 g) −1 ], respectively. During the Chemical Stimulation of the VLPA, SCBF increased in response to the changes in arterial PaCO 2 indicating that the reactivity of spinal cord vasculature was intact ( n = 5). Microinjections of l -glutamate into an area adjacent to the VLPA had no effect on spinal cord circulation ( n = 5). These results suggest that the neurons within the VLPA may play a role in the control of spinal cord circulation.
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Chemical Stimulation of the rostral ventrolateral medullary pressor area decreases cerebral blood flow in anesthetized rats.
Brain Research, 1991Co-Authors: Masanobu Maeda, A. J. Krieger, M Nakai, Hreday N. SapruAbstract:In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral medullary pressor area (VLPA) were Chemically stimulated by microinjections of L-glutamate (1.7-5.0 nmole in 100 nl of 0.9% sodium chloride solution) and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres (57Co, 113Sn and 46Sc). In one group of rats (n = 11), unilateral Chemical Stimulation of the VLPA produced a significant (P less than 0.01) increase in arterial blood pressure (ABP), a significant (P less than 0.05) decrease in CBF, and a significant (P less than 0.01) increase in cerebrovascular resistance (CVR) in the cerebral cortex ipsilateral to the stimulated VLPA. The CBF was 52 +/- 3 (mean +/- S.E.M.) and 48 +/- 4 ml.min-1.(100 g)-1 before and during the Chemical Stimulation of VLPA; the CVR was 1.9 +/- 0.1 and 2.6 +/- 0.3 mmHg per ml.min-1.(100 g)-1 before and during the Stimulation. In order to measure CBF at normotension, moderate hypotension was induced by controlled hemorrhage in another group of rats (n = 8). Unilateral Chemical Stimulation of the VLPA in these rats increased ABP but it remained within normotensive range. The CBFs of ipsilateral and contralateral cerebral cortices decreased significantly (P less than 0.05) from 57 +/- 14 to 41 +/- 9 and from 50 +/- 12 to 39 +/- 9 ml.min-1.(100 g)-1, respectively. The CVRs of ipsilateral and contralateral cortices increased significantly (P less than 0.05) from 2.6 +/- 0.6 to 3.5 +/- 0.8 and from 2.7 +/- 0.5 to 3.5 +/- 0.8 mmHg/[ml.min-1.(100 g)-1], respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Lu-yuan Lee - One of the best experts on this subject based on the ideXlab platform.
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Ca2+ transient evoked by Chemical Stimulation is enhanced by PGE2 in vagal sensory neurons: role of cAMP/PKA signaling pathway.
Journal of Neurophysiology, 2003Co-Authors: Kevin Kwong, Lu-yuan LeeAbstract:The effect of prostaglandin E2 (PGE2) on Chemical Stimulation-evoked calcium (Ca2+) transient was investigated in isolated vagal sensory neurons of the rat using fura-2-based ratiometric Ca2+ imagi...
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ca2 transient evoked by Chemical Stimulation is enhanced by pge2 in vagal sensory neurons role of camp pka signaling pathway
Journal of Neurophysiology, 2003Co-Authors: Kevin Kwong, Lu-yuan LeeAbstract:The effect of prostaglandin E2 (PGE2) on Chemical Stimulation-evoked calcium (Ca2+) transient was investigated in isolated vagal sensory neurons of the rat using fura-2-based ratiometric Ca2+ imagi...
H Sequeira - One of the best experts on this subject based on the ideXlab platform.
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Activation of ventrolateral medullary neurons projecting to spinal autonomic areas after Chemical Stimulation of the central nucleus of amygdala: a neuroanatomical study in the rat.
Brain Research, 2001Co-Authors: N. Salomé, S Leman, O Viltart, H SequeiraAbstract:Several studies have shown that the central nucleus of amygdala is involved in cardiovascular regulation. The control of this function may be mediated by activation of the ventrolateral medulla neurons that project to preganglionic neurons located in the intermediolateral nucleus of the spinal cord. The aim of the present study was to examine whether Stimulation of the central nucleus of amygdala activated ventrolateral medulla neurons projecting to the intermediolateral nucleus. For this purpose, the injection of a retrograde tracer, the cholera toxin b subunit (CTb), into the intermediolateral nucleus of the T2 segment was combined with immunohistoChemical detection of Fos protein following Chemical Stimulation of the central nucleus of amygdala. Results showed that retrogradely labeled neurons were found throughout the ventrolateral medulla. Moreover, Chemical Stimulation of the central nucleus of amygdala induced: (1) a decrease of arterial blood pressure; (2) an expression of Fos protein mainly in sub-populations of neurons located in the intermediate and caudal parts of the ventrolateral medulla; (3) a significantly higher number of double labeled neurons (CTb-immunoreactive/Fos-immunoreactive) in the rostral part of the ventrolateral medulla than in the other parts of this region. These results show that the central nucleus of amygdala influences the activity of brainstem neurons projecting to the intermediolateral nucleus. Data were discussed in terms of descending amygdalofugal pathways involved in the hypotension.
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Expression of Fos protein in adrenal preganglionic neurons following Chemical Stimulation of the rostral ventrolateral medulla of the rat.
Brain Research, 2000Co-Authors: S Leman, O Viltart, H SequeiraAbstract:The ventrolateral medulla is known to be involved in the regulation of arterial blood pressure, especially via its connections with sympathetic preganglionic neurons (SPNs) mainly located in the intermediolateral nucleus of the spinal cord. It has been shown that Stimulation of the rostral part of the ventrolateral medulla (RVLM) elicits a release of catecholamines from the adrenal medulla. The aim of the present study was to demonstrate the existence of a functional pathway between the RVLM and adrenal SPNs using the combination of a retrograde tract tracing technique (cholera toxin B subunit) with the immunohistoChemical detection of Fos protein following the Chemical Stimulation of RVLM. The data obtained showed that: (1) Chemical Stimulation of the RVLM induced Fos immunoreactivity in the intermediolateral nucleus and particularly in SPNs projecting to the adrenal medulla; (2) along the thoracic segments T2-T12, 26.1% of retrogradely identified adrenal SPNs were Fos-immunoreactive with the greatest percentage (30.9%) in the T8 segment. These results favored a functional control of the RVLM on adrenal SPNs which may contribute to a substantial activation of the cardiovascular system via the release of adrenal catecholamines.