Navegando por Palavras-chave "nucleus of the solitary tract"
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- ItemSomente MetadadadosAblation of NK1 receptor bearing neurons in the nucleus of the solitary tract blunts cardiovascular reflexes in awake rats(Elsevier B.V., 2006-11-13) Abdala, Ana Paula L.; Schoorlemmer, Gerhardus Hermanus Maria [UNIFESP]; Colombari, Eduardo; Universidade Federal de São Paulo (UNIFESP); Univ Estadual PaulistaThe nucleus of the solitary tract (NTS) receives primary afferents involved in cardiovascular regulation. We investigated the role of NK1-receptor bearing neurons in the NTS on cardiovascular reflexes in awake rats fitted with chronic venous and arterial cannulae. These neurons were lesioned selectively with saporin conjugated with substance P (SP-SAP, 2 mu M, bilateral injections of 20 nL in the subpostremal NTS, or 200 nL in both the subpostremal and the commissural NTS). Before, and 7 and 14 days after injection of SP-SAP, we measured changes in blood pressure and heart rate induced by i.v. injection of phenylephrine and nitroprusside (baroreceptor reflex), cyanide (arterial chemoreceptor reflex), and phenylbiguanide (Bezold-Jarisch reflex). the smaller injections with SP-SAP completely abolished NK1 receptor staining in the subpostremal NTS. the larger injections abolished NK1 receptor immunoreactivity in an area that extended from the commissural NTS to the rostral end of the subpostremal NTS. the lesions seemed to affect only a limited number of neurons, since neutral red stained sections did not show any obvious reduction in cell number. the smaller lesions reduced the gain of baroreflex bradycardia and the hypotension induced by phenylbiguanide. the larger lesions completely abolished the response to phenylbiguanide, blocked the baroreflex bradycardia induced by phenylephrine, severely blunted the baroreflex tachycardia, and blocked the bradycardia and reduced the hypertension induced by cyanide. Thus, these responses depend critically on NK1-receptor bearing neurons in the NTS. (c) 2006 Elsevier B.V. All rights reserved.
- ItemSomente MetadadadosEffect of nitric oxide on excitatory amino acid-evoked discharge of neurons in NTS(Amer Physiological Soc, 2003-01-01) Dias, ACR; Colombari, E.; Mifflin, S. W.; Univ Texas; Universidade Federal de São Paulo (UNIFESP)N-methyl-D-aspartate (NMDA) and non-NMDA excitatory amino acid (EAA) receptor subtypes are involved in the integration of visceral afferent inputs within the nucleus of the solitary tract (NTS). Microinjection studies indicate interactions between nitric oxide (NO) and EAA receptors within the NTS. To examine these interactions at the single cell level, this study characterized the effects of the NO synthase inhibitor N-G-nitro-L-arginine methyl ester (L-NAME) and the NO donor 3-[2-hydroxy-2-nitroso-1-propylhydrazino]-1-propanamine (PAPA-NONOate) on the excitatory responses of vagus nerve (VN)-evoked NTS neurons to the activation of (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and NMDA receptors in rats. Iontophoresis of L-NAME did not alter spontaneous or VN-evoked discharges, but significantly decreased the number of action potentials (APs) evoked by iontophoretic application of AMPA. the effects of L-NAME on NMDA-evoked discharge were variable; for the population, L-NAME did not change the number of APs evoked by NMDA. PAPA-NONOate enhanced the spontaneous discharge and the number of APs elicited by AMPA but not NMDA. Iontophoresis of the inactive enantiomers N-G-nitro-D-arginine methyl ester and hydroxydiazenesulfonic acid 1-oxide disodium salt had no effect on AMPA-evoked discharge. Our data suggest that NO facilitates AMPA-mediated neuronal transmission within the NTS.
