Relevant bibliographies by topics / Ventrolateral Medulla / Journal articles

Journal articles on the topic 'Ventrolateral Medulla'

To see the other types of publications on this topic, follow the link: Ventrolateral Medulla.
Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Ventrolateral Medulla.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Mandal, Aloke K., Pingyu Zhong, Kenneth J. Kellar, and Richard A. Gillis. "Ventrolateral Medulla." Journal of Cardiovascular Pharmacology 15 (1990): S49—S60. http://dx.doi.org/10.1097/00005344-199000157-00007.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Mandal, Aloke K., Pingyu Zhong, Kenneth J. Kellar, and Richard A. Gillis. "Ventrolateral Medulla." Journal of Cardiovascular Pharmacology 15 (January 1990): S49—S60. http://dx.doi.org/10.1097/00005344-199001001-00007.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

McCall, R. B. "GABA-mediated inhibition of sympathoexcitatory neurons by midline medullary stimulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255, no. 4 (October 1, 1988): R605—R615. http://dx.doi.org/10.1152/ajpregu.1988.255.4.r605.

Full text
Abstract:
The present investigation determined whether the effects of electrical stimulation of depressor sites in midline medullary raphe nuclei were a result of inhibition of sympathoexcitatory medullospinal neurons in the rostral ventrolateral medulla of anesthetized cats. Electrical stimulation of the raphe inhibited inferior cardiac sympathetic activity. Microinjections of glutamate mimicked the effects of electrical stimulation. Electrical stimulation inhibited sympathoexcitatory neurons in the rostral ventrolateral medulla. The onset of the sympathoinhibition recorded from the inferior cardiac nerve (72 ms) was equal to the sum of the onset latency of the sympathoexcitatory response elicited from the rostral ventrolateral medulla (49 ms) plus the conduction time in the raphe to rostral ventrolateral sympathoinhibitory pathway (23 ms). Raphe stimulation excited a second set of neurons in the rostral ventrolateral medulla with an onset of 21 ms. Microiontophoretically applied bicuculline increased the discharge of sympathoexcitatory neurons and blocked the raphe-evoked inhibition. Iontophoretic glutamate excited sympathoexcitatory neurons but failed to antagonize raphe-elicited inhibition. These data suggest that neuronal elements in medullary raphe nuclei tonically inhibit sympathoexcitatory medullospinal neurons in the rostral ventrolateral medulla by activating closely adjacent gamma-aminobutyric acid (GABA) interneurons.
APA, Harvard, Vancouver, ISO, and other styles
4

Sun, Wei, and W. Michael Panneton. "The caudal pressor area of the rat: its precise location and projections to the ventrolateral medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 3 (September 1, 2002): R768—R778. http://dx.doi.org/10.1152/ajpregu.00184.2002.

Full text
Abstract:
Investigators have demonstrated pressor areas in the medullas of various species. The present study precisely localized the pressor area in the caudal medulla of the rat and determined its projections to the caudal and rostral ventrolateral medulla. The caudal medulla first was mapped grossly in rats with injections (30 nl) of glutamate (30-, 15-, and 7.5-nmol doses) placed 0.5, 1.0, and 1.5 mm caudal to the calamus scriptorius, 1.0, 1.5, and 2.0 mm lateral to the midline, and 1.8, 1.7, and 1.6 mm ventral to the dorsal medullary surface, respectively, and their arterial pressures were recorded. One of these nine injections showed significant increases in arterial pressure. We micromapped this area with a total of 27 injections of glutamate (10 nl; 5 nmol) placed 300 μm apart at 3 different dorsoventral levels. This micromapping study pinpointed the precise location of caudal pressor area (CPA) neurons in a restricted region lateral to the caudal end of the lateral reticular nucleus and ventromedial to the medullary dorsal horn near the level of the pyramidal decussation. Injections of glutamate into this spot, 1.0 mm caudal to the calamus scriptorius, 2.0 mm lateral to the midline, and 1.7 mm ventral from the dorsal surface of the medulla, induced significant increases in arterial pressure. The neuroanatomic connections of neurons in the CPA to the ventrolateral medulla were then investigated with iontophoretic injections of either the anterograde tracer biotinylated dextran amine (BDA) made into the CPA or the retrograde tracer FluoroGold (FG) injected into either the caudal or rostral ventrolateral medulla. BDA injections resulted in bouton-laden fibers throughout both caudal and rostral portions of the ventrolateral medulla. Either of the FG injections resulted in numerous spindle-shaped neurons interspersed between the longitudinal fiber bundles running through the CPA area. The proximity of the CPA neurons to the A1 catecholaminergic cell group is discussed.
APA, Harvard, Vancouver, ISO, and other styles
5

Bergamaschi, Cássia T., Ruy R. Campos, and Oswaldo U. Lopes. "Rostral Ventrolateral Medulla." Hypertension 34, no. 4 (October 1999): 744–47. http://dx.doi.org/10.1161/01.hyp.34.4.744.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Kubo, T., H. Amano, and Y. Misu. "Caudal ventrolateral medulla." Naunyn-Schmiedeberg's Archives of Pharmacology 328, no. 4 (February 1985): 368–72. http://dx.doi.org/10.1007/bf00692902.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Li, Y. W., Z. J. Gieroba, R. M. McAllen, and W. W. Blessing. "Neurons in rabbit caudal ventrolateral medulla inhibit bulbospinal barosensitive neurons in rostral medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 1 (July 1, 1991): R44—R51. http://dx.doi.org/10.1152/ajpregu.1991.261.1.r44.

Full text
Abstract:
We made extracellular recordings from 104 spinally projecting neurons in the rostral ventrolateral medulla of urethan-anesthetized rabbits to test whether inhibitory vasomotor neurons in the caudal ventrolateral medulla act by inhibiting rostral sympathoexcitatory neurons. The median conduction velocity was 8.3 m/s, and the median discharge rate was 2.9 spikes/s. Raising arterial pressure with intravenous phenylephrine inhibited 88% of 77 neurons tested. The remaining units were excited. Lowering arterial pressure with nitroprusside excited 90% of 30 neurons tested. Remaining units were unaffected. Ninety-one percent of 58 rostral neurons inhibited by phenylephrine were also inhibited by injection of L-glutamate into the caudal ventrolateral medulla and 81% of 43 tested were excited by caudal injection of gamma-aminobutyric acid. These results confirm our suggestion [Brain Res. 253: 161-171, 1982; Am. J. Physiol. 254 (Heart Circ. Physiol. 23): H686-H692, 1988] and the findings of S. K. Agarwal, A. J. Gelsema, and F. R. Calaresu [Am. J. Physiol. 257 (Regulatory Integrative Comp. Physiol. 26): R265-R270, 1989]. The depressor neurons in the caudal medulla act substantially by inhibition of spinally projecting sympathoexcitatory neurons in the rostral medulla. All rostral units excited by phenylephrine were also excited by injections of L-glutamate into the caudal ventrolateral medulla, suggesting that some sympathoinhibition of baroreceptor and caudal medullary origin may take place in the spinal cord and be mediated by a subpopulation of rostral sympathoinhibitory neurons.
APA, Harvard, Vancouver, ISO, and other styles
8

Blessing, W. W. "Depressor neurons in rabbit caudal medulla act via GABA receptors in rostral medulla." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 4 (April 1, 1988): H686—H692. http://dx.doi.org/10.1152/ajpheart.1988.254.4.h686.

