Cardiorespiratory responses to glutamatergic antagonists in the caudal ventrolateral medulla of rats

Jung, Ranu; Bruce, Eugene N.; Katona, Péter

doi:10.1016/0006-8993(91)91465-d

Cited by 31 publications

(19 citation statements)

References 29 publications

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“…11 When the mixture of AP7 and DNQX was microinjected in the CVLM, we observed significant increases in baseline blood pressure and SNA. This finding is compatible with the observation of Jung et al, 12 who showed that kynurenic acid injection in the CVLM increased blood pressure. This glutamatergic input to CVLM neurons appears to represent a component of the baroreceptor reflex arc since injection of kynurenic acid 26 or NMDA antagonists 11 were effective in abolishing the depressor response to aortic depressor nerve stimulation.…”

Section: Discussionsupporting

confidence: 82%

Metabotropic glutamate receptors in the ventrolateral medulla of rats.

Tsuchihashi

Averill

1993

Hypertension

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We investigated the hypothesis that stimulation of metabotropic excitatory amino acid receptors in the ventrolateral medulla evokes cardiovascular responses. Thus, (15,3/?)-l-aminocyclopentane-l,3-dicarboxylic acid [(1S,3/J)-ACPD], a selective agonist of metabotropic excitatory amino acid receptors, was microinjected into the rostral or caudal ventrolateral medulla of halothane-anesthetized Sprague-Dawley rats. Microinjections of (lS,3/f)-ACPD (100 pmol-1 nmol) into the rostral ventrolateral medulla produced dose-dependent increases in mean arterial pressure (+20±4 mm Hg by 100 praol and +35±2 mm Hg by 1 nmol, p< 0.01 versus artificial cerebrospinal fluid) and integrated splanchnic sympathetic nerve activity (+17±3% and +46±4%, respectively, p<0.01), whereas (15,3/f)-ACPD microinjected into the caudal ventrolateral medulla decreased mean arterial pressure (-28±2 mm Hg by 100 pmol and -48±6 mm Hg by 1 nmol, p<0.01 versus artificial cerebrospinal fluid) and splanchnic sympathetic nerve activity (-24±4% and -49±5%, p<0.01). The blockade of ionotropic excitatory amino acid receptors by the combined injection of 2-amino-7-phosphonoheptanoic acid (200 pmol) and 6,7-dinitroquinoxaline-2,3-dione ( t is well appreciated that L-glutamate (Glu) is a primary excitatory neurotransmitter in the central nervous system. Glu or other excitatory amino acids (EAA) may act at receptors that are ligand-gated ion channels and are referred to as ionotropic EAA receptors.1 These receptors exhibit selective responsiveness to 7V-methyl-D-aspartic acid (NMDA), kainic acid, or a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA);

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Section: Discussionsupporting

confidence: 82%

Metabotropic glutamate receptors in the ventrolateral medulla of rats.

Tsuchihashi

Averill

1993

Hypertension

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“…The time course of the development of the respiratory effects was similar to that observed with microinjection of EAA receptor antagonists in other studies (e.g. [1,2,4,29]). The antagonist concentrations employed were in the same range as those reported previously to block the medullary ionotropic EAA receptors in vivo selectively (e.g.…”

Section: Discussionsupporting

confidence: 65%

Respiratory responses to ionotropic glutamate receptor antagonists in the ventral respiratory group of the rabbit

Bongianni

Mutolo

Carfì

et al. 2002

Pfl�gers Archiv European Journal of Physiology

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Selective excitatory amino acid receptor antagonists acting on either N-methyl-D-aspartic acid (NMDA) or non-NMDA receptors were microinjected (30-50 nl) bilaterally into different subregions of the ventral respiratory group (VRG) of a-chloralose-urethane anaesthetized, vagotomized, paralysed and artificially ventilated rabbits. Blockade of NMDA receptors by d(-)-2-amino-5-phosphonopentanoic acid (D-AP5; 1 or 10 mM) within the inspiratory portion of the VRG (iVRG) dose-dependently decreased the peak amplitude and rate of rise of phrenic nerve activity, without significant changes in respiratory timing. Decreases in respiratory frequency and peak phrenic amplitude up to apnoea were evoked by 20 mM D-AP5; phrenic nerve activity was restored transiently by hypoxic or hypercapnic stimulation during D-AP5-induced apnoea. Microinjections of the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 1, 10 or 20 mM) into the iVRG provoked less intense depressant respiratory effects. No significant respiratory responses were evoked by microinjections of these antagonists into more caudal VRG subregions. The results suggest that ionotropic glutamate receptors within the iVRG are involved mainly in the control of the intensity of inspiratory activity, with a major role played by NMDA receptors. Glutamate receptor antagonism in the iVRG does not seem to impair the basic mechanisms underlying respiratory rhythm generation.

