The Experts below are selected from a list of 6381 Experts worldwide ranked by ideXlab platform
Wilson Abrão Saad - One of the best experts on this subject based on the ideXlab platform.
-
medial Septal Area ang ii receptor subtypes in the regulation of urine and sodium excretion induced by vasopressin
Journal of the Renin-Angiotensin-Aldosterone System, 2011Co-Authors: Gabriela Maria Pavan De Arruda Camargo, Luiz Antonio De Arruda Camargo, Wilson Abrão SaadAbstract:Introduction. The present study was designed to determine the effects of selective antagonists of angiotensin II receptor types AT1 and AT2 on the flow of urine and sodium excretion induced by arginine vasopressin (AVP). Materials and methods. To this end, the drugs were microinjected into the medial Septal Area (MSA) of the brains of male Holtzman rats. Intravenous infusion of hypotonic saline was used to promote urinary flow, which was collected for one hour. Results. MSA microinjections of AVP decreased the urinary flow and increased sodium excretion in a dose-dependent manner. Microinjection into MSA of an AT2 antagonist (PD-123319) had a significantly greater effect than with an AT1 antagonist (losartan) in increasing urinary flow and decreasing sodium excretion. These effects were more pronounced when both antagonists were injected together, before the AVP. Conclusions. These results indicate that MSA AT1 and AT2 receptors act synergistically in the regulation of urine and sodium excretion induced by AVP.
-
on a possible dual role for the lateral Septal Area 5 ht1a receptor system in the regulation of water intake and urinary excretion
Behavioural Brain Research, 2010Co-Authors: Gabriela Maria Pavan De Arruda Camargo, Luiz Antonio De Arruda Camargo, Wilson Abrão SaadAbstract:Abstract The 5-hydroxytryptamine (5-HT) 1A receptor system plays a prominent role in a variety of physiological functions and behavior and regulation of this responsiveness of the receptor system has been implicated in the central regulation of water intake and urinary excretion. The lateral Septal Area (LSA) exhibits a high density of 5-HT 1A receptors, as well as a subpopulation of oxytocin (OT) receptors. Here we report the effects of pMPPF (a selective 5-HT 1A antagonist), d(CH 2 ) 5 [Tyr(Me) 2 Thr 4 , Orn 5 , Tyr(NH 2 ) 9 ]-vasotocin (an OT antagonist), and that 5-HT 1A receptor system is regulated as a consequence of activation of the Na + channel by veratridine. Cannulae were implanted into the LSA of rats to enable the introduction of the drugs. Injections of 8-OH-DPAT (a 5-HT 1A agonist) blocked water intake and increased urinary excretion, while pMPPF or the OT antagonist injected bilaterally before 8-OH-DPAT blocked its inhibitory effect on water intake and its diuretic effect. In contrast, increases in extracellular sodium levels induced by the sodium channel modulator, veratridine, enhanced 5-HT 1A responsiveness for water intake and reduced the diuretic effects induced by 8-OH-DPAT. These trials demonstrated that the responsiveness of the 5-HT 1A receptor system in the LSA can be enhanced or depressed as a consequence of an induced rise in extracellular sodium.
-
involvement of the intermediate nucleus of the lateral Septal Area on angiotensin ii induced dipsogenic and pressor responses
Regulatory Peptides, 2009Co-Authors: Andre Henrique Freiriaoliveira, Jose Vanderlei Menani, Luiz Antonio De Arruda Camargo, Graziela Torres Blanch, Wilson Abrão SaadAbstract:Abstract Previous studies have shown that different parts of the Septal Area may have opposite roles in the control of water intake and cardiovascular responses. In the present study we investigated the effects of electrolytic lesions of the intermediate nucleus of the lateral Septal Area (LSI) on cardiovascular and dipsogenic responses to intracerebroventricular (icv) angiotensin II (ANG II) and water intake induced by other different stimuli. Male Holtzman rats (280–320 g of body weight, n = 6–16/group) with sham or electrolytic lesions of the LSI and a stainless steel cannula implanted into the lateral ventricle (LV) were used. The LSI lesions did not affect body weight or daily water intake. However, LSI lesions reduced water intake and pressor responses induced by icv ANG II (4.10 − 2 nmol). The LSI lesions also slightly reduced water intake induced by 24 h of water deprivation or isoproterenol (30 μg/kg) subcutaneously, but did not affect water intake induced by intragastric 2 ml of 2 M NaCl load. The results suggest that LSI is part of the forebrain circuitry activated by ANG II to produce pressor and dipsogenic responses. However, the same nucleus is not involved in the dipsogenic responses to central osmoreceptor activation.