Full text
Abstract:
Experiments were conducted in urethan-anesthetized rabbits to determine whether vasomotor effects elicited by activation or inhibition of the caudal ventrolateral medulla depend on gamma-aminobutyric acid (GABA)ergic, glycinergic, or alpha-adrenergic receptors in the region of the rostral ventrolateral medulla, which contains the bulbospinal sympathoexcitatory neurons. Bilateral injection of bicuculline methiodide into the rostral medulla caused a dose-related reduction in the fall in arterial pressure and in the inhibition of renal sympathetic nerve activity normally elicited by chemical stimulation of neurons in the caudal medulla using local injection of L-glutamate. When both bicuculline and muscimol were injected into the rostral medulla at the same time, resting arterial pressure was maintained at base-line levels, and the sympathoexcitatory neurons remained normally excitable by local injection of L-glutamate into the rostral medulla. In the presence of this mixed antagonist-agonist GABAergic blockade, both decreases and increases in arterial pressure elicited by excitation or inhibition of neuronal function in the caudal medulla were abolished. Similar effects were not observed after blockade of glycinergic or alpha-adrenergic receptors in the rostral ventrolateral medulla. Results suggest that the depressor neurons in the caudal ventrolateral medulla alter peripheral sympathetic vasomotor activity almost entirely by an action on GABAergic receptors in the rostral ventrolateral medulla.
APA, Harvard, Vancouver, ISO, and other styles
9

Naraghi, Ramin, Michael R. Gaab, Gerhard F. Walter, and Berthold Kleineberg. "Arterial hypertension and neurovascular compression at the ventrolateral medulla." Journal of Neurosurgery 77, no. 1 (July 1992): 103–12. http://dx.doi.org/10.3171/jns.1992.77.1.0103.

Full text
Abstract:
✓ Intraoperative observations and animal experiments suggest that neurovascular compression at the left ventrolateral medulla is a possible etiological factor in essential hypertension. In pursuing this hypothesis, the authors examined the neurovascular relations in the posterior cranial fossa of 24 patients with essential hypertension, of 10 with renal hypertension, and of 21 normotensive control patients. Artificial perfusion of the vessels and microsurgical investigations during autopsy identified the vascular relations at the brain stem and at the root entry zone of the caudal cranial nerves. There was no evidence of neurovascular compression at the ventrolateral medulla on the left side in any patient from the control group or among those with renal hypertension. Two normotensive patients had neurovascular compression at the right ventrolateral medulla by the posterior inferior cerebellar artery. In contrast, all patients with essential hypertension had definite neurovascular compression at the left ventrolateral medulla. Additional compression of the right side was seen in three of these patients. Based on the anatomical appearance, it was possible to define three distinct types of neurovascular compression at the ventrolateral medulla. Common to all three types is the compression of the medulla oblongata at its rostral part just caudal to the pontomedullary junction and lateral to the olive in the retro-olivary sulcus. Comparative histopathological study of the microsurgically examined brain-stem specimens revealed no differences between patients with essential hypertension, those with renal hypertension, and normal controls. There was a structural integrity at the site of neurovascular compression at the ventrolateral medulla. The microanatomical findings of this study show that neurovascular relations at the ventrolateral medulla in essential hypertension give rise to pulsatile compression on the left. This supports Jannetta's hypothesis of neurovascular compression at the left ventrolateral medulla as an etiology of essential hypertension.
APA, Harvard, Vancouver, ISO, and other styles
10

Steinbacher, B. C., and B. J. Yates. "Processing of vestibular and other inputs by the caudal ventrolateral medullary reticular formation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 4 (October 1, 1996): R1070—R1077. http://dx.doi.org/10.1152/ajpregu.1996.271.4.r1070.

Full text
Abstract:
Lesions of the lateral medullary reticular formation caudal to the obex abolish vestibulosympathetic and somatosympathetic responses; this area also contains neurons that mediate baroreceptor reflexes. Recordings were made from neurons in the caudal medullary reticular formation of cats that were decerebrate or anesthetized using alpha-chloralose-urethan to determine whether common neurons responded to electrical stimulation of vestibular and hindlimb afferents and had cardiac-related (i.e., baroreceptor) inputs. Many neurons in the ventrolateral portion of the caudal reticular formation received labyrinthine inputs, and they were interspersed with neurons that received baroreceptor signals. However, virtually none of the units received convergent baroreceptor and vestibular inputs, suggesting that separate pathways from the caudal ventrolateral medulla mediate baroreceptor and vestibulosympathetic reflexes. Furthermore, the neurons that received labyrinthine signals could not be antidromically activated from electrodes inserted into the rostral ventrolateral medulla, which is known to mediate vestibulosympathetic responses; thus an indirect pathway must convey vestibular inputs from the caudal to rostral medullary reticular formation. Over 75% of both neurons with baroreceptor inputs and cells with vestibular signals responded to sciatic nerve stimulation, suggesting that more than one pathway from the caudal medulla may mediate somatosympathetic responses.
APA, Harvard, Vancouver, ISO, and other styles
11

Porter, J. P., and M. J. Brody. "Neural projections from paraventricular nucleus that subserve vasomotor functions." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 248, no. 3 (March 1, 1985): R271—R281. http://dx.doi.org/10.1152/ajpregu.1985.248.3.r271.

Full text
Abstract:
Descending projections from the paraventricular nucleus of the hypothalamus (PVN) either terminate in the dorsal medulla or pass through the ventrolateral medulla to terminate in the intermediolateral column of the spinal cord. We sought to determine whether a cardiovascular function is subserved by these pathways. Electrical stimulation of the PVN in urethan-anesthetized rats produced increases in blood pressure and mesenteric and renal vascular resistances while hindquarter resistance decreased. This integrated cardiovascular response appeared to be neurogenically mediated because it was virtually abolished by ganglionic blockade and unaffected by blockade of peripheral vascular vasopressin receptors. Adrenal catecholamines appeared to contribute since adrenalectomy reduced the response, especially the hindquarter vasodilation. Interruption with a knife cut of the PVN-dorsal medullary pathway did not affect the response to PVN stimulation except for hindquarter vasodilation, which was reduced significantly. Interruption of the PVN-ventrolateral medullary pathway by local microinjection of lidocaine blocked the pressor and vasoconstrictor responses to PVN stimulation but enhanced the hindquarter vasodilation. These data suggest that fibers descending from the PVN responsible for skeletal muscle vasodilation pass to or through the dorsal medulla, whereas efferent vasoconstrictor pathways from the PVN appear to course through, or synapse in, the ventrolateral medulla.
APA, Harvard, Vancouver, ISO, and other styles
12

Guyenet, Patrice G., Ruth L. Stornetta, Benjamin B. Holloway, George M. P. R. Souza, and Stephen B. G. Abbott. "Rostral Ventrolateral Medulla and Hypertension." Hypertension 72, no. 3 (September 2018): 559–66. http://dx.doi.org/10.1161/hypertensionaha.118.10921.

