Role of the medial prefrontal cortex in cardiovascular responses to acute restraint in rats

Tavares, Rodrigo Fiacadori; Corrêa, Fernando Morgan de Aguiar

doi:10.1016/j.neuroscience.2006.07.030

Cited by 67 publications

(60 citation statements)

References 56 publications

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“…CoCl 2 injections into brain stem nuclei have previously been shown to disrupt neuronal transmission (2,13,27). CoCl 2 injections have also been used to block transmission in cardiovascular pathways with a similar time course to that observed in this study (2,13,20,26,27,30). This interruption of neuronal transmission with CoCl 2 has been shown to be due to a reversible inactivation of calcium channels on the presynaptic terminals (18,22,23).…”

Section: Discussionsupporting

confidence: 72%

“…Micropipettes were lowered stereotaxically into the caudal mNTS bilaterally (stereotaxic coordinates: 0.5 mm rostral to calamus scriptorius, 0.6 mm lateral to the midline, and 0.5 mm ventral to the dorsal surface of the medulla). Cardiovascular responsive sites in the PSTN region were retested following the bilateral injections into the mNTS of the synaptic blocker CoCl 2 (5 mM in 0.9% physiological saline; 100 nl; Fisher Scientific, Fair Lawn, NJ) (13,20,27,30). The same stimulation site in the PSTN region identified previously that produced a cardiovascular response was retested at 2, 5, 10, and 20 min postinjection of either the synaptic blocker or vehicle (0.9% physiological saline).…”

Section: Methodsmentioning

confidence: 99%

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Medullary pathways mediating the parasubthalamic nucleus depressor response

Ciriello¹,

Solano-Flores²,

Rosas‐Arellano³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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The parasubthalamic nucleus (PSTN) projects extensively to the nucleus of the solitary tract (NTS); however, the function of PSTN in cardiovascular regulation is unknown. Experiments were done in ␣-chloralose anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of glutamate (10 nl, 0.25 M) activation of PSTN neurons on mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA). Glutamate stimulation of PSTN elicited depressor (Ϫ20.4 Ϯ 0.7 mmHg) and bradycardia (Ϫ26.0 Ϯ 1.0 beats/min) responses and decreases in RSNA (67 Ϯ 17%). Administration (intravenous) of atropine methyl bromide attenuated the bradycardia response (46%), but had no effect on the MAP response. Subsequent intravenous administration of hexamethonium bromide blocked both the remaining bradycardia and depressor responses. Bilateral microinjection of the synaptic blocker CoCl 2 into the caudal NTS region attenuated the PSTN depressor and bradycardia responses by 92% and 94%, respectively. Additionally, prior glutamate activation of neurons in the ipsilateral NTS did not alter the magnitude of the MAP response to stimulation of PSTN, but potentiated HR response by 35%. Finally, PSTN stimulation increased the magnitude of the reflex bradycardia to activation of arterial baroreceptors. These data indicate that activation of neurons in the PSTN elicits a decrease in MAP due to sympathoinhibition and a cardiac slowing that involves both vagal excitation and sympathoinhibition. In addition, these data suggest that the PSTN depressor effects on circulation are mediated in part through activation of NTS neurons involved in baroreflex function. lateral hypothalamus; blood pressure; bradycardia; baroreceptor reflex; nucleus of the solitary tract

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Section: Discussionsupporting

confidence: 72%

Section: Methodsmentioning

confidence: 99%

Medullary pathways mediating the parasubthalamic nucleus depressor response

Ciriello¹,

Solano-Flores²,

Rosas‐Arellano³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This structure is activated during aversive situations (Pezzone et al 1992;Duncan et al 1993;Beck and Fibiger 1995;Kubo et al 2002) and sends projections to brain regions involved in the behavioral and cardiovascular responses to aversive stimuli (LeDoux et al 1988;Resstel et al 2006aResstel et al , 2008aTavares and Correa 2006;Tavares et al 2009). There is evidence that the LSA modulates the autonomic responses to stress and emotional threat situations (Kubo et al 2002).…”

mentioning

confidence: 99%

Involvement of the lateral septal area in the expression of fear conditioning to context

