Parabrachial neurons mediate dorsal periaqueductal gray evoked respiratory responses in the rat

2004 ◽  
Vol 96 (3) ◽  
pp. 1146-1154 ◽  
Author(s):  
Linda F. Hayward ◽  
Mabelin Castellanos ◽  
Paul W. Davenport
Keyword(s):  
Heart Rate ◽  
Significant Role ◽  
Defense Response ◽  
Pressor Response ◽  
Defense Responses ◽  
Periaqueductal Gray ◽  
Parabrachial Nucleus ◽  
Ventrolateral Medulla ◽  
Descending Pathways ◽  
Behavioral Defense

The neural substrates mediating autonomic components of the behavioral defense response reside in the periaqueductal gray (PAG). The cardiovascular components of the defense response evoked from the dorsal PAG (DPAG) have been well described and are dependent, in part, on the integrity of neurons in the region of the parabrachial nucleus as well as the rostral ventrolateral medulla. Descending pathways mediating the ventilatory response associated with activation of DPAG neurons are unknown. The present study was undertaken to test the hypothesis that parabrachial area neurons are also involved in mediating the respiratory response to DPAG stimulation. In urethane-anesthetized, spontaneously breathing rats, electrical stimulation of the DPAG significantly increased respiratory rate, arterial pressure, and heart rate. Changes in respiratory frequency were associated with significant decreases in inspiratory and expiratory durations. After bilateral inhibition of neurons in the lateral parabrachial nucleus (LPBN) region with 5 mM muscimol ( n = 6), DPAG-evoked increases in respiration and heart rate were attenuated by 90 ± 6 and 72 ± 13%, respectively. The pressor response evoked by DPAG stimulation, however, was attenuated by only 57 ± 6%. Bilateral blockade of glutamate receptors with 20 mM kynurenic acid ( n = 6) in the LPBN also markedly attenuated DPAG-evoked increases in respiration and heart rate (65 ± 15 and 53 ± 9% reduction, respectively) but only modestly changed the DPAG-evoked pressor response (34 ± 16% reduction). These results demonstrate that LPBN neurons play a significant role in the DPAG-mediated respiratory component of behavioral defense responses. This finding supports previous work demonstrating that the dorsolateral pons plays a significant role in mediating most physiological adjustments associated with activation of the DPAG.

scholarly journals Respiratory response to activation or disinhibition of the dorsal periaqueductal gray in rats

2003 ◽  
Vol 94 (3) ◽  
pp. 913-922 ◽  
Author(s):  
Linda F. Hayward ◽  
Camille L. Swartz ◽  
Paul W. Davenport
Keyword(s):  
Defense Response ◽  
Defense Responses ◽  
Neural Substrates ◽  
Periaqueductal Gray ◽  
Similar Response ◽  
Respiratory Change ◽  
Behavioral Defense ◽  
Expiration Time ◽  
Spontaneously Breathing ◽  
Dose Dependent

The neural substrates mediating autonomic components of the behavioral defense response have been shown to reside in the periaqueductal gray (PAG). The cardiovascular components of the behavioral defense response have been well described and are tonically suppressed by GABAergic input. The ventilatory response associated with disinhibition of the dorsal PAG (dPAG) neurons is unknown. In urethane-anesthetized, spontaneously breathing rats, electrical stimulation of the dPAG was shown to decrease the expiration time and increase respiratory frequency, with no change in time of inspiration. Baseline and the change in diaphragm electromyograph also increased, resulting in an increase in neural minute activity. Microinjection of bicuculline methobromide, a GABAA-receptor antagonist, into the dPAG produced a similar response, which was dose dependent. Disinhibition of the dPAG also produced a decrease in inspiration time. These results suggest that GABAA-mediated suppression of dPAG neurons plays a role in the respiratory component of behavioral defense responses. The respiratory change is due in part to a change in brain stem respiratory timing and phasic inspiratory output. In addition, there is an increase in tonic diaphragm activity.