Full text
APA, Harvard, Vancouver, ISO, and other styles
13

Guyenet, P. G., R. A. Darnall, and T. A. Riley. "Rostral ventrolateral medulla and sympathorespiratory integration in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 259, no. 5 (November 1, 1990): R1063—R1074. http://dx.doi.org/10.1152/ajpregu.1990.259.5.r1063.

Full text
Abstract:
The respiratory modulation of the lumbar sympathetic nerve discharge (LSND) was examined in halothane-anesthetized, paralyzed, and vagotomized rats by means of phrenic nerve discharge (PND)-triggered histograms. The respiratory modulation was 1) proportional to PND amplitude during chemoreceptor activation with CO2 and 2) reduced at elevated arterial pressure. Bilateral injections of bicuculline [gamma-aminobutyric acid (GABA)A receptor antagonist, n = 5] into the rostral ventrolateral medulla (RVLM), but not into medullary raphe, reversibly increased mean arterial pressure (MAP) and resting LSND, decreased the baroreflex, reduced PND amplitude and central respiratory rate, and greatly magnified the respiratory modulation of LSND. Injections of strychnine (glycine receptor antagonist, n = 5) or phaclofen (GABAB receptor antagonist, n = 2) into RVLM were without effect. Injections of kynurenic acid (excitatory amino acid receptor antagonist) into RVLM (n = 8), but not raphe (n = 3), reduced PND amplitude, increased central respiratory rate, reduced MAP, elevated resting LSND slightly, and greatly reduced the respiratory modulation of LSND. These data suggest that the rostral tip of the ventrolateral medulla represents a critical link between the central respiratory rhythm generator and the vasomotor outflow. Also, it indicates that the respiratory modulation of SND does not involve a gating of the activity of the medullary neurons that convey baroreceptor information to RVLM sympathoexcitatory neurons.
APA, Harvard, Vancouver, ISO, and other styles
14

Adams, M., T. Chonan, N. S. Cherniack, and C. von Euler. "Effects on respiratory pattern of focal cooling in the medulla of the dog." Journal of Applied Physiology 65, no. 5 (November 1, 1988): 2004–10. http://dx.doi.org/10.1152/jappl.1988.65.5.2004.

Full text
Abstract:
Studies in cats have shown that, in addition to respiratory neuron groups in the dorsomedial (DRG) and ventrolateral (VRG) medulla, neural structures in the most ventral medullary regions are important for the maintenance of respiratory rhythm. The purpose of this study was to determine whether a similar superficially located ventral region was present in the dog and to assess the role of each of the other regions in the canine medulla important in the control of breathing, in 20 anesthetized, vagotomized, and artificially ventilated dogs, a cryoprobe was used to cool selected regions of the medulla to 15-20 degrees C. Respiratory output was determined from phrenic nerve or diaphragm electrical activity. Cooling in or near the nucleus of the solitary tract altered timing and produced little change in the amplitude or rate of rise of inspiratory activity; lengthening of inspiratory time was the most common timing effect observed. Cooling in ventrolateral regions affected the amplitude and rate of rise of respiratory activity. Depression of neural tidal volume and apnea could be produced by unilateral cooling in two ventrolateral regions: 1) near the nucleus ambiguus and nucleus para-ambiguus and 2) just beneath the ventral medullary surface. These findings indicate that in the dog dorsomedial neural structures influence respiratory timing, whereas more ventral structures are important to respiratory drive.
APA, Harvard, Vancouver, ISO, and other styles
15

Badoer, Emilio, Michael J. McKinley, Brian J. Oldfield, and Robin M. McAllen. "Localization of barosensitive neurons in the caudal ventrolateral medulla which project to the rostral ventrolateral medulla." Brain Research 657, no. 1-2 (September 1994): 258–68. http://dx.doi.org/10.1016/0006-8993(94)90975-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
16

Gieroba, Z. J., Y. W. Li, and W. W. Blessing. "Characteristics of caudal ventrolateral medullary neurons antidromically activated from rostral ventrolateral medulla in the rabbit." Brain Research 582, no. 2 (June 1992): 196–207. http://dx.doi.org/10.1016/0006-8993(92)90133-t.

Full text
APA, Harvard, Vancouver, ISO, and other styles
17

Vizzard, M. A., A. Standish, and W. S. Ammons. "Renal afferent input to the ventrolateral medulla of the cat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 2 (August 1, 1992): R412—R422. http://dx.doi.org/10.1152/ajpregu.1992.263.2.r412.

Full text
Abstract:
Experiments were performed to determine if information from the kidneys projects to the rostral ventrolateral medulla. Extracellular action potentials were recorded from 148 cells within the rostral ventrolateral medulla of alpha-chloralose-anesthetized cats. Cells within the rostral ventrolateral medulla were tested for responses to electrical stimulation of both left and right renal nerves. Electrical stimulation of renal nerves excited 144 cells (97.3%) and inhibited 4. The majority of cells received either bilateral or contralateral renal nerve input. Cells with bilateral renal nerve input responded to contralateral renal nerve stimulation with a significantly greater number of impulses compared with ipsilateral renal nerve stimulation (P less than 0.05). All cells but one responding to renal nerve stimulation had convergent somatic input. Comparisons between thresholds for cell responses and activation thresholds for the A and C volleys of the compound action potential recorded in the least splanchnic nerve revealed that 44 cells required activation of A delta-fibers, and 12 cells required activation of both A delta- and C-fibers. A conditioning stimulus applied to renal nerves on one side significantly decreased the response elicited by a test stimulus applied to the renal nerves on the opposite side for at least 300 ms (P less than 0.05). The demonstration that an afferent connection exists between the kidneys and the ventrolateral medulla suggests that the rostral ventrolateral medulla may play a role in mediating supraspinal reflexes of renal origin.
APA, Harvard, Vancouver, ISO, and other styles
18

Xing, Xiao-Hui, Ling Wang, Zhi-Ren Rao, and Jing-Zao Chen. "Infrasonic Stimulation Induced Fos Expression in Medullary Catecholaminergic Neurons in Rats." Journal of Low Frequency Noise, Vibration and Active Control 17, no. 3 (September 1998): 133–39. http://dx.doi.org/10.1177/026309239801700303.

Full text
Abstract:
To clarify the effects of infrasound on the medulla, catecholaminergic neurons in the medulla expressing Fos were investigated in the rats by immunohistochemical method. After exposure to infrasound (8Hz, 120dB) for 2 hours, animals were sacrificed and sections of the medulla were stained immunohistochemically for Fos and tyrosine hydroxylase (TH). Many Fos-like immunoreactive neurons were found in the nucleus tractus solitarii (NTS) and Ventrolateral medulla (VLM) at the middle and caudal levels of medulla, only a few of them scattered in the reticular formation between NTS and VLM. Some Fos immunoreactive neurons were also labeled with TH. These results indicated that medulla was sensitive to infrasonic stimulation and some medullary catecholaminergic neurons might be involved in the responses to the stress produced by infrasound.
APA, Harvard, Vancouver, ISO, and other styles
19

Lindsey, B. G., L. S. Segers, K. F. Morris, Y. M. Hernandez, S. Saporta, and R. Shannon. "Distributed actions and dynamic associations in respiratory-related neuronal assemblies of the ventrolateral medulla and brain stem midline: evidence from spike train analysis." Journal of Neurophysiology 72, no. 4 (October 1, 1994): 1830–51. http://dx.doi.org/10.1152/jn.1994.72.4.1830.

Full text
Abstract:
1. Considerable evidence indicates that neurons in the brain stem midline and ventrolateral medulla participate in the control of breathing. This work was undertaken to detect and evaluate evidence for functional links that coordinate the parallel operations of neurons distributed in these two domains. 2. Data were from 51 Dial-urethan-anesthetized, bilaterally vagotomized, paralyzed, artificially ventilated cats. Planar arrays of tungsten microelectrodes were used to monitor simultaneously spike trains in two or three of the following regions: n. raphe obscurus-n. raphe pallidus, n. raphe magnus, rostral ventrolateral medulla, and caudal ventrolateral medulla. Efferent phrenic nerve activity was recorded to indicate the phases of the respiratory cycle. Electrodes in the ventral spinal cord (C3) were used in antidromic stimulation tests for spinal projections of neurons. 3. Spike trains of 1,243 neurons were tested for respiratory modulated firing rates with cycle-triggered histograms and an analysis of variance with the use of a subjects-by-treatments experimental design. Functional associations were detected and evaluated with cross-correlograms, snowflakes, and the gravity method. 4. Each of 2,310 pairs of neurons studied included one neuron monitored within 0.6 nm of the brain stem midline and a second cell recorded in the ventrolateral medulla; 117 of these pairs (5%) included a neuron with a spinal projection, identified with antidromic stimulation methods, that extended to at least the third cervical segment. Short-time scale correlations were detected in 110 (4.7%) pairs of neurons. Primary cross-correlogram features included 40 central peaks, 47 offset peaks, 4 central troughs, and 19 offset troughs. 5. In 14 data sets, multiple short-time scale correlations were found among three or more simultaneously recorded neurons distributed between both midline and ventrolateral domains. The results suggested that elements of up to three layers of interneurons were monitored simultaneously. Evidence for concurrent serial and parallel regulation of impulse synchrony was detected. Gravitational representations demonstrated respiratory-phase dependent synchrony among neurons distributed in both brain stem regions. 6. The results support a model of the brain stem respiratory network composed of coordinated distributed subassemblies and provide evidence for several hypotheses. 1) Copies of respiratory drive information from rostral ventrolateral medullary (RVLM) respiratory neurons are transmitted to midline neurons. 2) Midline neurons act on respiratory-related neurons in the RVLM to modulate phase timing. 3) Impulse synchrony of midline neurons is influenced by concurrent divergent actions of both midline and ventrolateral neurons.(ABSTRACT TRUNCATED AT 400 WORDS)
APA, Harvard, Vancouver, ISO, and other styles
20

Terui, Naohito, Noboru Masuda, Yuka Saeki, Naohiro Koshiya, and Mamoru Kumada. "Electrophysiological evidence that neurons in the caudal ventrolateral medulla inhibit sympathoexcitatory neurons in the rostral ventrolateral medulla." Neuroscience Research Supplements 15 (January 1990): S20. http://dx.doi.org/10.1016/0921-8696(90)90093-i.

Full text
APA, Harvard, Vancouver, ISO, and other styles
21

Terui, Naohito, Noboru Masuda, Yuka Saeki, Naohiro Koshiya, and Mamoru Kumada. "Electrophysiological evidence that neurons in the caudal ventrolateral medulla inhibit sympathoexcitatory neurons in the rostral ventrolateral medulla." Neuroscience Research Supplements 11 (January 1990): S20. http://dx.doi.org/10.1016/0921-8696(90)90516-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
22

Li, J., G. A. Hand, J. T. Potts, L. B. Wilson, and J. H. Mitchell. "c-Fos expression in the medulla induced by static muscle contraction in cats." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 1 (January 1, 1997): H48—H56. http://dx.doi.org/10.1152/ajpheart.1997.272.1.h48.

Full text
Abstract:
In this study, we examined Fos-like immunoreactivity (FLI) in the medulla after static muscle contraction induced by stimulation of L7 and S1 ventral roots of the spinal cord in anesthetized cats. The results show that FLI increases in the lateral reticular nucleus, nucleus of the solitary tract, lateral tegmental field, vestibular nucleus, subretrofacial nucleus, and A1 region of the medulla in comparison with these same areas in sham-operated animals (P < 0.05 in each region). In the rostral ventrolateral medulla, FLI distribution in neurons containing phenylethanolamine-N-methyltransferase (PNMT, the synthetic enzyme for epinephrine) was also observed utilizing double-labeling methods. The majority of neurons with PNMT also expressed FLI (66 +/- 4%). These data are in contrast to the results from sham-operated animals showing that 24 +/- 3% of the neurons costained with PNMT (P < 0.05). Our findings indicate that expression of FLI can be used to identify neurons activated during static muscle contraction and support previous studies implicating the ventrolateral medulla as a critical region for expression of the exercise pressor reflex. Furthermore, neurons in the rostral ventrolateral medulla containing PNMT were activated during static muscle contraction.
APA, Harvard, Vancouver, ISO, and other styles
23

Lin, A. M. Y., Y. Wang, J. S. Kuo, and C. Y. Chai. "Homocysteic acid elicits pressor responses from ventrolateral medulla and dorsomedial medulla." Brain Research Bulletin 22, no. 4 (April 1989): 627–31. http://dx.doi.org/10.1016/0361-9230(89)90081-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
24

Connelly, J. C., L. W. McCallister, and M. P. Kaufman. "Stimulation of the caudal ventrolateral medulla decreases total lung resistance in dogs." Journal of Applied Physiology 63, no. 3 (September 1, 1987): 912–17. http://dx.doi.org/10.1152/jappl.1987.63.3.912.