-
interaction between supraoptic nucleus and Septal Area in the control of water sodium intake and arterial blood pressure induced by injection of angiotensin ii
Pharmacology Biochemistry and Behavior, 2004Co-Authors: Wilson Abrão Saad, Luiz Antonio De Arruda Camargo, Ismael Francisco Motta Siqueira Guarda, Talmir Augusto Faria Brisola Dos Santos, William Abrao Saad, Sylvio Simoes, Renata Saad Guarda, Jose Antunes RodriguesAbstract:We investigated the effects of injection into the supraoptic nucleus (SON) of losartanand PD 123319 (nonpeptide AT(1) and AT(2)-angiotensin II [ANG II] receptor antagonists, respectively); d(CH(2))(5)-Tyr(Me)-AVP (AVPA; an arginine-vasopressin [AVP] V(1) receptor antagonist), FK 409 (a nitric oxide [NO] donor), and N(W)-nitro-l-arginine methyl ester (l-NAME; an NO synthase inhibitor) on water intake, sodium chloride 3% (NaCl) intake and arterial blood pressure induced by injection of ANG II into the lateral Septal Area (LSA). Male Holtzman rats (250-300 g) were implanted with cannulae into SON and LSA unilaterally. The drugs were injected in 0.5 microl over 30-60 s. Controls were injected with a similar volume of 0.15 M NaCl. ANG II was injected at a dose of 10 pmol. ANG II antagonists and AVPA were injected at doses of 80 nmol. FK 409 and l-NAME were injected at doses of 20 and 40 microg, respectively. Water and NaCl intake was measured over a 2-h period. Prior administration of losartan into the SON decreased water and NaCl intake induced by injection of ANG II. While there was a decrease in water intake, ANG II-induced NaCl intake was significantly increased following injection of AVPA. FK 409 injection decreased water intake and sodium intake induced by ANG II. l-NAME alone increased water and sodium intake and induced a pressor effect. l-NAME-potentiated water and sodium intake induced by ANG II. PD 123319 produced no changes in water or sodium intake induced by ANG II. The prior administration of losartan or AVPA decreased mean arterial pressure (MAP) induced by ANG II. PD 123319 decreased the pressor effect of ANG II to a lesser degree than losartan. FK 409 decreased the pressor effect of ANG II while l-NAME potentiated it. These results suggest that both ANG II AT(1) and AVP V(1) receptors and NO within the SON may be involved in water intake, NaCl intake and the pressor response were induced by activation of ANG II receptors within the LSA. These results do not support the involvement of LSA AT(2) receptors in the mediation of water and NaCl intake responses induced by ANG II, but influence the pressor response.
-
influence of arginine vasopressin receptors and angiotensin receptor subtypes on the water intake and arterial blood pressure induced by vasopressin injected into the lateral Septal Area of the rat
Autonomic Neuroscience: Basic and Clinical, 2004Co-Authors: Wilson Abrão Saad, Luiz Antonio De Arruda Camargo, Ismael Francisco Motta Siqueira Guarda, William Abrao Saad, Paulo Sergio Cerri, Silvio Jorge Coelho Simoes, Gustavo Garcia, Laura Izabel Gutierrez, Renata Saad GuardaAbstract:In this study we investigated the influence of d(CH2)5-Tyr(Me)-[Arg8]vasopressin (AAVP) and [adamanteanacetyl1,0-ET-d-Tyr2,Val4,aminobutyryl6,Arg8,9]-[Arg8]vasopressin (ATAVP), which are antagonists of vasopressin V1 and V2 receptors, and the effects of losartan, a selective angiotensin AT1 receptor antagonist, and CGP42112A, a selective AT2 receptor antagonist, injected into the lateral Septal Area (LSA) on thirst and hypertension induced by [Arg8]vasopressin (AVP). AAVP and ATAVP injected into the LSA reduced the drinking responses elicited by injecting AVP into the LSA. Both the AT1 and AT2 ligands administered into the LSA elicited a concentration-dependent decrease in the water intake induced by AVP injected into the LSA, but losartan was more effective than CGP42112A. The increase in MAP, due to injection of AVP into the LSA, was reduced by prior injection of AAVP from 18 +/- 1 to 6 +/- 1 mm Hg. Losartan injected into the LSA prior to AVP reduced the increase in MAP to 7 +/- 0.8 mm Hg. ATAVP and CGP42112A produced no changes in the pressor effect of AVP. These results suggest that the dipsogenic effects induced by injecting AVP into the LSA were mediated primarily by AT1 receptors. However, doses of losartan were more effective when combined with CGP42112A than when given alone, suggesting that the thirst induced by AVP injections into LSA may involve activation of multiple AVP and angiotensin II receptor subtypes. The pressor response of AVP was reduced by losartan and by AAVP. CGP42112A and ATAVP did not change the AVP pressor response. These results suggest that facilitator effects of AVP on water intake are mediated through the activation of V1 receptors and that the inhibitory effect requires V2 receptors. The involvement of AT1 and AT2 receptors can be postulated. Based on the present findings, we suggest that the AVP in the LSA may play a role in the control of water and arterial blood pressure balance.
Luiz Antonio De Arruda Camargo - One of the best experts on this subject based on the ideXlab platform.