Effects of ventrolateral medullary AMPA-receptor antagonism on pressor response during muscle contraction

1997 ◽  
Vol 272 (6) ◽  
pp. H2774-H2781 ◽  
Author(s):  
T. Kobayashi ◽  
D. Caringi ◽  
D. J. Mokler ◽  
A. Ally
Keyword(s):  
Heart Rate ◽  
Muscle Contraction ◽  
Ampa Receptors ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Contrast Administration ◽  
Tibial Nerve Stimulation ◽  
Before And After

Effects of administering 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) at a concentration that preferentially blocks alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors into rostral ventrolateral medulla (rVLM) or caudal ventrolateral medulla (cVLM) on cardiovascular responses elicited during static muscle contraction were investigated using anesthetized rats. Two microdialysis probes were inserted bilaterally into either the rVLM or the cVLM using stereotaxic guides. A tibial nerve stimulation-evoked static muscle contraction for 30 s increased mean arterial pressure (MAP) and heart rate (HR) by 27 +/- 3 mmHg and 28 +/- 4 beats/min, respectively. Microdialysis of CNQX into the rVLM for 30 min attenuated the contraction-evoked increases in MAP and HR (10 +/- 2 mmHg and 12 +/- 2 beats/min). Developed tensions were similar during the contractions before and after microdialyzing CNQX. In contrast, administration of CNQX into the cVLM potentiated the muscle contraction-evoked cardiovascular responses (MAP, 25 +/- 4 vs. 39 +/- 6 mmHg; HR, 27 +/- 3 vs. 42 +/- 3 beats/min), with no change in developed tensions. Results demonstrate that AMPA receptors within the rVLM and the cVLM appear to play opposite modulatory roles in the central integration of cardiovascular responses elicited during static muscle contraction.

Sympathoinhibition from ventrolateral periaqueductal gray mediated by 5-HT1A receptors in the RVLM

2001 ◽  
Vol 280 (4) ◽  
pp. R976-R984 ◽  
Author(s):  
M. Bago ◽  
C. Dean
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Periaqueductal Gray ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Pentobarbital Sodium ◽  
Arterial Blood ◽  
Way 100635

The role of 5-hydroxytryptamine 1A (5-HT1A) receptors located in the rostral ventrolateral medulla (RVLM) in the mediation of a sympathoinhibitory and depressor response elicited from the ventrolateral periaqueductal gray (vlPAG) matter of the midbrain was examined in pentobarbital sodium-anesthetized rats. Activation of neurons in the vlPAG evoked a decrease in renal and lumbar sympathetic nerve activities and a decrease in arterial blood pressure. After microinjection of the specific 5-HT1A-receptor antagonist WAY-100635 into the pressor area of the RVLM, the vlPAG-evoked sympathoinhibition and hypotension was attenuated to control levels (7 of 15 animals) or converted into a sympathoexcitation and pressor response (8 of 15 animals). Baroreflex inhibition of sympathetic nerve activity was not impaired by microinjection of WAY into the sympathoexcitatory region of the RVLM. These data suggest that sympathoinhibition and hypotension elicited by activation of neurons in the vlPAG are mediated by 5-HT1A receptors in the RVLM.

Descending pathways of powerful pressor response elicited by suprapontine cerebral ischemia in rabbits

1994 ◽  
Vol 266 (6) ◽  
pp. R1832-R1839 ◽  
Author(s):  
J. Horiuchi ◽  
T. Takeuchi
Keyword(s):  
Cerebral Ischemia ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Global Cerebral Ischemia ◽  
Ventrolateral Medulla ◽  
Descending Pathways ◽  
Renal Sympathetic Nerve Activity ◽  
Ventromedial Medulla ◽  
Control Response ◽  
Renal Sympathetic