Full text
Abstract:
Although the role played by the caudal ventrolateral medulla in the regulation of the cardiovascular system has been extensively investigated, little is known about the role played by this area in the regulation of airway caliber. Therefore, in alpha-chloralose-anesthetized dogs, we used both electrical and chemical means to stimulate the caudal ventrolateral medulla while we monitored changes in total lung resistance breath by breath. We found that electrical stimulation (25 microA) of 26 sites in this area significantly decreased total lung resistance from 7.1 +/- 0.4 to 5.7 +/- 0.3 cmH2O.1'1.s (P less than 0.001). The bronchodilation evoked by electrical stimulation was unaffected by beta-adrenergic blockade but was abolished by cholinergic blockade. In addition, chemical stimulation of seven sites in the caudal ventrolateral medulla with microinjections of DL-homocysteic acid (0.2 M; 66 nl), which stimulates cell bodies but not fibers of passage, also decreased total lung resistance from 8.3 +/- 1.1 to 6.5 +/- 0.8 cmH2O.l'1.s (P less than 0.01). In contrast, microinjections of DL-homocysteic acid into the nucleus ambiguus (n = 6) increased total lung resistance from 7.5 +/- 0.5 to 9.2 +/- 0.4 cmH2O.l'1.s (P less than 0.05). We conclude that the caudal ventrolateral medulla contains a pool of cell bodies whose excitation causes bronchodilation by withdrawing cholinergic input to airway smooth muscle.
APA, Harvard, Vancouver, ISO, and other styles
25

Blessing, WW. "Inhibitory Vasomotor Neurons in the Caudal Ventrolateral Medulla Oblongata." Physiology 6, no. 3 (June 1, 1991): 139–41. http://dx.doi.org/10.1152/physiologyonline.1991.6.3.139.

Full text
Abstract:
Tonically active, probably GABAergic, neurons in the caudal ventrolateral medulla oblongata decrease sympathetic vasomotor tone by directly inhibiting sympathoexcitatory premotor neurons in the rostral medulla. These caudal inhibitory vasomotor neurons may constitute the inhibitory link in the central baroreceptor-vasomotor pathway.
APA, Harvard, Vancouver, ISO, and other styles
26

Beluli, D. J., and L. C. Weaver. "Differential control of renal and splenic nerves without medullary topography." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 4 (April 1, 1991): H1072—H1079. http://dx.doi.org/10.1152/ajpheart.1991.260.4.h1072.

Full text
Abstract:
A previous study in our laboratory showed that pharmacological blockade of neurons in the rostral ventrolateral medulla has greater influence on the electrical activity of renal than splenic nerves (K. Hayes and L. C. Weaver, J. Physiol. Lond. 428: 371-385, 1990). This differential control of sympathetic nerves innervating different organs may be due to viscerotopic representation of the kidney and spleen within medullary neurons that control the vasculature. To search for this topographical organization, 15 nl (2.5 nmol) of the excitatory amino acid DL-homocysteic acid (DLH) was microinjected into the ventrolateral medulla (VLM) of rats anesthetized with urethan. No distinct viscerotopic organization was found in the rostral or caudal VLM. However, renal nerve responses were consistently greater than splenic by a fixed proportion. In summary, stimulation of rostral and caudal VLM neurons causes differential renal and splenic excitatory responses, but mechanisms providing this selective control do not involve spatial organization of neuronal groups in the VLM.
APA, Harvard, Vancouver, ISO, and other styles
27

Kubo, T. "Involvement of the ventrolateral medulla in the mediation of pressor responses of the rat to afferent vagal stimulation." Canadian Journal of Physiology and Pharmacology 63, no. 12 (December 1, 1985): 1612–14. http://dx.doi.org/10.1139/y85-266.

Full text
Abstract:
Electrical stimulation of afferent vagal fibres evoked a pressor response in rats after transection of the spinal cord. The pressor response was accounted for by an increased release of vasopressin because it was abolished by the intravenous injection of a vasopressin antagonist. Bilateral electrolytic lesions at the sites of the caudal ventrolateral medulla markedly reduced the pressor response to afferent vagal stimulation but not that to carotid occlusion. It is concluded that the area of the caudal ventrolateral medulla is involved in mediation of the vasopressin-induced pressor response to afferent vagal stimulation.
APA, Harvard, Vancouver, ISO, and other styles
28

Jeske, I., S. F. Morrison, S. L. Cravo, and D. J. Reis. "Identification of baroreceptor reflex interneurons in the caudal ventrolateral medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 1 (January 1, 1993): R169—R178. http://dx.doi.org/10.1152/ajpregu.1993.264.1.r169.

Full text
Abstract:
Interrupting neuronal activity in the caudal ventrolateral medulla (CVL) abolishes baroreceptor-mediated sympathoinhibition and vasodepressor responses. In the present study we identified CVL neurons that function as interneurons in the baroreceptor reflex arc. The mean antidromic onset latency of CVL neurons (5 ms) after stimulation in the rostral ventrolateral medulla (RVL) suggests that they transmit information to the RVL via unmyelinated axons. Stimulation of baroreceptor afferents in the aortic depressor nerve (ADN) excited CVL neurons projecting to the RVL with onset latencies between 15 and 45 ms. The short-latency ADN stimulus-evoked excitation of CVL barosensory interneurons preceded the onset of the ADN stimulus-evoked inhibition of RVL-spinal sympathoexcitatory neurons. Longer-latency ADN-evoked CVL neuronal responses may arise from activation of unmyelinated ADN afferents that can prolong the inhibition of RVL sympathoexcitatory neurons. The excitation of CVL barosensory interneurons resulting from the systolic pressure rise was followed by a period of decreased excitability of RVL sympatho-excitatory neurons, which was of comparable duration to the increase in the discharge probability of CVL neurons. Our characterization of baroreceptor reflex interneurons in the CVL suggests that transmission of baroreceptor information involves a complex activation of medullary interneurons responding selectively to different aspects of the arterial pressure stimulus.
APA, Harvard, Vancouver, ISO, and other styles
29

Huangfu, D. H., and P. G. Guyenet. "Sympatholytic response to stimulation of superior laryngeal nerve in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 2 (February 1, 1991): R290—R297. http://dx.doi.org/10.1152/ajpregu.1991.260.2.r290.