- ItemSomente MetadadadosEnhanced pressor response to carotid occlusion in commNTS-lesioned rats: possible efferent mechanisms(Amer Physiological Soc, 2000-05-01) Sato, Monica Akemi [UNIFESP]; Menani, Jose Vanderlei; Lopes, Oswaldo Ubriaco [UNIFESP]; Colombari, Eduardo [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Estadual PaulistaBilateral common carotid occlusion (BCO) over a period of 60 s in conscious rats produces a biphasic presser response, consisting of an early (peak) and late (plateau) phase. In this study we investigated 1) the effects of lesions of the commissural nucleus of the solitary tract (commNTS) on the cardiovascular responses produced by BCO in conscious rats and 2) the autonomic and humoral mechanisms activated to produce the presser response to BCO in sham- and commNTS-lesioned rats. Both the peak and plateau of the presser response produced by BCO increased in commNTS-lesioned rats despite the impairment of chemoreflex responses induced by intravenous potassium cyanide. In sham rats sympathetic blockade with intravenous prazosin and metoprolol, but not vasopressin receptor blockade with the Manning compound, reduced both components of BCO. In commNTS-lesioned rats the sympathetic blockade or vasopressin receptor blockade reduced both components of BCO. The results showed 1) the sympathetic nervous system, but not vasopressin, is important for the presser response to BCO during 60 s in conscious sham rats; 2) in commNTS-lesioned rats, despite chemoreflex impairment, BCO produces an increased presser response dependent on sympathetic activity associated with vasopressin release; and 3) the increment in the presser response to BCO in commNTS-lesioned rats seems to depend only on vasopressin secretion.
- ItemRestritoLesions of the commissural subnucleus of the nucleus of the solitary tract increase isoproterenol-induced water intake(Assoc Bras Divulg Cientifica, 2007-08-01) Blanch, Graziela Torres; Freiria-Oliveira, Andre Henrique; Colombari, Eduardo [UNIFESP]; Menani, Jose Vanderlei; Colombari, Debora Simões de Almeida [UNIFESP]; UNESP; Universidade Federal de São Paulo (UNIFESP)The nucleus of the solitary tract (NTS) is the primary site of the cardiovascular afferent information about arterial blood pressure and volume. the NTS projects to areas in the central nervous system involved in cardiovascular regulation and hydroelectrolyte balance, such as the anteroventral third ventricle region and the lateral parabrachial nucleus. the aim of the present study was to investigate the effects of electrolytic lesion of the commissural NTS on water and 0.3 M NaCl intake and the cardiovascular responses to subcutaneous injection of isoproterenol. Male Holtzman rats weighing 280 to 320 g were submitted to sham lesion or electrolytic lesion of the commissural NTS (N = 6-15/group). the sham-lesioned rats had the electrode placed along the same coordinates, except that no current was passed. Water intake induced by subcutaneous isoproterenol (30 mu g/kg body weight) significantly increased in chronic (15 days) commissural NTS-lesioned rats (to 2.4 +/- 0.2 vs sham: 1.9 +/- 0.2 mL 100 g body weight(-1) 60 min(-1)). Isoproterenol did not induce any sodium intake in sham or in commissural NTS-lesioned rats. the isoproterenol-induced hypotension (sham: -27 +/- 4 vs commissural NTS-lesioned rats: -22 +/- 4 mmHg/20 min) and tachycardia (sham: 168 +/- 10 vs commissural NTS: 144 +/- 24 bpm/20 min) were not different between groups. the present results suggest that the commissural NTS is part of an inhibitory neural pathway involved in the control of water intake induced by subcutaneous isoproterenol, and that the overdrinking observed in lesioned rats is not the result of a cardiovascular imbalance in these animals.