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“…3) and the ability of cyclothiazide (an agent which has been shown to prevent desensitization of AMPA receptors; Patneau et al 1993;Wong & Mayer, 1993) to increase both amplitude and rate of breathing. The arrest of breathing following NBQX instillation into the fourth ventricle CSF in unanaesthetized fetal sheep is similar to microinjections of CNQX in the caudal ventrolateral medulla of adult rats (Dillon et al 1991;Jung et al 1991) under urethane anaesthesia and to bath applications in the isolated neonatal rat brainstem-spinal cord preparation (Greer et al 1991). In contrast in decerebrate adult cats neither injection of CNQX into the retrotrapezoid nucleus (Nattie et al 1993) nor systemic infusion of NBQX consistently produced apnoea (Pierrefiche et al 1994).…”

Section: Discussionmentioning

confidence: 71%

“…In anaesthetized adult rats CNQX showed an increase in breath frequency (Jung et al 1991) while in decerebrate adult cats NBQX did not change inspiratory or expiratory timing (Pierrefiche et al Non-NMDA receptors and fetal respiration 1994). In fetal sheep both Ti and Te were lengthened by CNQX, in contrast to observations in adult animals.…”

Section: Discussionmentioning

confidence: 99%

“…Intracellular recordings from phrenic motoneurones in this preparation showed that glutamate acting at non-NMDA receptors mediates the synaptic transmission necessary for inspiratory drive (Liu, Feldman & Smith, 1990). In anaesthetized spontaneously breathing rats, injection of the non-NMDA antagonist CNQX in the caudal ventrolateral medulla resulted in apnoea (Jung, Bruce & Katona, 1991), as did the broader spectrum antagonist kynurenic acid (Dillon, Welsh & Waldrop, 1991). In contrast experiments in decerebrate cats which had been vagotomized showed that the non-NMDA antagonist 2,3-dihydro-6-nitro-7-sulphamoyl-benzo(f) quinoxaline (NBQX) given intravenously did not consistently result in apnoea when given alone (Pierrefiche, Foutz, Champagnat & Denavit-Saubi e, 1994).…”

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confidence: 84%

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Non‐NMDA receptors modulate respiratory drive in fetal sheep

Bissonnette

Hohimer

Knopp

1997

The Journal of Physiology

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Experiments were carried out in unanaesthetized fetal sheep to evaluate the significance of non‐N‐methyl‐d‐aspartate (non‐NMDA) receptor neurotransmission in the expression of fetal breathing movements. Catheters placed in the trachea and amniotic fluid and electrodes beneath the parietal bones and in the nuchal muscle were used to monitor breath amplitude and frequency and fetal behavioural state. Experiments were carried out by instillation of neurotransmitter agonists, antagonists or receptor modulators into the cerebrospinal fluid (CSF) of the fourth ventricle by means of a chronic catheter introduced through the foramen magnum. The non‐NMDA receptor antagonist 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX) decreased respiratory rate in a dose dependent manner by lengthening both inspiratory time (Ti) and expiratory time (Te). Kainate and (R,S)‐α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid (AMPA) increased breath amplitude. Instillation of the antagonist 2,3‐dihydro‐6‐nitro‐7‐sulphamoyl‐benzo(f) quinoxaline (NBQX) prior to administering AMPA resulted in apnoea, which was not overcome by the agonist. Cyclothiazide, which has been shown to prevent desensitization of AMPA receptors, caused an increase in both breath amplitude (152 ± 73%; mean ±s.d.; P= 0.004) and frequency (46 ± 37%; P= 0.049). These data suggest that glutamate acting at non‐NMDA receptors is an essential component for the expression of fetal breathing movements, and that under resting conditions these non‐NMDA receptors are desensitized following glutamate synaptic release.

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Cardiorespiratory responses to glutamatergic antagonists in the caudal ventrolateral medulla of rats

Cited by 31 publications

References 29 publications

Metabotropic glutamate receptors in the ventrolateral medulla of rats.

Metabotropic glutamate receptors in the ventrolateral medulla of rats.

Respiratory responses to ionotropic glutamate receptor antagonists in the ventral respiratory group of the rabbit

Non‐NMDA receptors modulate respiratory drive in fetal sheep

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