We determined the magnitude of the pressor and sympathoexcitatory responses elicited by suprapontine cerebral ischemia (SCI) and the descending pathways in the rostral medulla mediating them. The suprapontine structures of anesthetized and artificially ventilated rabbits were selectively exposed to cerebral ischemia, by combined occlusions of basilar and common carotid artery. SCI produced a pressor response of 78 +/- 9 (SE) mmHg and an increase in renal sympathetic nerve activity of 289 +/- 21% compared with preischemic levels. The magnitude of the pressor and sympathoexcitatory response to SCI was comparable to those in response to global cerebral ischemia. Microinjection of the neurotoxin kainic acid into the pressor sites of the rostral ventrolateral medulla significantly (P < 0.05) reduced the SCI pressor response to 34 +/- 11% of the prelesion control response. Chemical lesions of the pressor sites in the rostral medial and ventromedial medulla resulted in a significant decrease in the pressor response to SCI to 78 +/- 12% of the control response. These results indicate that the suprapontine structures play an important role in the generation of the powerful pressor response elicited by cerebral ischemia and that the pressor response to SCI is mediated by pressor neurons in the rostral medulla.

Cannabinoid and GABA modulation of sympathetic nerve activity and blood pressure in the dorsal periaqueductal gray of the rat

2011 ◽  
Vol 301 (6) ◽  
pp. R1765-R1772 ◽  
Author(s):  
C. Dean
Keyword(s):  
Blood Pressure ◽  
Gabaa Receptor ◽  
Defense Response ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Acute Stress ◽  
Pressor Response ◽  
Periaqueductal Gray ◽  
Nerve Activity ◽  
Gabaergic Neurotransmission

Sympathoexcitation and increased blood pressure evoked by central networks integrating defensive behavior are fundamental to the acute stress response. A balance between excitatory glutamatergic and inhibitory GABAergic neurotransmission in the dorsal periaqueductal gray (dPAG) results in a tonic level of activity in the alerting system. Neuromodulators such as endocannabinoids have been shown to influence the sympathoexcitatory and pressor components of acute stress in the dPAG, exemplified by the defense response as a model, but the mechanism of integration remains unknown. The present study examines the role of GABA and its interaction with endocannabinoids in modulating sympathetic nerve activity and blood pressure related to the defense response. Microinjection of the broad-spectrum excitatory amino acid dl-homocysteic acid (DLH) identified sites of the defense pathway in the dPAG from which an increase in renal sympathetic nerve activity and blood pressure could be evoked, and subsequent microinjections were made at the same site through a multibarrelled micropipette. Blockade of GABAA receptors or microinjection of the cannabinoid 1 receptor agonist anandamide elicited a renal sympathoexcitation and pressor response. Prior microinjection of the GABAA receptor antagonist gabazine attenuated the sympathoexcitation and pressor response associated with anandamide microinjection. In contrast, the sympathetic response to DLH was enhanced by GABAA receptor blockade. These data demonstrate that sympathoexcitatory neurons in the dPAG are under tonic inhibition by GABA and that endocannabinoids modulate this GABAergic neurotransmission to help regulate components of the defense response.

scholarly journals Deletion of the SACPD-C Locus Alters the Symbiotic Relationship Between Bradyrhizobium japonicum USDA110 and Soybean, Resulting in Elicitation of Plant Defense Response and Nodulation Defects

2016 ◽  
Vol 29 (11) ◽  
pp. 862-877 ◽  
Author(s):  
Hari B. Krishnan ◽  
Alaa A. Alaswad ◽  
Nathan W. Oehrle ◽  
Jason D. Gillman
Keyword(s):  
Plant Defense ◽  
Defense Response ◽  
Acyl Carrier Protein ◽  
Defense Responses ◽  
Nodule Development ◽  
Plant Defense Response ◽  
Wild Type ◽  
Two Dimensional Gel Electrophoresis ◽  
Symbiotic Associations ◽  
Soybean Nodule

Legumes form symbiotic associations with soil-dwelling bacteria collectively called rhizobia. This association results in the formation of nodules, unique plant-derived organs, within which the rhizobia are housed. Rhizobia-encoded nitrogenase facilitates the conversion of atmospheric nitrogen into ammonia, which is utilized by the plants for its growth and development. Fatty acids have been shown to play an important role in root nodule symbiosis. In this study, we have investigated the role of stearoyl-acyl carrier protein desaturase isoform C (SACPD-C), a soybean enzyme that catalyzes the conversion of stearic acid into oleic acid, which is expressed in developing seeds and in nitrogen-fixing nodules. In-depth cytological investigation of nodule development in sacpd-c mutant lines M25 and MM106 revealed gross anatomical alteration in the sacpd-c mutants. Transmission electron microscopy observations revealed ultrastructural alterations in the sacpd-c mutants that are typically associated with plant defense response to pathogens. In nodules of two sacpd-c mutants, the combined jasmonic acid (JA) species (JA and the isoleucine conjugate of JA) were found to be reduced and 12-oxophytodienoic acid (OPDA) levels were significantly higher relative to wild-type lines. Salicylic acid levels were not significantly different between genotypes, which is divergent from previous studies of sacpd mutant studies on vegetative tissues. Soybean nodule phytohormone profiles were very divergent from those of roots, and root profiles were found to be almost identical between mutant and wild-type genotypes. The activities of antioxidant enzymes, ascorbate peroxidase, and superoxide dismutase were also found to be higher in nodules of sacpd-c mutants. PR-1 gene expression was extremely elevated in M25 and MM106, while the expression of nitrogenase was significantly reduced in these sacpd-c mutants, compared with the parent ‘Bay’. Two-dimensional gel electrophoresis and matrix-assisted laser desorption-ionization time of flight mass spectrometry analyses confirmed sacpd-c mutants also accumulated higher amounts of pathogenesis-related proteins in the nodules. Our study establishes a major role for SACPD-C activity as essential for proper maintenance of soybean nodule morphology and physiology and indicates that OPDA signaling is likely to be involved in attenuation of nodule biotic defense responses.

Neurotransmission in the medulla mediating insular cortical and lateral hypothalamic sympathetic responses

1998 ◽  
Vol 76 (7-8) ◽  
pp. 737-746 ◽  
Author(s):  
Kenneth S Butcher ◽  
David F Cechetto
Keyword(s):  
Receptor Antagonist ◽  
Sympathetic Nerve ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Bipolar Electrode ◽  
Hypothalamic Area ◽  
Renal Nerve ◽  
Lateral Hypothalamic ◽  
Baseline Activity ◽  
Sympathetic Responses

Previous evidence has shown sympathetic nerve responses to insular cortical (IC) stimulation are mediated by synapses within the lateral hypothalamic area (LHA) and ventrolateral medulla (VLM). The present study was aimed at determining the neurotransmitter(s) and receptor(s) involved at the synapse in the VLM. Twenty male Wistar rats were instrumented for renal nerve, arterial pressure, and heart rate recording. The IC or the LHA was stimulated with a bipolar electrode (200-1000 µA; 2 ms; 0.8 Hz) to elicit sympathetic nerve responses. Antagonists were then pressure-injected into the VLM (300 nL). Bilateral and unilateral kynurenate (25 mM) resulted in 100% block of IC- and LHA-stimulated sympathetic nerve responses. Bilateral injection of the non-NMDA (N-methyl-D-aspartate) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 200 µM) also resulted in up to 100% block of IC and LHA sympathetic responses. In addition, unilateral injections of CNQX were made in two animals, resulting in 100 and 83% block of LHA sympathetic responses. Bilateral injection of the NMDA receptor antagonist DL-2-amino-5-phosphonopentanoic acid (AP5; 200µM) did not affect the response to IC or LHA stimulation. Kynurenate, CNQX, and AP5 all resulted in an elevation of baseline sympathetic nerve activity and a pressor response. Kynurenate resulted in a 263 ± 79% increase in baseline activity, while CNQX and AP5 resulted in 83 ± 19% and 91 ± 21% increases, respectively. Bilateral injections of antagonists for GABAA (bicuculline; 0.1 µM), acetylcholine (atropine; 0.1 µM) and catecholaminergic alpha and beta receptors (phentolamine and propranolol: 0.1 µM) had no effect on LHA sympathetic responses. Thus, sympathetic responses originating in the IC and LHA are mediated by a non-NMDA receptors in the VLM, which are likely AMPA receptors.Key words: insular cortex, ventrolateral medulla, glutamate, sympathetic activity.

Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

Cardiovascular effects of opioid antagonist naloxone in rostral ventrolateral medulla of rabbits

1990 ◽  
Vol 258 (2) ◽  
pp. R325-R331 ◽  
Author(s):  
D. A. Morilak ◽  
G. Drolet ◽  
J. Chalmers
Keyword(s):  
Pressor Response ◽  
Cardiovascular Effects ◽  
Rostral Ventrolateral Medulla ◽  
Endogenous Opioids ◽  
Opioid Antagonist ◽  
Ventrolateral Medulla ◽  
Inhibitory Influence ◽  
Beneficial Effects ◽  
Arterial Blood ◽  
Depressor Effect

We have examined the influence of endogenous opioids on the basal and reflex control of arterial blood pressure in the pressor region of the rostral ventrolateral medulla (RVLM) of chloralose-anesthetized rabbits. We tested basal effects both in intact animals and after hypotensive hemorrhage. Bilateral administration of the opiod antagonist naloxone (20 nmol, 100 nl) directly into the RVLM induced a gradual and prolonged increase in mean arterial pressure (MAP) (+17 +/- 2 mmHg). This was preceded by a brief and mild depressor effect (-9 +/- 3 mmHg), which was attributable to a transient reduction in excitability immediately after naloxone injection. When naloxone was administered into the RVLM after hemorrhage (20 ml/kg), it improved recovery of MAP relative to saline controls, again producing a gradual, prolonged pressor response (+29 +/- 5 mmHg). The effect of naloxone on a baroreflex in intact animals was only transient, with a brief, nonsignificant attenuation of the reflex depressor response to aortic nerve stimulation. We conclude that endogenous opioids exert a tonic inhibitory influence on RVLM pressor neurons and that this input remains active after hemorrhage. The RVLM may thus be one site for the beneficial effects of naloxone in preventing circulatory decompensation after hemorrhage. In contrast, opioid neurons are not an essential component of baroreflex-mediated sympathoinhibition in the RVLM.

scholarly journals Transcriptomic Analysis of Arabidopsis Seedlings in Response to an Agrobacterium-Mediated Transformation Process

2018 ◽  
Vol 31 (4) ◽  
pp. 445-459 ◽  
Author(s):  
Kaixuan Duan ◽  
Christopher J. Willig ◽  
Joann R. De Tar ◽  
William G. Spollen ◽  
Zhanyuan J. Zhang
Keyword(s):  
Agrobacterium Tumefaciens ◽  
Defense Response ◽  
Time Course ◽  
Basic Research ◽  
Defense Responses ◽  
Transformation Process ◽  
Host Responses ◽  
Nucleic Acid Metabolism ◽  
Agrobacterium Strain ◽  
Agrobacterium Mediated Transformation

Agrobacterium tumefaciens is a plant pathogen that causes crown gall disease. This pathogen is capable of transferring the T-DNA from its Ti plasmid to the host cell and, then, integrating it into the host genome. To date, this genetic transformation ability has been harnessed as the dominant technology to produce genetically modified plants for both basic research and crop biotechnological applications. However, little is known about the interaction between Agrobacterium tumefaciens and host plants, especially the host responses to Agrobacterium infection and its associated factors. We employed RNA-seq to follow the time course of gene expression in Arabidopsis seedlings infected with either an avirulent or a virulent Agrobacterium strain. Gene Ontology analysis indicated many biological processes were involved in the Agrobacterium-mediated transformation process, including hormone signaling, defense response, cellular biosynthesis, and nucleic acid metabolism. RNAseq and quantitative reverse transcription-polymerase chain reaction results indicated that expression of genes involved in host plant growth and development were repressed but those involved in defense response were induced by Agrobacterium tumefaciens. Further analysis of the responses of transgenic Arabidopsis lines constitutively expressing either the VirE2 or VirE3 protein suggested Vir proteins act to enhance plant defense responses in addition to their known roles facilitating T-DNA transformation.

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