-
medial Septal Area ang ii receptor subtypes in the regulation of urine and sodium excretion induced by vasopressin
Journal of the Renin-Angiotensin-Aldosterone System, 2011Co-Authors: Gabriela Maria Pavan De Arruda Camargo, Luiz Antonio De Arruda Camargo, Wilson Abrão SaadAbstract:Introduction. The present study was designed to determine the effects of selective antagonists of angiotensin II receptor types AT1 and AT2 on the flow of urine and sodium excretion induced by arginine vasopressin (AVP). Materials and methods. To this end, the drugs were microinjected into the medial Septal Area (MSA) of the brains of male Holtzman rats. Intravenous infusion of hypotonic saline was used to promote urinary flow, which was collected for one hour. Results. MSA microinjections of AVP decreased the urinary flow and increased sodium excretion in a dose-dependent manner. Microinjection into MSA of an AT2 antagonist (PD-123319) had a significantly greater effect than with an AT1 antagonist (losartan) in increasing urinary flow and decreasing sodium excretion. These effects were more pronounced when both antagonists were injected together, before the AVP. Conclusions. These results indicate that MSA AT1 and AT2 receptors act synergistically in the regulation of urine and sodium excretion induced by AVP.
-
on a possible dual role for the lateral Septal Area 5 ht1a receptor system in the regulation of water intake and urinary excretion
Behavioural Brain Research, 2010Co-Authors: Gabriela Maria Pavan De Arruda Camargo, Luiz Antonio De Arruda Camargo, Wilson Abrão SaadAbstract:Abstract The 5-hydroxytryptamine (5-HT) 1A receptor system plays a prominent role in a variety of physiological functions and behavior and regulation of this responsiveness of the receptor system has been implicated in the central regulation of water intake and urinary excretion. The lateral Septal Area (LSA) exhibits a high density of 5-HT 1A receptors, as well as a subpopulation of oxytocin (OT) receptors. Here we report the effects of pMPPF (a selective 5-HT 1A antagonist), d(CH 2 ) 5 [Tyr(Me) 2 Thr 4 , Orn 5 , Tyr(NH 2 ) 9 ]-vasotocin (an OT antagonist), and that 5-HT 1A receptor system is regulated as a consequence of activation of the Na + channel by veratridine. Cannulae were implanted into the LSA of rats to enable the introduction of the drugs. Injections of 8-OH-DPAT (a 5-HT 1A agonist) blocked water intake and increased urinary excretion, while pMPPF or the OT antagonist injected bilaterally before 8-OH-DPAT blocked its inhibitory effect on water intake and its diuretic effect. In contrast, increases in extracellular sodium levels induced by the sodium channel modulator, veratridine, enhanced 5-HT 1A responsiveness for water intake and reduced the diuretic effects induced by 8-OH-DPAT. These trials demonstrated that the responsiveness of the 5-HT 1A receptor system in the LSA can be enhanced or depressed as a consequence of an induced rise in extracellular sodium.
-
involvement of the intermediate nucleus of the lateral Septal Area on angiotensin ii induced dipsogenic and pressor responses
Regulatory Peptides, 2009Co-Authors: Andre Henrique Freiriaoliveira, Jose Vanderlei Menani, Luiz Antonio De Arruda Camargo, Graziela Torres Blanch, Wilson Abrão SaadAbstract:Abstract Previous studies have shown that different parts of the Septal Area may have opposite roles in the control of water intake and cardiovascular responses. In the present study we investigated the effects of electrolytic lesions of the intermediate nucleus of the lateral Septal Area (LSI) on cardiovascular and dipsogenic responses to intracerebroventricular (icv) angiotensin II (ANG II) and water intake induced by other different stimuli. Male Holtzman rats (280–320 g of body weight, n = 6–16/group) with sham or electrolytic lesions of the LSI and a stainless steel cannula implanted into the lateral ventricle (LV) were used. The LSI lesions did not affect body weight or daily water intake. However, LSI lesions reduced water intake and pressor responses induced by icv ANG II (4.10 − 2 nmol). The LSI lesions also slightly reduced water intake induced by 24 h of water deprivation or isoproterenol (30 μg/kg) subcutaneously, but did not affect water intake induced by intragastric 2 ml of 2 M NaCl load. The results suggest that LSI is part of the forebrain circuitry activated by ANG II to produce pressor and dipsogenic responses. However, the same nucleus is not involved in the dipsogenic responses to central osmoreceptor activation.
-
interaction between paraventricular nucleus and medial Septal Area on the renal effects induced by adrenaline
Autonomic Neuroscience: Basic and Clinical, 2004Co-Authors: W A Saad, Luiz Antonio De Arruda Camargo, Patricia De Souza VillaAbstract:Abstract The aim of the present study was to analyze the role of α1, α2-adrenoceptors, and the effects of losartan and PD123319 (selective ligands of the AT1 and AT2 angiotensin receptors, respectively) injected into the paraventricular nucleus (PVN) on the diuresis, natriuresis, and kaliuresis induced by administration of adrenaline into the medial Septal Area (MSA). Male Holtzman rats with a stainless steel cannula implanted into the MSA and bilaterally into the PVN were used. The administration of adrenaline into the MSA increased in a dose-dependent manner the urine, sodium, and potassium excretions. The previous administration of prazosin (an α1-adrenoceptor antagonist) injected into the PVN abolished the above effects of adrenaline, whereas yohimbine (an α2-adrenoceptor antagonist) doesn't affect the diuresis, natriuresis, and kaliuresis induced by adrenaline. Pretreatment with losartan into the PVN decreased in a dose-dependent manner the urine, sodium, and potassium excretions induced by MSA administration of adrenaline (50 ng), while PVN PD123319 was without effect. These results indicate that urinary and electrolyte excretion effects induced by adrenaline into the MSA are mediated primarily by PVN AT1 receptors. However, the doses of losartan were more effective when combined with the doses of PD123319 than given alone, suggesting that the urinary, natriuretic, and kaliuretic effects of MSA adrenaline may involve activation of multiple angiotensin II receptors subtypes into the PVN.
-
interaction between supraoptic nucleus and Septal Area in the control of water sodium intake and arterial blood pressure induced by injection of angiotensin ii
Pharmacology Biochemistry and Behavior, 2004Co-Authors: Wilson Abrão Saad, Luiz Antonio De Arruda Camargo, Ismael Francisco Motta Siqueira Guarda, Talmir Augusto Faria Brisola Dos Santos, William Abrao Saad, Sylvio Simoes, Renata Saad Guarda, Jose Antunes RodriguesAbstract:We investigated the effects of injection into the supraoptic nucleus (SON) of losartanand PD 123319 (nonpeptide AT(1) and AT(2)-angiotensin II [ANG II] receptor antagonists, respectively); d(CH(2))(5)-Tyr(Me)-AVP (AVPA; an arginine-vasopressin [AVP] V(1) receptor antagonist), FK 409 (a nitric oxide [NO] donor), and N(W)-nitro-l-arginine methyl ester (l-NAME; an NO synthase inhibitor) on water intake, sodium chloride 3% (NaCl) intake and arterial blood pressure induced by injection of ANG II into the lateral Septal Area (LSA). Male Holtzman rats (250-300 g) were implanted with cannulae into SON and LSA unilaterally. The drugs were injected in 0.5 microl over 30-60 s. Controls were injected with a similar volume of 0.15 M NaCl. ANG II was injected at a dose of 10 pmol. ANG II antagonists and AVPA were injected at doses of 80 nmol. FK 409 and l-NAME were injected at doses of 20 and 40 microg, respectively. Water and NaCl intake was measured over a 2-h period. Prior administration of losartan into the SON decreased water and NaCl intake induced by injection of ANG II. While there was a decrease in water intake, ANG II-induced NaCl intake was significantly increased following injection of AVPA. FK 409 injection decreased water intake and sodium intake induced by ANG II. l-NAME alone increased water and sodium intake and induced a pressor effect. l-NAME-potentiated water and sodium intake induced by ANG II. PD 123319 produced no changes in water or sodium intake induced by ANG II. The prior administration of losartan or AVPA decreased mean arterial pressure (MAP) induced by ANG II. PD 123319 decreased the pressor effect of ANG II to a lesser degree than losartan. FK 409 decreased the pressor effect of ANG II while l-NAME potentiated it. These results suggest that both ANG II AT(1) and AVP V(1) receptors and NO within the SON may be involved in water intake, NaCl intake and the pressor response were induced by activation of ANG II receptors within the LSA. These results do not support the involvement of LSA AT(2) receptors in the mediation of water and NaCl intake responses induced by ANG II, but influence the pressor response.
Fernando M A Correa - One of the best experts on this subject based on the ideXlab platform.
-
the medial amygdaloid nucleus is involved in the cardiovascular pathway activated by noradrenaline into the lateral Septal Area of rats
European Journal of Neuroscience, 2012Co-Authors: America A Scopinho, Eduardo Albino Trindade Fortaleza, Fernando M A CorreaAbstract:We have previously reported that noradrenaline (NA) microinjected into the lateral Septal Area (LSA) caused pressor and bradicardic responses that were mediated by vasopressin release into the circulation through the paraventricular nucleus of hypothalamus (PVN). Although PVN is the final structure involved in the cardiovascular responses caused by NA in the LSA, there is no evidence of direct connections between these Areas, suggesting that some structures could be links in this pathway. In the present study, we verified the effect of reversible synaptic inactivation of the medial amygdaloid nucleus (MeA), bed nucleus of stria terminalis (BNST) or diagonal band of Broca (DBB) with Cobalt Chloride (CoCl(2) ) on the cardiovascular response to NA microinjection into the LSA of unanesthetized rats. Male Wistar rats had guide cannulae implanted into the LSA and the MeA, BNST or DBB for drug administration, and a femoral catheter for blood pressure and heart rate recordings. Local microinjection of CoCl(2) (1 mm in 100 nL) into the MeA significantly reduced the pressor and bradycardic responses caused by NA microinjection (21 nmol in 200 nL) into the LSA. In contrast, microinjection of CoCl(2) into the BNST or DBB did not change the cardiovascular responses to NA into the LSA. The results indicate that synapses within the MeA, but not in BNST or DBB, are involved in the cardiovascular pathway activated by NA microinjection into the LSA.