Full text
Abstract:
The central pathway mediating a sympatholytic response to stimulation of the superior laryngeal nerve (SLN) was studied in halothane-anesthetized, paralyzed rats. Single-pulse stimulation of SLN inhibited lumbar sympathetic nerve discharge (LSND) with onset latency of 113 +/- 1.7 ms. LSND inhibition was markedly attenuated by bilateral microinjection of kynurenic acid (Kyn, glutamate receptor antagonist, 4.5 nmol/side) into the caudal ventrolateral medulla (CVL) or by bilateral administration of bicuculline methiodide (Bic; gamma-aminobutyric acid-receptor antagonist, 225 pmol/side) into the rostral ventrolateral medulla (RVL). In 13 of 14 cases, the baroreceptor reflex was also severely reduced. Injections of Bic or Kyn elsewhere in the medullary reticular formation were ineffective. Single-pulse stimulation of SLN inhibited 19 of 26 RVL reticulospinal barosensitive cells (onset latency 46 +/- 1.4 ms). This inhibition was attenuated (from 92 +/- 6 to 14 +/- 12%) by iontophoretic application of Bic (n = 7), which also reduced the cells' inhibitory response to aortic coarctation. The remaining seven barosensitive neurons were unaffected by SLN stimulation. In conclusion, the sympathetic baroreflex and the sympathoinhibitory response to SLN stimulation appear to be mediated by similar medullary pathways.
APA, Harvard, Vancouver, ISO, and other styles
30

Smith, J. K., and K. W. Barron. "GABAergic responses in ventrolateral medulla in spontaneously hypertensive rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 2 (February 1, 1990): R450—R456. http://dx.doi.org/10.1152/ajpregu.1990.258.2.r450.

Full text
Abstract:
Gamma-Aminobutyric acid (GABA) and the GABA antagonist bicuculline methiodide were used to investigate the role of GABAergic transmission in the rostral and caudal ventrolateral medulla in 12- to 13-wk-old spontaneously hypertensive (SH) (n = 7) and normotensive, control Wistar-Kyoto (WKY) (n = 7) rats. Animals were anesthetized with urethan (1.25 g/kg sc), paralyzed with gallamine triethiodide (10 mg/kg iv), and artificially ventilated. Femoral arterial and venous catheters were inserted for the measurement of mean arterial pressure (MAP) and heart rate responses and for intravenous infusions. The ventral surface of the brain stem then was exposed. The responsiveness of the rostral ventrolateral medulla to GABA was compared in SH and WKY rats using unilateral microinjections (30 nl) of GABA at 1, 10, and 100 mM concentrations, which produced significantly (P less than 0.05) larger decreases of MAP in SH rats compared with WKY at the 10 and 100 mM concentrations (-37.3 +/- 2.8 mmHg for SH vs. -27.3 +/- 2.7 mmHg for WKY at 100 mM). Tonic GABAergic inhibition was gauged using bilateral microinjections (30 nl) of bicuculline (2 and 4 mM) into the rostral ventrolateral medulla, which caused significantly larger increases in MAP in the WKY group (+84.8 +/- 8.5 mmHg at 4 mM) compared with the SH group (+14.9 +/- 5.8 mmHg at 4 mM). In contrast, the ability to drive sympathetic outflow by microinjection of L-glutamate in the rostral ventrolateral medulla was not significantly different between WKY and SH rats.(ABSTRACT TRUNCATED AT 250 WORDS)
APA, Harvard, Vancouver, ISO, and other styles
31

Chen, Chiung-Tong, Ling-Ling Hwang, Jaw-Kang Chang, and Nae J. Dun. "Pressor effects of orexins injected intracisternally and to rostral ventrolateral medulla of anesthetized rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 3 (March 1, 2000): R692—R697. http://dx.doi.org/10.1152/ajpregu.2000.278.3.r692.

Full text
Abstract:
Orexin A and B, two recently isolated hypothalamic peptides, have been reported to increase food consumption upon intracerebroventricular injections in rats. In addition to the hypothalamus, orexin A-immunoreactive fibers have been observed in several areas of the medulla that are associated with cardiovascular functions. The present study was undertaken to evaluate the hypothesis that orexins may influence cardiovascular response by interacting with neurons in the medulla. Intracisternal injections of orexins A (0.0056–7.0 nmol) or B (0.028–0.28 nmol) dose dependently increased mean arterial pressure (MAP) by 4–27 mmHg and heart rate (HR) by 26–80 beats/min in urethan-anesthetized rats, with orexin A being more effective in this regard. MAP and HR were not changed by intravenous injection of orexins at higher concentrations. Microinjection of orexin A (14 pmol/50.6 nl) to the rostral ventrolateral medulla, which was confirmed by histological examination, increased MAP and HR. Our results indicate that, in addition to a role in positive feeding behavior, orexins may enhance cardiovascular response via an action on medullary neurons.
APA, Harvard, Vancouver, ISO, and other styles
32

Chalmers, John, Vimal Kapoor, Eric Mills, Jane Minson, Margaret Morris, Paul Pilowsky, and Malcolm West. "Do pressor neurons in the ventrolateral medulla release amines and neuropeptides?" Canadian Journal of Physiology and Pharmacology 65, no. 8 (August 1, 1987): 1598–604. http://dx.doi.org/10.1139/y87-251.

Full text
Abstract:
Activation of neurons arising in the rostral ventrolateral medulla evokes a pressor response in the rat and the rabbit. This region of the medulla gives rise to bulbospinal neurons containing many different neurotransmitters, including amines such as adrenaline, noradrenaline and serotonin, and neuropeptides such as substance P and neuropeptide Y. Colocalization of amines and neuropeptides has been described in some neurons descending from the rostral ventrolateral medulla. In this paper we discuss the evidence that bulbospinal serotonin-containing neurons (B3) and adrenaline-containing neurons (C1) arising from this part of the medulla exert pressor effects by distinct central pathways and conclude that they do. We also consider the possibility that the pressor effects of activating these two groups of neurons are associated with release of neuropeptides and highlight evidence that substance P is released into the spinal cord by activation of descending serotonin-containing neurons, while neuropeptide Y may be released by activation of bulbospinal adrenaline-containing neurons.
APA, Harvard, Vancouver, ISO, and other styles
33

Patodia, Smriti, Alyma Somani, Megan O’Hare, Ranjana Venkateswaran, Joan Liu, Zuzanna Michalak, Matthew Ellis, et al. "The ventrolateral medulla and medullary raphe in sudden unexpected death in epilepsy." Brain 141, no. 6 (March 28, 2018): 1719–33. http://dx.doi.org/10.1093/brain/awy078.

Full text
APA, Harvard, Vancouver, ISO, and other styles
34

Hilaire, Gérard, Céline Bou, and Roger Monteau. "Rostral ventrolateral medulla and respiratory rhythmogenesis in mice." Neuroscience Letters 224, no. 1 (March 1997): 13–16. http://dx.doi.org/10.1016/s0304-3940(97)13458-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
35

Guyenet, Patrice G., Ruth L. Stornetta, Ann M. Schreihofer, Nicole M. Pelaez, Abdallah Hayar, Sue Aicher, and Ida J. Llewellyn-Smith. "Opioid Signalling In The Rat Rostral Ventrolateral Medulla." Clinical and Experimental Pharmacology and Physiology 29, no. 3 (March 2002): 238–42. http://dx.doi.org/10.1046/j.1440-1681.2002.03636.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
36

Andreatta-Van Leyen, S., D. B. Averill, and C. M. Ferrario. "Cardiovascular actions of vasopressin at the ventrolateral medulla." Hypertension 15, no. 2_Suppl (February 1, 1990): I102. http://dx.doi.org/10.1161/01.hyp.15.2_suppl.i102.

Full text
APA, Harvard, Vancouver, ISO, and other styles
37

Cherniack, N. S., J. Mitra, N. R. Prabhakar, and E. M. Adams. "Respiratory and Vasomotor Influences of the Ventrolateral Medulla." Clinical and Experimental Hypertension. Part A: Theory and Practice 10, sup1 (January 1988): 1–9. http://dx.doi.org/10.3109/10641968809075959.

Full text
APA, Harvard, Vancouver, ISO, and other styles
38

Kulchitsky, V. A. "The capsaicin-sensitive area of the ventrolateral medulla." Neuropeptides 26 (April 1994): 51. http://dx.doi.org/10.1016/0143-4179(94)90266-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
39

Siddall, P. J., R. A. L. Dampney, and J. W. Polson. "Descending antinociceptive pathways in the rostral ventrolateral medulla." Pain 41 (January 1990): S447. http://dx.doi.org/10.1016/0304-3959(90)93009-m.

Full text
APA, Harvard, Vancouver, ISO, and other styles
40

de Toledo Bergamaschi, Cássia, Bruno de Arruda Carillo, Henrique Azevedo Futuro Neto, and Ruy Ribeiro de Campos. "Differential baroreceptor modulation mediated by the ventrolateral medulla." Autonomic Neuroscience 126-127 (June 2006): 156–62. http://dx.doi.org/10.1016/j.autneu.2006.02.012.

Full text
APA, Harvard, Vancouver, ISO, and other styles
41

Koshiya, Naohiro, Donghai Huangfu, and Patrice G. Guyenet. "Ventrolateral medulla and sympathetic chemoreflex in the rat." Brain Research 609, no. 1-2 (April 1993): 174–84. http://dx.doi.org/10.1016/0006-8993(93)90871-j.

Full text
APA, Harvard, Vancouver, ISO, and other styles
42

Hsieh, J. H., J. J. Wu, C. T. Yen, and C. Y. Chai. "The depressor caudal ventrolateral medulla: Its correlation with the pressor dorsomedial and ventrolateral medulla and the depressor paramedian reticular nucleus." Journal of the Autonomic Nervous System 70, no. 1-2 (May 1998): 103–14. http://dx.doi.org/10.1016/s0165-1838(98)00043-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
43

Terui, Naohito, Noboru Masuda, Yuka Saeki, and Mamoru Kumada. "Activity of barosensitive neurons in the caudal ventrolateral medulla that send axonal projections to the rostral ventrolateral medulla in rabbits." Neuroscience Letters 118, no. 2 (October 1990): 211–14. http://dx.doi.org/10.1016/0304-3940(90)90629-n.

Full text
APA, Harvard, Vancouver, ISO, and other styles
44

Aicher, Sue A., Oliver S. Kurucz, Donald J. Reis, and Teresa A. Milner. "Nucleus tractus solitarius efferent terminals synapse on neurons in the caudal ventrolateral medulla that project to the rostral ventrolateral medulla." Brain Research 693, no. 1-2 (September 1995): 51–63. http://dx.doi.org/10.1016/0006-8993(95)00660-i.

Full text
APA, Harvard, Vancouver, ISO, and other styles
45

Ma, Anyun, Lie Gao, Ahmed M. Wafi, Li Yu, Tara Rudebush, Wenxian Zhou, and Irving H. Zucker. "Overexpression of Central ACE2 (Angiotensin-Converting Enzyme 2) Attenuates the Pressor Response to Chronic Central Infusion of Ang II (Angiotensin II)." Hypertension 76, no. 5 (November 2020): 1514–25. http://dx.doi.org/10.1161/hypertensionaha.120.15681.

Full text
Abstract:
We investigated the mechanism by which ACE2 (angiotensin-converting enzyme 2) overexpression alters neurohumoral outflow and central oxidative stress. Nrf2 (nuclear factor [erythroid-derived 2]-like 2) is a master antioxidant transcription factor that regulates cytoprotective and antioxidant genes. We hypothesized that upregulation of central ACE2 inhibits the pressor response to Ang II (angiotensin II) by reducing reactive oxygen species through a Nrf2/antioxidant enzyme–mediated mechanism in the rostral ventrolateral medulla. Synapsin human Angiotensin Converting Enzyme 2 positive (SynhACE2 +/+ ) mice and their littermate controls synhACE2 −/− were used to evaluate the consequence of intracerebroventricular infusion of Ang II. In control mice, Ang II infusion evoked a significant increase in blood pressure and norepinephrine excretion, along with polydipsia and polyuria. The pressor effect of central Ang II was completely blocked in synhACE2 +/+ mice. Polydipsia, norepinephrine excretion, and markers of oxidative stress in response to central Ang II were also reduced in synhACE2 +/+ mice. The MasR (Mas receptor) agonist Ang 1–7 and blocker A779 had no effects on blood pressure. synhACE2 +/+ mice showed enhanced expression of Nrf2 in the rostral ventrolateral medulla which was blunted following Ang II infusion. Ang II evoked nuclear translocation of Nrf2 in cultured Neuro 2A (N2A) cells. In synhACE2 −/− mice, the central Ang II pressor response was attenuated by simultaneous intracerebroventricular infusion of the Nrf2 activator sulforaphane; blood pressure was enhanced by knockdown of Nrf2 in the rostral ventrolateral medulla in Nrf2 floxed (Nrf2 f/f ) mice. These data suggest that the hypertensive effects of intracerebroventricular Ang II are attenuated by selective overexpression of brain synhACE2 and may be mediated by Nrf2-upregulated antioxidant enzymes in the rostral ventrolateral medulla.
APA, Harvard, Vancouver, ISO, and other styles
46

Barman, Susan M. "2019 Ludwig Lecture: Rhythms in sympathetic nerve activity are a key to understanding neural control of the cardiovascular system." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 318, no. 2 (February 1, 2020): R191—R205. http://dx.doi.org/10.1152/ajpregu.00298.2019.

Full text
Abstract:
This review is based on the Carl Ludwig Distinguished Lecture, presented at the 2019 Experimental Biology Meeting in Orlando, FL, and provides a snapshot of >40 years of work done in collaboration with the late Gerard L. Gebber and colleagues to highlight the importance of considering the rhythmic properties of sympathetic nerve activity (SNA) and brain stem neurons when studying the neural control of autonomic regulation. After first providing some basic information about rhythms, I describe the patterns and potential functions of rhythmic activity recorded from sympathetic nerves under various physiological conditions. I review the evidence that these rhythms reflect the properties of central sympathetic neural networks that include neurons in the caudal medullary raphe, caudal ventrolateral medulla, caudal ventrolateral pons, medullary lateral tegmental field, rostral dorsolateral pons, and rostral ventrolateral medulla. The role of these brain stem areas in mediating steady-state and reflex-induced changes in SNA and blood pressure is discussed. Despite the common appearance of rhythms in SNA, these oscillatory characteristics are often ignored; instead, it is common to simply quantify changes in the amount of SNA to make conclusions about the function of the sympathetic nervous system in mediating responses to a variety of stimuli. This review summarizes work that highlights the need to include an assessment of the changes in the frequency components of SNA in evaluating the cardiovascular responses to various manipulations as well as in determining the role of different brain regions in the neural control of the cardiovascular system.
APA, Harvard, Vancouver, ISO, and other styles
47

Chen, Z., J. Hedner, and T. Hedner. "Substance P in the ventrolateral medulla oblongata regulates ventilatory responses." Journal of Applied Physiology 68, no. 6 (June 1, 1990): 2631–39. http://dx.doi.org/10.1152/jappl.1990.68.6.2631.

Full text
Abstract:
Local injection of substance P (SP) into the ventral portion of the nucleus gigantocellularis, nucleus reticularis lateralis, and nucleus retrofacialis of the ventrolateral medulla oblongata (VLM) or direct application on the ventral surface of the medulla oblongata caused marked stimulation of tidal volume (VT) and/or minute ventilation (VE). The ventilatory response to hypoxia was significantly blunted after SP in the VLM but not in the dorsal medulla oblongata (DM) (nucleus tractus solitarius). The SP antagonist [D-Pro2,D-Trp7,9]SP almost completely inhibited this response when applied locally to a wide area of the superficial layer of the VLM but not of the DM. Unilateral or bilateral application of 0.3-1.5 nmol of the SP antagonist in the VLM (corpus trapezoideum and the caudal region extending from the rootlets of the nucleus hypoglossus to the first cervical segment) markedly attenuated the response to a 5% CO2 inhalation. The inhibition of the CO2 response was seen after [D-Pro2,D-Trp7,9]SP in the rostral areas of the medulla oblongata corresponding to the corpus trapezoideum and the caudal region extending from the rootlets of the nucleus hypoglossus to the first cervical segment of the cervical cord. Electric somatosensory-induced ventilatory stimulation could be depressed by approximately 70% by [D-Pro2,D-Trp7,9]SP locally applied on the surface of the VLM. We conclude that SP is involved in the hypoxic, hypercapnic, and somatosensory ventilatory responses in the rat. However, these respiratory reflexes are mediated via different neuronal pools in the medulla oblongata, mainly the VLM.
APA, Harvard, Vancouver, ISO, and other styles
48

Masuda, Noboru, Youichirou Ootsuka, and Naohito Terui. "Neurons in the caudal ventrolateral medulla mediate the somato-sympathetic inhibitory reflex response via GABA receptors in the rostral ventrolateral medulla." Journal of the Autonomic Nervous System 40, no. 2 (September 1992): 91–98. http://dx.doi.org/10.1016/0165-1838(92)90020-h.

Full text
APA, Harvard, Vancouver, ISO, and other styles
49

Bonham, A. C., and I. Jeske. "Cardiorespiratory effects of DL-homocysteic acid in caudal ventrolateral medulla." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 3 (March 1, 1989): H688—H696. http://dx.doi.org/10.1152/ajpheart.1989.256.3.h688.

Full text
Abstract:
We carried out experiments in urethan-anesthetized rats to determine 1) whether increasing the activity of small groups of neurons in the caudal ventrolateral medulla (CVLM) by injecting picomoles of an excitatory amino acid altered cardiovascular and/or respiratory homeostasis and 2) whether the depressor responses after chemical excitation in the CVLM were elicited only from the immunohistochemically identified catecholamine-containing cell group. In discrete sites in the CVLM, unilateral injections of 1-12 nl (20-240 pmol) of DL-homocysteic acid (DLH; 20 mM, pH 7.4) selectively or concomitantly inhibited arterial pressure, heart rate, and diaphragm electromyogram (EMG) activity. In the region in which chemical excitation slowed breathing, units were recorded extracellularly that discharged with respiratory periodicity. Sites where the smallest volumes of DLH decreased arterial pressure were located outside the immunohistochemically identified DBH-positive cell bodies. These data suggest that either the same or neighboring neurons in the CVLM are involved in the central neural circuitry for both cardiovascular and respiratory control and that cells other than the catecholaminergic cell group are important in medullary depressor responses.
APA, Harvard, Vancouver, ISO, and other styles
50

Abbott, Stephen B. G., and Paul M. Pilowsky. "Galanin microinjection into rostral ventrolateral medulla of the rat is hypotensive and attenuates sympathetic chemoreflex." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 4 (April 2009): R1019—R1026. http://dx.doi.org/10.1152/ajpregu.90885.2008.

Full text
Abstract:
Galanin is present in neurons in the brain that are important in the control of arterial pressure, and intracisternal administration of galanin evokes hypotension, but the site of action is unknown. In urethane-anesthetized, vagotomized mechanically ventilated Sprague-Dawley rats ( n = 34), we investigated the effects of microinjecting galanin (1 mM, 50 nl, 50 pmol) into the rostral ventrolateral medulla on resting splanchnic sympathetic nerve activity, arterial pressure, heart rate, and phrenic nerve activity. Second, we determined the effect of microinjecting galanin into the rostral ventrolateral medulla on the cardiovascular response to stimulation of central and peripheral chemoreceptors, arterial baroreceptors, and the somatosympathetic reflex. Galanin caused a prolonged reduction in resting splanchnic sympathetic nerve activity (−37.0 ± 7.2% of baseline), mean arterial pressure (−17.0 ± 3.5 mmHg), and heart rate (−25.0 ± 9.1 beats/min). Galanin increased the sympathoinhibitory response to aortic depressor nerve stimulation by 51.8%, had no effect on the somatosympathetic reflex, and markedly attenuated the effect of hypercapnia and hypoxia on arterial pressure (by 65% and 92.4% of control, respectively). These results suggest a role for galanin neurotransmission in the integration of the cardiovascular responses to hypoxia, hypercapnia, and the sympathetic baroreflex in the rostral ventrolateral medulla. The data suggest that galanin may be an important peptide in the homeostatic regulation of chemosensory reflexes.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Ventrolateral Medulla' for other source types:
Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography