Pressor effects of acetylcholine injected into the lateral septal area of conscious rats

Peres-Polon, Vera Lúcia; Corrêa, Fernando Morgan de Aguiar

doi:10.1016/0028-3908(94)90127-9

Cited by 27 publications

(10 citation statements)

References 31 publications

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“…At this dose, d(CH 2 ) 5 Tyr(Me)AVP was shown to inhibit the vasopressinergic component of pressor responses to either intracerebroventricular or intracortical microinjection of noradrenaline (Corrêa et al, 1985;Fernandez et al, 2003), or the intraseptal injection of acetylcholine (Peres-Polon and Corrêa, 1994). The pretreatment with d(CH 2 ) 5 -Tyr(Me)AVP did not change the pressor response to EE of the MPFC, thus ruling out involvement of the vasopressinergic system in this response.…”

Section: Discussionmentioning

confidence: 92%

“…Classically, stimuli that promote vasopressin release are plasma osmolality elevation, blood volume reduction, blood pressure decrease, increased circulating angiotensin II levels, various stressors, fever and pain (Cunningham and Sawchenko, 1991;Share, 1996). Intracerebral injection of catecholamines (Hoffman, 1979;Corrêa et al, 1985;Corrêa and Peres-Polon, 1995), acetylcholine (Peres-Polon and Corrêa, 1994), or L-glutamate was reported to elicit pressor responses in rats, which are consequent to acute vasopressin release. Fernandes et al (2003) have demonstrated an important Fig.…”

Section: Discussionmentioning

confidence: 97%

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Pressor effects of electrical stimulation of medial prefrontal cortex in unanesthetized rats

Tavares

Antunes‐Rodrigues

Corrêa

2004

J of Neuroscience Research

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The medial prefrontal cortex (MPFC) is involved in central nervous system (CNS)-mediated cardiovascular modulation. We compared the cardiovascular effects of electrical stimulation (EE) of the MPFC in unanesthetized rats to those observed after stimulation of the same area in urethane-anesthetized rats. Electrical stimulation (35, 106, 177, 247, 318, and 389 microA rms/10 sec, 60-Hz sine wave) of the MPFC of urethane-anesthetized rats caused depressor responses of stimulus-related intensity. The cardiovascular response to electrical stimulation of the MPFC in unanesthetized rats was characterized by stimulus-related pressor responses. No significant heart rate changes were observed during the EE period in any case. The pressor response to electrical stimulation (106 microA rms/10 sec, 60-Hz sine wave) of the MPFC was not affected by intravenous pretreatment with the vasopressin antagonist dTyr(CH(2))(5)(Me)AVP (50 microg/kg, intravenously), by hypophysectomy, or by intravenous pretreatment with the angiotensin II antagonist losartan (1 mg/kg, intravenously). The pressor response was blocked by intravenous pretreatment with the ganglionic blocker mecamylamine (2 mg/kg, intravenously) but was not affected by adrenal demedullation, thus suggesting involvement of the neural component of the sympathetic nervous system without a major involvement of its hormonal component. Our results confirmed the occurrence of depressor responses after electrical stimulation of the MPFC in urethane-anesthetized rats and evidenced that only pressor responses are observed after its stimulation in unanesthetized rats. The fact that the pressor response to the stimulation of the MPFC was blocked by a ganglioplegic suggests that the MPFC has functional excitatory actions over the sympathetic nervous system.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 97%

Pressor effects of electrical stimulation of medial prefrontal cortex in unanesthetized rats

Tavares

Antunes‐Rodrigues

Corrêa

2004

J of Neuroscience Research

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“…Electrical stimulation of this region evokes blood pressure decreases or increases in anesthetized [45], [46] or unanesthetized rats [47], respectively. Cardiovascular changes are also reported after neurotransmitter agonist injections into the LSA, with glutamate decreasing [48] and acetylcholine, bradykinin and noradrenaline increasing MAP [49], [50], [51], [52], [53]. In addition, acute synaptic inhibition of the LSA enhances baroreflex responses, indicating an inhibitory influence of this region in this reflex [3].…”