-
lateral Septal Area α1 and α2 adrenoceptors differently modulate baroreflex activity in unanaesthetized rats
Experimental Physiology, 2012Co-Authors: America A Scopinho, Fernando M A Correa, Leonardo B M Resstel, Fernando H F Alves, Carlos C CrestaniAbstract:The lateral Septal Area (LSA) is a limbic structure involved in autonomic, neuroendocrine and behavioural responses. An inhibitory influence of the LSA on baroreflex activity has been reported; however, the local neurotransmitter involved in this modulation is still unclear. In the present study, we verified the involvement of local LSA adrenoceptors in modulating cardiac baroreflex activity in unanaesthetized rats. Bilateral microinjection of the selective α1-adrenoceptor antagonist WB4101 (10 nmol in a volume of 100 nl) into the LSA decreased baroreflex bradycardia evoked by blood pressure increases, but had no effect on reflex tachycardia evoked by blood pressure decreases. Nevertheless, bilateral administration of the selective α2-adrenoceptor antagonist RX821002 (10 nmol in 100 nl) increased baroreflex tachycardia without affecting reflex bradycardia. Treatment of the LSA with a cocktail containing WB4101 and RX821002 decreased baroreflex bradycardia and increased reflex tachycardia. The non-selective β-adrenoceptor antagonist propranolol (10 nmol in 100 nl) did not affect either reflex bradycardia or tachycardia. Microinjection of noradrenaline into the LSA increased reflex bradycardia and decreased the baroreflex tachycardic response, an opposite effect compared with those observed after double blockade of α1- and α2-adrenoceptors, and this effect of noradrenaline was blocked by local LSA pretreatment with the cocktail containing WB4101 and RX821002. The present results provide advances in our understanding of the baroreflex neural circuitry. Taken together, data suggest that local LSA α1- and α2-adrenoceptors modulate baroreflex control of heart rate differently. Data indicate that LSA α1-adrenoceptors exert a facilitatory modulation on baroreflex bradycardia, whereas local α2-adrenoceptors exert an inhibitory modulation on reflex tachycardia.
-
brain pathways involved in the modulatory effects of noradrenaline in lateral Septal Area on cardiovascular responses
Cellular and Molecular Neurobiology, 2012Co-Authors: America A Scopinho, Leonardo B M Resstel, Francisco Silveira Guimaraes, Daniele C Aguiar, Fernando M A CorreaAbstract:We have previously reported that stimulation of alpha-1 adrenoceptors by noradrenaline (NA) injected into the lateral Septal Area (LSA) of anaesthetized rats causes pressor and bradycardic responses that are mediated by acute vasopressin release into the circulation through activation of the paraventricular nucleus (PVN). Although the PVN is the final structure of this pathway, the LSA has no direct connections with the PVN, suggesting that other structures may connect these Areas. To address this issue, the present study employed c-Fos immunohistochemistry to investigate changes caused by NA microinjection into the LSA in neuronal activation in brain structures related to systemic vasopressin release. NA microinjected in the LSA caused pressor and bradycardic responses, which were blocked by intraSeptal administration of α-1 adrenoceptor antagonist (WB4101, 10 nmol/200 nL) or systemic V-1 receptor antagonist (dTyr(CH2)5(Me)AVP, 50 μg/kg). NA also increased c-Fos immunoreactivity in the prelimbic cortex (PL), infralimbic cortex (IL), dorsomedial periaqueductal gray (dmPAG), bed nucleus of the stria terminalis (BNST), PVN, and medial amygdala (MeA). No differences in the diagonal band of Broca, cingulate cortex, and dorsolateral periaqueductal gray (dlPAG) were found. Systemic administration of the vasopressin receptor antagonist dTyr AVP (CH2)5(Me) did not change the increase in c-Fos expression induced by intra-Septal NA. This latter effect, however, was prevented by local injection of the alpha-1 adrenoceptor antagonist WB4101. These results suggest that Areas such as the PL, IL, dmPAG, BNST, MeA, and PVN could be part of a circuit responsible for vasopressin release after activation of alpha-1 adrenoceptors in the LSA.
-
behavioral and autonomic responses to acute restraint stress are segregated within the lateral Septal Area of rats
PLOS ONE, 2011Co-Authors: Daniel G Reis, Fernando M A Correa, America A Scopinho, Francisco Silveira Guimaraes, Leonardo B M ResstelAbstract:Background The Lateral Septal Area (LSA) is involved with autonomic and behavior responses associated to stress. In rats, acute restraint (RS) is an unavoidable stress situation that causes autonomic (body temperature, mean arterial pressure (MAP) and heart rate (HR) increases) and behavioral (increased anxiety-like behavior) changes in rats. The LSA is one of several brain regions that have been involved in stress responses. The aim of the present study was to investigate if the neurotransmission blockade in the LSA would interfere in the autonomic and behavioral changes induced by RS.
-
involvement of the lateral Septal Area in the expression of fear conditioning to context
Learning & Memory, 2010Co-Authors: Daniel G Reis, Fernando M A Correa, America A Scopinho, Francisco Silveira Guimaraes, Leonardo B M ResstelAbstract:Considering the evidence that the lateral Septal Area (LSA) modulates defensive responses, the aim of the present study is to verify if this structure is also involved in contextual fear conditioning responses. Neurotransmission in the LSA was reversibly inhibited by bilateral microinjections of cobalt chloride (CoCl(2), 1 mM) 10 min before or after conditioning or 10 min before re-exposure to the aversively conditioned chamber. Only those animals that received CoCl(2) before re-exposure showed a decrease in both cardiovascular and behavioral conditioned responses. These results suggest that the LSA participates in the expression, but not acquisition or consolidation, of contextual fear conditioning.
America A Scopinho - One of the best experts on this subject based on the ideXlab platform.
-
the medial amygdaloid nucleus is involved in the cardiovascular pathway activated by noradrenaline into the lateral Septal Area of rats
European Journal of Neuroscience, 2012Co-Authors: America A Scopinho, Eduardo Albino Trindade Fortaleza, Fernando M A CorreaAbstract:We have previously reported that noradrenaline (NA) microinjected into the lateral Septal Area (LSA) caused pressor and bradicardic responses that were mediated by vasopressin release into the circulation through the paraventricular nucleus of hypothalamus (PVN). Although PVN is the final structure involved in the cardiovascular responses caused by NA in the LSA, there is no evidence of direct connections between these Areas, suggesting that some structures could be links in this pathway. In the present study, we verified the effect of reversible synaptic inactivation of the medial amygdaloid nucleus (MeA), bed nucleus of stria terminalis (BNST) or diagonal band of Broca (DBB) with Cobalt Chloride (CoCl(2) ) on the cardiovascular response to NA microinjection into the LSA of unanesthetized rats. Male Wistar rats had guide cannulae implanted into the LSA and the MeA, BNST or DBB for drug administration, and a femoral catheter for blood pressure and heart rate recordings. Local microinjection of CoCl(2) (1 mm in 100 nL) into the MeA significantly reduced the pressor and bradycardic responses caused by NA microinjection (21 nmol in 200 nL) into the LSA. In contrast, microinjection of CoCl(2) into the BNST or DBB did not change the cardiovascular responses to NA into the LSA. The results indicate that synapses within the MeA, but not in BNST or DBB, are involved in the cardiovascular pathway activated by NA microinjection into the LSA.
-
lateral Septal Area α1 and α2 adrenoceptors differently modulate baroreflex activity in unanaesthetized rats
Experimental Physiology, 2012Co-Authors: America A Scopinho, Fernando M A Correa, Leonardo B M Resstel, Fernando H F Alves, Carlos C CrestaniAbstract:The lateral Septal Area (LSA) is a limbic structure involved in autonomic, neuroendocrine and behavioural responses. An inhibitory influence of the LSA on baroreflex activity has been reported; however, the local neurotransmitter involved in this modulation is still unclear. In the present study, we verified the involvement of local LSA adrenoceptors in modulating cardiac baroreflex activity in unanaesthetized rats. Bilateral microinjection of the selective α1-adrenoceptor antagonist WB4101 (10 nmol in a volume of 100 nl) into the LSA decreased baroreflex bradycardia evoked by blood pressure increases, but had no effect on reflex tachycardia evoked by blood pressure decreases. Nevertheless, bilateral administration of the selective α2-adrenoceptor antagonist RX821002 (10 nmol in 100 nl) increased baroreflex tachycardia without affecting reflex bradycardia. Treatment of the LSA with a cocktail containing WB4101 and RX821002 decreased baroreflex bradycardia and increased reflex tachycardia. The non-selective β-adrenoceptor antagonist propranolol (10 nmol in 100 nl) did not affect either reflex bradycardia or tachycardia. Microinjection of noradrenaline into the LSA increased reflex bradycardia and decreased the baroreflex tachycardic response, an opposite effect compared with those observed after double blockade of α1- and α2-adrenoceptors, and this effect of noradrenaline was blocked by local LSA pretreatment with the cocktail containing WB4101 and RX821002. The present results provide advances in our understanding of the baroreflex neural circuitry. Taken together, data suggest that local LSA α1- and α2-adrenoceptors modulate baroreflex control of heart rate differently. Data indicate that LSA α1-adrenoceptors exert a facilitatory modulation on baroreflex bradycardia, whereas local α2-adrenoceptors exert an inhibitory modulation on reflex tachycardia.
-
brain pathways involved in the modulatory effects of noradrenaline in lateral Septal Area on cardiovascular responses
Cellular and Molecular Neurobiology, 2012Co-Authors: America A Scopinho, Leonardo B M Resstel, Francisco Silveira Guimaraes, Daniele C Aguiar, Fernando M A CorreaAbstract:We have previously reported that stimulation of alpha-1 adrenoceptors by noradrenaline (NA) injected into the lateral Septal Area (LSA) of anaesthetized rats causes pressor and bradycardic responses that are mediated by acute vasopressin release into the circulation through activation of the paraventricular nucleus (PVN). Although the PVN is the final structure of this pathway, the LSA has no direct connections with the PVN, suggesting that other structures may connect these Areas. To address this issue, the present study employed c-Fos immunohistochemistry to investigate changes caused by NA microinjection into the LSA in neuronal activation in brain structures related to systemic vasopressin release. NA microinjected in the LSA caused pressor and bradycardic responses, which were blocked by intraSeptal administration of α-1 adrenoceptor antagonist (WB4101, 10 nmol/200 nL) or systemic V-1 receptor antagonist (dTyr(CH2)5(Me)AVP, 50 μg/kg). NA also increased c-Fos immunoreactivity in the prelimbic cortex (PL), infralimbic cortex (IL), dorsomedial periaqueductal gray (dmPAG), bed nucleus of the stria terminalis (BNST), PVN, and medial amygdala (MeA). No differences in the diagonal band of Broca, cingulate cortex, and dorsolateral periaqueductal gray (dlPAG) were found. Systemic administration of the vasopressin receptor antagonist dTyr AVP (CH2)5(Me) did not change the increase in c-Fos expression induced by intra-Septal NA. This latter effect, however, was prevented by local injection of the alpha-1 adrenoceptor antagonist WB4101. These results suggest that Areas such as the PL, IL, dmPAG, BNST, MeA, and PVN could be part of a circuit responsible for vasopressin release after activation of alpha-1 adrenoceptors in the LSA.
-
behavioral and autonomic responses to acute restraint stress are segregated within the lateral Septal Area of rats
PLOS ONE, 2011Co-Authors: Daniel G Reis, Fernando M A Correa, America A Scopinho, Francisco Silveira Guimaraes, Leonardo B M ResstelAbstract:Background The Lateral Septal Area (LSA) is involved with autonomic and behavior responses associated to stress. In rats, acute restraint (RS) is an unavoidable stress situation that causes autonomic (body temperature, mean arterial pressure (MAP) and heart rate (HR) increases) and behavioral (increased anxiety-like behavior) changes in rats. The LSA is one of several brain regions that have been involved in stress responses. The aim of the present study was to investigate if the neurotransmission blockade in the LSA would interfere in the autonomic and behavioral changes induced by RS.
-
involvement of the lateral Septal Area in the expression of fear conditioning to context
Learning & Memory, 2010Co-Authors: Daniel G Reis, Fernando M A Correa, America A Scopinho, Francisco Silveira Guimaraes, Leonardo B M ResstelAbstract:Considering the evidence that the lateral Septal Area (LSA) modulates defensive responses, the aim of the present study is to verify if this structure is also involved in contextual fear conditioning responses. Neurotransmission in the LSA was reversibly inhibited by bilateral microinjections of cobalt chloride (CoCl(2), 1 mM) 10 min before or after conditioning or 10 min before re-exposure to the aversively conditioned chamber. Only those animals that received CoCl(2) before re-exposure showed a decrease in both cardiovascular and behavioral conditioned responses. These results suggest that the LSA participates in the expression, but not acquisition or consolidation, of contextual fear conditioning.
Leonardo B M Resstel - One of the best experts on this subject based on the ideXlab platform.
-
lateral Septal Area α1 and α2 adrenoceptors differently modulate baroreflex activity in unanaesthetized rats
Experimental Physiology, 2012Co-Authors: America A Scopinho, Fernando M A Correa, Leonardo B M Resstel, Fernando H F Alves, Carlos C CrestaniAbstract:The lateral Septal Area (LSA) is a limbic structure involved in autonomic, neuroendocrine and behavioural responses. An inhibitory influence of the LSA on baroreflex activity has been reported; however, the local neurotransmitter involved in this modulation is still unclear. In the present study, we verified the involvement of local LSA adrenoceptors in modulating cardiac baroreflex activity in unanaesthetized rats. Bilateral microinjection of the selective α1-adrenoceptor antagonist WB4101 (10 nmol in a volume of 100 nl) into the LSA decreased baroreflex bradycardia evoked by blood pressure increases, but had no effect on reflex tachycardia evoked by blood pressure decreases. Nevertheless, bilateral administration of the selective α2-adrenoceptor antagonist RX821002 (10 nmol in 100 nl) increased baroreflex tachycardia without affecting reflex bradycardia. Treatment of the LSA with a cocktail containing WB4101 and RX821002 decreased baroreflex bradycardia and increased reflex tachycardia. The non-selective β-adrenoceptor antagonist propranolol (10 nmol in 100 nl) did not affect either reflex bradycardia or tachycardia. Microinjection of noradrenaline into the LSA increased reflex bradycardia and decreased the baroreflex tachycardic response, an opposite effect compared with those observed after double blockade of α1- and α2-adrenoceptors, and this effect of noradrenaline was blocked by local LSA pretreatment with the cocktail containing WB4101 and RX821002. The present results provide advances in our understanding of the baroreflex neural circuitry. Taken together, data suggest that local LSA α1- and α2-adrenoceptors modulate baroreflex control of heart rate differently. Data indicate that LSA α1-adrenoceptors exert a facilitatory modulation on baroreflex bradycardia, whereas local α2-adrenoceptors exert an inhibitory modulation on reflex tachycardia.
-
brain pathways involved in the modulatory effects of noradrenaline in lateral Septal Area on cardiovascular responses
Cellular and Molecular Neurobiology, 2012Co-Authors: America A Scopinho, Leonardo B M Resstel, Francisco Silveira Guimaraes, Daniele C Aguiar, Fernando M A CorreaAbstract:We have previously reported that stimulation of alpha-1 adrenoceptors by noradrenaline (NA) injected into the lateral Septal Area (LSA) of anaesthetized rats causes pressor and bradycardic responses that are mediated by acute vasopressin release into the circulation through activation of the paraventricular nucleus (PVN). Although the PVN is the final structure of this pathway, the LSA has no direct connections with the PVN, suggesting that other structures may connect these Areas. To address this issue, the present study employed c-Fos immunohistochemistry to investigate changes caused by NA microinjection into the LSA in neuronal activation in brain structures related to systemic vasopressin release. NA microinjected in the LSA caused pressor and bradycardic responses, which were blocked by intraSeptal administration of α-1 adrenoceptor antagonist (WB4101, 10 nmol/200 nL) or systemic V-1 receptor antagonist (dTyr(CH2)5(Me)AVP, 50 μg/kg). NA also increased c-Fos immunoreactivity in the prelimbic cortex (PL), infralimbic cortex (IL), dorsomedial periaqueductal gray (dmPAG), bed nucleus of the stria terminalis (BNST), PVN, and medial amygdala (MeA). No differences in the diagonal band of Broca, cingulate cortex, and dorsolateral periaqueductal gray (dlPAG) were found. Systemic administration of the vasopressin receptor antagonist dTyr AVP (CH2)5(Me) did not change the increase in c-Fos expression induced by intra-Septal NA. This latter effect, however, was prevented by local injection of the alpha-1 adrenoceptor antagonist WB4101. These results suggest that Areas such as the PL, IL, dmPAG, BNST, MeA, and PVN could be part of a circuit responsible for vasopressin release after activation of alpha-1 adrenoceptors in the LSA.
-
behavioral and autonomic responses to acute restraint stress are segregated within the lateral Septal Area of rats
PLOS ONE, 2011Co-Authors: Daniel G Reis, Fernando M A Correa, America A Scopinho, Francisco Silveira Guimaraes, Leonardo B M ResstelAbstract:Background The Lateral Septal Area (LSA) is involved with autonomic and behavior responses associated to stress. In rats, acute restraint (RS) is an unavoidable stress situation that causes autonomic (body temperature, mean arterial pressure (MAP) and heart rate (HR) increases) and behavioral (increased anxiety-like behavior) changes in rats. The LSA is one of several brain regions that have been involved in stress responses. The aim of the present study was to investigate if the neurotransmission blockade in the LSA would interfere in the autonomic and behavioral changes induced by RS.
-
involvement of the lateral Septal Area in the expression of fear conditioning to context
Learning & Memory, 2010Co-Authors: Daniel G Reis, Fernando M A Correa, America A Scopinho, Francisco Silveira Guimaraes, Leonardo B M ResstelAbstract:Considering the evidence that the lateral Septal Area (LSA) modulates defensive responses, the aim of the present study is to verify if this structure is also involved in contextual fear conditioning responses. Neurotransmission in the LSA was reversibly inhibited by bilateral microinjections of cobalt chloride (CoCl(2), 1 mM) 10 min before or after conditioning or 10 min before re-exposure to the aversively conditioned chamber. Only those animals that received CoCl(2) before re-exposure showed a decrease in both cardiovascular and behavioral conditioned responses. These results suggest that the LSA participates in the expression, but not acquisition or consolidation, of contextual fear conditioning.
-
α1 adrenoceptors in the lateral Septal Area modulate food intake behaviour in rats
British Journal of Pharmacology, 2009Co-Authors: America A Scopinho, Leonardo B M Resstel, F M A CorreaAbstract:Background and purpose: Control of food intake is a complex behaviour which involves many interconnected brain structures. The present work assessed if the noradrenergic system in the lateral septum (LS) was involved in the feeding behaviour of rats. Experimental approach: In the first protocol, the food intake of rats was measured. Then non-food-deprived animals received either 100 nL of 21 nmol of noradrenaline or vehicle unilaterally in the LS 10 min after local 10 nmol of WB4101, an a1-adrenoceptor antagonist, or vehicle. In the second protocol, different doses of WB4101 (1, 10 or 20 nmol in 100 nL) were microinjected bilaterally into the LS of rats, deprived of food for 18 h and food intake was compared to that of satiated animals. Key results: One-sided microinjection of noradrenaline into the LS of normal-fed rats evoked food intake, compared with vehicle-injected control animals, which was significantly reduced by a1-adrenoceptor antagonism. In a further investigation, food intake was significantly higher in food-deprived animals, compared to satiated controls. Pretreatment of the LS with WB4101 reduced food intake in only food-deprived animals in a dose-related manner, suggesting that the LS noradrenergic system was involved in the control of food intake. Conclusion and implications: Activation by local microinjection of noradrenaline of a1-adrenoceptors in the LS evoked food intake behaviour in rats. In addition, blockade of the LS a1-adrenoceptors inhibited food intake in food-deprived animals, suggesting that the LS noradrenergic system modulated food intake behaviour and satiation.