Reis

Scopinho²,

Guimarães³

et al. 2010

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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.The lateral septal area (LSA) has been related to the modulation of several cognitive and emotional processes including learning, memory, anxiety, and regulation of autonomic responses (Covian 1966;Paxinos 1995;Sheehan et al. 2004;Scopinho et al. 2006Scopinho et al. , 2007. This structure is activated during aversive situations (Pezzone et al. 1992;Duncan et al. 1993;Beck and Fibiger 1995;Kubo et al. 2002) and sends projections to brain regions involved in the behavioral and cardiovascular responses to aversive stimuli (LeDoux et al. 1988;Resstel et al. 2006aResstel et al. , 2008aTavares and Correa 2006;Tavares et al. 2009). There is evidence that the LSA modulates the autonomic responses to stress and emotional threat situations (Kubo et al. 2002). Also, the anxiolytic-like effect evoked by systemic administration of diazepam in rats submitted to fear conditioning to context is associated with a decrease in LSA neuronal activity (Beck and Fibiger 1995). Taken together, these data support a possible regulatory role of the LSA on behavioral and cardiovascular responses associated with aversive situations such as fear conditioning.Conditioned fear to context is evoked by re-exposing an animal to an environment (context) that has been previously paired with an aversive or unpleasant stimulus (Blanchard and Blanchard 1969;Fanselow 1980Fanselow , 2000Resstel et al. 2006b). This re-exposure causes freezing immobility and increases in mean arterial pressure (MAP) and heart rate (HR) (Fanselow 1980;LeDoux et al. 1988; Resstel et al. 2008a,b). These responses are modulated by structures connected with the LSA, such as the medial prefrontal cortex, amygdala, and bed nucleus of the stria terminalis (Swanson and Cowan 1977;Risold and Swanson 1997;Kuniecki et al. 2002;Vertes 2004; Resstel et al. 2008a,b). Therefore, the LSA could be part of the brain circuitry involved in contextual fear conditioning. However, the precise role of the LSA in contextual fear conditioning is still not completely understood, with contradictory evidence found in the literature. For example, freezing behavior elicited by an aversively conditioned context was reported to be potentiated in rats with LSA lesion (Sparks and LeDoux 1995), whereas a recent study showed that LSA reversible inhibition by lidocaine before the conditioning session reduces freezin...

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“…Sabe-se, ainda, que o estresse pode levar a alterações no sistema circulatório, dependendo do tipo de estressor envolvido (Esch et al, 2002), uma vez que a exposição ao estresse provoca o aumento da PA e da FC (Irvine et al, 1997, Barres et al, 2004, Carrive, 2006, Tavares and Correa, 2006. Adicionalmente, alterações cardiovasculares provocadas por pelo estresse crônico são seguidas por alterações da atividade do barorreflexo (Duarte et al, 2015a) O barorreflexo é um dos mecanismos neurais responsáveis pelo ajuste em curto prazo da PA através da modulação de atividades simpática e parassimpática para o sistema cardiovascular, influenciando FC e resistência vascular (Huang et al, 2010).…”

Section: Sumáriounclassified

“…Além dessas alterações no peso e comportamento, vários estudos demonstram que o estresse pode levar a alterações no sistema circulatório, dependendo do tipo de estressor envolvido (Esch et al, 2002), uma vez que a exposição ao estresse provoca o aumento da PA e da FC (Irvine et al, 1997, Barres et al, 2004, Carrive, 2006, Tavares and Correa, 2006, Grippo et al, 2008, Duarte et al, 2015b. Nossos achados estão em conformidade com estudos de Grippo et al, (2006) Embora as alterações cardiovasculares sejam comuns frente à exposição ao estresse, elas podem variar de acordo com os diferentes estressores utilizados (Crestani et al, 2010c).…”

Section: Figura 38 (Ab)unclassified

Efeitos do estresse crônico sobre as respostas cardiovasculares e ventilatórias ativadas pelo quimiorreflexo e barorreflexo em ratos

Silva¹

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Efeitos do estresse crônico sobre as respostas cardiovasculares e ventilatórias ativadas pelo quimiorreflexo e barorreflexo em ratos LISTA DE ABREVIATURAS ABSTRACT Abstract _______________________________________________________________ 18 ABSTRACTThe body is submitted to various stressful stimuli that may affect many physiological processes. Although blood pressure and heart rate oscilations are common during exposure to stress, they can vary according to the different stressors type, duration, frequency and intensity of the aversive stimulus.

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Role of the medial prefrontal cortex in cardiovascular responses to acute restraint in rats

Cited by 67 publications

References 56 publications

Medullary pathways mediating the parasubthalamic nucleus depressor response

Medullary pathways mediating the parasubthalamic nucleus depressor response

Involvement of the lateral septal area in the expression of fear conditioning to context

Efeitos do estresse crônico sobre as respostas cardiovasculares e ventilatórias ativadas pelo quimiorreflexo e barorreflexo em ratos

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