Section: Discussionmentioning

confidence: 99%

Behavioral and Autonomic Responses to Acute Restraint Stress Are Segregated within the Lateral Septal Area of Rats

et al. 2011

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BackgroundThe 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.Methodology/Principal FindingsMale Wistar rats with bilateral cannulae aimed at the LSA, an intra-abdominal datalogger (for recording internal body temperature), and an implanted catheter into the femoral artery (for recording and cardiovascular parameters) were used. They received bilateral microinjections of the non-selective synapse blocker cobalt chloride (CoCl2, 1 mM/ 100 nL) or vehicle 10 min before RS session. The tail temperature was measured by an infrared thermal imager during the session. Twenty-four h after the RS session the rats were tested in the elevated plus maze (EPM).Conclusions/SignificanceInhibition of LSA neurotransmission reduced the MAP and HR increases observed during RS. However, no changes were observed in the decrease in skin temperature and increase in internal body temperature observed during this period. Also, LSA inhibition did not change the anxiogenic effect induced by RS observed 24 h later in the EPM. The present results suggest that LSA neurotransmission is involved in the cardiovascular but not the temperature and behavioral changes induced by restraint stress.

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“…Microinjection of a glutamatergic agonist into the LSA caused depressor responses (Gelsema and Calaresu, 1987). Microinjection of acetylcholine, bradykinin, or noradrenaline (NA) increased arterial pressure and decreased heart rate (Corrêa and Graeff, 1975; Pirola et al, 1987; Peres‐Polon and Corrêa, 1992, 1994; Scopinho et al, 2006), suggesting the involvement of LSA synapses in cardiovascular control.…”

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confidence: 99%

Non‐N‐methyl‐D‐aspartate glutamate receptors in the paraventricular nucleus of hypothalamus mediate the pressor response evoked by noradrenaline microinjected into the lateral septal area in rats

Scopinho

Tavares

Busnardo

et al. 2008

J of Neuroscience Research

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The lateral septal area (LSA) is a part of the limbic system and is involved in cardiovascular modulation. We previously reported that microinjection of noradrenaline (NA) into the LSA of unanesthetized rats caused pressor responses that are mediated by acute vasopressin release. Magnocellular neurons of the paraventricular (PVN) and supraoptic (SON) of the hypothalamus synthesize vasopressin. In the present work, we studied which of these nuclei is involved in the pressor pathway activated by unilateral NA injection into the LSA as well as the local neurotransmitter involved. Chemical ablation of the SON by unilateral injection of the nonspecific synapses blocker cobalt chloride (1 mM/100 nl) did not affect the pressor response evoked by NA (21 nmol/200 nl) microinjection into the LSA. However, the response to NA was blocked when cobalt chloride (1 mM/100 nl) was microinjected into the PVN, indicating that this hypothalamic nucleus is responsible for the mediation of the pressor response. There is evidence in the literature pointing to glutamate as a putative neurotransmitter activating magnocellular neurons. Pretreatment of the PVN with the selective non-N-methyl-D-asparate (NMDA) antagonist NBQX (2 nmol/100 nl) blocked the pressor response to NA microinjected into the LSA, whereas pretreatment with the selective NMDA antagonist LY235959 (2 nmol/100 nl) did not affect the response to NA. Our results implicate the PVN as the final structure in the pressor pathway activated by the microinjection of NA into the LSA. They also indicate that local glutamatergic synapses and non-NMDA glutamatergic receptors mediate the response in the PVN.

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Pressor effects of acetylcholine injected into the lateral septal area of conscious rats

Cited by 27 publications

References 31 publications

Pressor effects of electrical stimulation of medial prefrontal cortex in unanesthetized rats

Pressor effects of electrical stimulation of medial prefrontal cortex in unanesthetized rats

Behavioral and Autonomic Responses to Acute Restraint Stress Are Segregated within the Lateral Septal Area of Rats

Non‐N‐methyl‐D‐aspartate glutamate receptors in the paraventricular nucleus of hypothalamus mediate the pressor response evoked by noradrenaline microinjected into the lateral septal area in rats

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