NMDA receptors in the intermediolateral column of the spinal cord mediate sympathoexcitatory cardiac responses elicited from the ventrolateral medullary pressor area

Sundaram, Kalyana; Sapru, Hreday N.

doi:10.1016/0006-8993(91)90882-v

Cited by 51 publications

(16 citation statements)

References 17 publications

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“…The stimulation of RVLM neurons was mediated via iGLURs because bilateral microinjections of iGLUR antagonists attenuated the increases in MAP and SNA. We have previously reported that the projection from the RVLM to the IML is glutamatergic (36). Our observation in the rat regarding the CPT-induced increase in GSNA is consistent with earlier reports in humans in which CPT increased muscle or skin SNA (5,10,40).…”

Section: Discussionsupporting

confidence: 93%

“…The rostral ventrolateral medullary pressor area (RVLM) (11,23,30,33,42) and the nucleus ambiguus (nAmb) (24) are final structures in the medulla that are involved in the regulation of AP and HR, respectively. It is also well established that the intermediolateral cell column in the thoracolumbar cord (IML) is the final station in the central nervous system that is involved in the regulation of AP, HR, and SNA (1,29,35,36). Therefore, this investigation was focused on the role of the RVLM, nAmb and spinal cord in mediating the cardiovascular responses to the CPT.…”

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confidence: 99%

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Cold pressor test in the rat: medullary and spinal pathways and neurotransmitters

Nakamura

Kawabe

Sapru³

2008

American Journal of Physiology-Heart and Circulatory Physiology

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This study was designed to delineate the medullary and spinal pathways mediating the cardiovascular responses to cold pressor test (CPT) and to identify neurotransmitters in these pathways. Experiments were done in barodenervated, urethane-anesthetized, male Wistar rats. The CPT was performed by immersing the limbs and ventral half of the body of the rat in ice-cold water (0.5 degrees C) for 2 min. CPT elicited an immediate increase in mean arterial pressure (MAP), heart rate (HR), and greater splanchnic nerve activity (GSNA). Bilateral blockade of ionotropic glutamate receptors (iGLURs) in the rostral ventrolateral medullary pressor area (RVLM) significantly attenuated the CPT-induced responses. Bilateral blockade of gamma-aminobutyric acid (GABA) receptors, but not iGLURs, in the nucleus ambiguus (nAmb) significantly reduced the CPT-induced increases in HR, but not MAP. Blockade of spinal iGLURs caused a significant reduction in CPT-induced increases in MAP and GSNA, whereas the increases in HR were reduced to a lesser extent. Combination of the blockade of spinal iGLURs and bilateral vagotomy or intravenous atropine almost completely blocked CPT-induced tachycardia. Midcollicular decerebration significantly reduced CPT-induced increases in MAP and HR. These results indicated that: 1) CPT-induced increases in MAP, HR, and GSNA were mediated by activation of iGLURs in the RVLM and spinal cord, 2) activation of GABA receptors in the nAmb also contributed to the CPT-induced tachycardic responses, and 3) brain areas rostral to the brain stem also participated in the CPT-induced pressor and tachycardic responses.

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Section: Discussionsupporting

confidence: 93%

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confidence: 99%

Cold pressor test in the rat: medullary and spinal pathways and neurotransmitters

Nakamura

Kawabe

Sapru³

2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…This projection is thought to mainly originate in the rostral ventrolateral medulla (RVLM, Morrison et al 1991;Mills et al 1990;Verberne et al 1990;Bazil & Gordon, 1991;Sundaram & Sapru, 1991;Kapoor et al 1992;Deuchars et al 1995). Since these RVLM neurones can be activated by stimulating neurones in the PVN (Yang & Coote, 1998), they may have participated in the PVN-induced excitatory effects on RSNA, which were blocked by intrathecal application of the broad spectrum ionotropic receptor antagonist kynurenic acid in the present experiments.…”

Section: Pvn-spinal Receptorsmentioning

confidence: 54%

Neuropeptides, Amines and Amino Acids as Mediators of the Sympathetic Effects of Paraventricular Nucleus Activation in the Rat

Yang¹,

Wheatley

Coote³

2002

Experimental Physiology

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The aim of the present study was to determine the influence on renal sympathetic nerve activity of the different chemically coded neuronal phenotypes that project from the paraventricular nucleus (PVN) to the spinal cord. Experiments were carried out on male Wistar rats anaesthetised with chloralose and urethane. Changes in renal sympathetic nerve activity were measured following activation of neurones in the PVN with D,L-homocysteic acid (100 nl, 200 mM), before and following intrathecal application of glutamate, vasopressin, oxytocin, dopamine and their receptor antagonists. Excitatory and inhibitory effects on renal sympathetic nerve activity were elicited by PVN stimulation. PVN excitatory effects were mimicked by intrathecal administration of glutamate and vasopressin and selectively antagonised by intrathecal administration of kynurenic acid and a V 1a receptor antagonist, respectively. A low dose of dopamine increased renal sympathetic activity and this was selectively antagonised by haloperidol; however, the latter was without effect on PVN excitatory responses. A high dose of dopamine decreased renal sympathetic nerve activity and this was selectively blocked by a D1 dopamine receptor antagonist (SCH 23390), which also antagonised a minority of inhibitory responses obtained from the caudal extension of the PVN. Oxytocin also had two actions: in 5 rats it inhibited and in 10 rats it increased renal sympathetic nerve activity, both actions being blocked selectively by oxytocin receptor antagonists. Neither of the PVN effects on renal sympathetic nerve activity appeared to be dependent on oxytocin pathways. Tests with intrathecal administration of bicuculline showed that PVN inhibition of renal sympathetic nerve activity was not dependent on spinal GABA A receptor activation. The results show that PVN-induced excitation of sympathetic activity to the kidney is mainly mediated by glutamate or vasopressin neurones whereas dopamine via D1 receptors may mediate some of the PVN inhibitory effects. Experimental Physiology (2002) METHODSThe experiments were approved by the local ethical committee of the University of Birmingham and were performed under a Home Office Licence in accordance with the UK Animals (Scientific Procedures) Act 1986. Animal preparationThe experiments were performed on 52 male rats (Wistar) weighing 292 ± 4.0 g, anaesthetised with a mixture of urethane and a-chloralose (650 mg kg _1 and 50 mg kg _1 , respectively) given I.V. after initial induction with enflurane. An adequate depth of anaesthesia was ensured by observing arterial blood pressure, heart rate and the absence of corneal and paw-pinch reflexes, and was maintained by regular hourly administration of additional anaesthetic (I.V.), or sooner if needed. The femoral artery was cannulated with a polyethylene catheter (PE-50 tubing) which was connected to a pressure transducer for continuous recording of arterial blood pressure. A femoral vein was also cannulated for administration of drugs.

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“…After complete spinal cord transection, NMDA receptor binding is decreased at 1 to 2 weeks (Krenz and Weaver, 1998) but not at 1 day (Sun and Faden, 1994). NMDA receptors underlie polysynaptic neurotransmission of somatic (Turski et al, 1990) and visceral reflexes (Mills et al, 1988;Sundaram and Sapru, 1991). Therefore, alteration in NMDA receptor function might mediate the decrease in reflexive function seen at 6 days after SCI (Thompson et al, 1992).…”

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confidence: 99%

Altered Glutamate Receptor Function during Recovery of Bladder Detrusor-External Urethral Sphincter Coordination in a Rat Model of Spinal Cord Injury

Pikov¹,

Wrathall²

2002

J Pharmacol Exp Ther

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Coordination of the bladder detrusor and the external urethral sphincter is a supraspinally controlled reflex that is essential for efficient micturition. This coordination is permanently lost after spinal cord transection but can recover chronically after incomplete spinal cord injury (SCI). As glutamatergic transmission plays a key role in all levels of detrusor-external urethral sphincter coordination, we examined the role of potential alterations in glutamatergic control in its recovery after SCI. Rats were subjected to standardized incomplete contusion injury. Detrusorexternal urethral sphincter coordination was evaluated urodynamically at 5 days (subacute) and 8 weeks (chronic) after SCI. Sensitivity of coordinated activation of the external urethral sphincter in response to bladder distension to the ␣ -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid/kainate antagonist 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo(f)quinoxaline-7-sulfonamide disodium (NBQX) and to the N-methyl-Daspartate (NMDA) antagonist R(Ϫ-3-(2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid (CPP) was determined by intrathecal application at the L6 spinal cord level during urodynamic recordings. We found that while detrusor contractions recovered at 5 days after SCI, coordinated activation of the external urethral sphincter was significantly impaired at 5 days and recovered only by 8 weeks. There was no difference in sensitivity of detrusor-external urethral sphincter coordination to NBQX at the subacute or chronic time points. However, external urethral sphincter response to bladder distension was sensitive to a 50% lower dose of CPP at 5 days compared with uninjured rats or chronic recovered SCI rats. Thus, alterations in NMDA receptor function appeared to be involved in recovery of detrusor-external urethral sphincter coordination after incomplete SCI.

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NMDA receptors in the intermediolateral column of the spinal cord mediate sympathoexcitatory cardiac responses elicited from the ventrolateral medullary pressor area

Cited by 51 publications

References 17 publications

Cold pressor test in the rat: medullary and spinal pathways and neurotransmitters

Cold pressor test in the rat: medullary and spinal pathways and neurotransmitters

Neuropeptides, Amines and Amino Acids as Mediators of the Sympathetic Effects of Paraventricular Nucleus Activation in the Rat

Altered Glutamate Receptor Function during Recovery of Bladder Detrusor-External Urethral Sphincter Coordination in a Rat Model of Spinal Cord Injury

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