- ItemSomente MetadadadosNitric oxide modulates the cardiovascular effects elicited by acetylcholine in the NTS of awake rats(Amer Physiological Soc, 2008-12-01) Silva, Liana Gouveia da [UNIFESP]; Dias, Ana Carolina Rodrigues [UNIFESP]; Furlan, Elaina [UNIFESP]; Colombari, Eduardo [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Estadual Paulistada Silva LG, Rodrigues Dias AC, Furlan E, Colombari E. Nitric oxide modulates the cardiovascular effects elicited by acetylcholine in the NTS of awake rats. Am J Physiol Regul Integr Comp Physiol 295: R1774-R1781, 2008. First published September 24, 2008; doi:10.1152/ajpregu.00559.2007.-Microinjection of acetylcholine chloride (ACh) in the nucleus of the solitary tract (NTS) of awake rats caused a transient and dose-dependent hypotension and bradycardia. Because it is known that cardiovascular reflexes are affected by nitric oxide (NO) produced in the NTS, we investigated whether these ACh-induced responses depend on NO in the NTS. Responses to ACh (500 pmol in 100 nl) were strongly reduced by ipsilateral microinjection of the NOS inhibitor N-G-nitro-L-arginine methyl ester (L-NAME; 10 nmol in 100 nl) in the NTS: mean arterial pressure (MAP) fell by 50 +/- 5 mmHg before L-NAME to 9 +/- 4 mmHg, 10 min after L-NAME, and HR fell by 100 +/- 26 bpm before L-NAME to 20 +/- 10 bpm, 10 min after L-NAME (both P < 0.05). Microinjection of the selective inhibitor of neuronal nitric oxide synthase (nNOS), 1-(2-trifluoromethylphenyl) imidazole (TRIM; 13.3 nmol in 100 nl), in the NTS also reduced responses to ACh: MAP fell from 42 +/- 3 mmHg before TRIM to 27 +/- 6 mmHg, 10 min after TRIM (P < 0.05). TRIM also tended to reduce ACh-induced bradycardia, but this effect was not statistically significant. ACh-induced hypotension and bradycardia returned to control levels 30-45 min after NOS inhibition. Control injections with D-NAME and saline did not affect resting values or the response to ACh. in conclusion, injection of ACh into the NTS of conscious rats induces hypotension and bradycardia, and these effects may be mediated at least partly by NO produced in NTS neurons.
- ItemSomente MetadadadosON THE VERGE OF A RESPIRATORY-TYPE PANIC ATTACK: SELECTIVE ACTIVATIONS OF ROSTROLATERAL AND CAUDOVENTROLATERAL PERIAQUEDUCTAL GRAY MATTER FOLLOWING SHORT-LASTING ESCAPE TO A LOW DOSE OF POTASSIUM CYANIDE(Pergamon-Elsevier Science Ltd, 2017) Torres Muller, Claudia Janaina; Quintino-Dos-Santos, Jeyce Willig; Schimitel, Fagna Giacomin; Tufik, Sergio [UNIFESP]; Beijamini, Vanessa; Canteras, Newton Sabino; Schenberg, Luiz CarlosIntravenous injections of potassium cyanide (KCN) both elicit escape by its own and facilitate escape to electrical stimulation of the periaqueductal gray matter (PAG). Moreover, whereas the KCN-evoked escape is potentiated by CO2, it is suppressed by both lesions of PAG and clinically effective treatments with panicolytics. These and other data suggest that the PAG harbors a hypoxiasensitive alarm system the activation of which could both precipitate panic and render the subject hypersensitive to CO2. Although prior c-Fos immunohistochemistry studies reported widespread activations of PAG following KCN injections, the employment of repeated injections of high doses of KCN (> 60 mu g) in anesthetized rats compromised both the localization of KCN-responsive areas and their correlation with escape behavior. Accordingly, here we compared the brainstem activations of saline-injected controls (air/saline) with those produced by a single intravenous injection of 40-mu g KCN (air/KCN), a 2-min exposure to 13% CO2 (CO2/saline), or a combined stimulus (CO2/KCN). Behavioral effects of KCN microinjections into the PAG were assessed as well. Data showed that whereas the KCN microinjections were ineffective, KCN intravenous injections elicited escape in all tested rats. Moreover, whereas the CO2 alone was ineffective, it potentiated the KCNevoked escape. Compared to controls, the nucleus tractus solitarius was significantly activated in both CO2/saline and CO2/KCN groups. Additionally, whereas the laterodorsal tegmental nucleus was activated by all treatments, the rostrolateral and caudoventrolateral PAG were activated by air/KCN only. Data suggest that the latter structures are key components of a hypoxia-sensitive suffocation alarm which activation may trigger a panic attack. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved.