Lung afferent activity: Implications for respiratory sensation

Dental pulp stem cells (DPSCs) are important in tooth physiology, contributing to development, repair, regeneration, and immunomodulatory processes. However, their role in inflammatory mechanisms underlying pulpitis is not well understood. We evaluated the influence of DPSCs stimulated with calcitonin gene-related peptide (CGRP), a proinflammatory neuropeptide, on the expression of mediators released from DPSCs and the effect of these mediators on sensory neuron activity. Human DPSCs were treated with either control media or media containing CGRP (10−8 M) for 7 d, and the conditioned media (CM) containing DPSC-released mediators was collected. The expression of cytokines and chemokines from DPSCs was evaluated by reverse transcription quantitative polymerase chain reaction. The effects of the CM from CGRP-primed DPSCs (primed DPSC-CM) were evaluated on sensory afferents by using primary cultures of mouse trigeminal neurons and an organotypic model of cultured human pulp slices. Mouse trigeminal neurons and human pulp explants were pretreated for 24 h with control or primed DPSC-CM and then stimulated with capsaicin. Afferent activity was measured by quantifying the response to capsaicin via live cell calcium imaging in mouse neurons and CGRP released from pulp explants. Gene expression analysis showed that primed DPSCs overexpressed some proinflammatory cytokines and chemokines, including chemokines CXCL1 and CXCL8, which are both agonists of the receptor CXCR2 expressed in sensory neurons. Primed DPSC-CM increased human pulp sensory afferent activity as compared with control DPSC-CM. Similarly, primed DPSC-CM increased the intensity of calcium responses in cultured mouse trigeminal neurons. Furthermore, the CXCR2 antagonist SB225002 prevented trigeminal neuron sensitization to capsaicin induced by primed DPSC-CM. In conclusion, mediators released by DPSCs, primed with the proinflammatory mediator CGRP, induce neuronal sensitization through CXCR2 receptor. These data suggest that DPSCs might contribute to pain symptoms that develop in pulpitis.

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Pericardial mechanoreceptors with phrenic afferents

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1993.264.6.h1836 ◽

1993 ◽

Vol 264 (6) ◽

pp. H1836-H1846 ◽

Cited By ~ 9

Author(s):

D. R. Kostreva ◽

S. P. Pontus

Keyword(s):

Phrenic Nerve ◽

Cardiac Rhythm ◽

Afferent Activity ◽

Fibrous Layer ◽

Anesthetized Dogs ◽

Anatomic Distribution ◽

Phrenic Nerves ◽

The Right

Pericardial mechanoreceptors with afferents in the phrenic nerves were studied in anesthetized dogs. The specific aims determined 1) if pericardial receptors with phrenic afferents exist in the dog; 2) the stimuli needed to activate these receptors; 3) the anatomic distribution of these pericardial receptors; and 4) which pericardial layer contains the receptors. Afferent activity was recorded from the phrenic nerves while the pericardium was probed. In 15 of 18 animals, pericardial receptors were found on the right side. In 12 of 18 animals pericardial receptors were located on the left side. Most of the mechanoreceptors were found in a band that paralleled the pericardiophrenic attachment, in the fibrous layer of the pericardium, overlying the atria and atrioventricular grooves. Some receptors had a cardiac rhythm, whereas others were stimulated by the inflating lung. None of the receptors were chemosensitive to capsaicin, bradykinin, or saline. This study is the first to demonstrate that the pericardium of the dog contains mechanosensitive receptors which are innervated by the phrenic nerve.

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Jejunal or portal vein infusions of lipids increase hepatic vagal afferent activity

Neuroreport ◽

10.1097/00001756-200110080-00024 ◽

2001 ◽

Vol 12 (14) ◽

pp. 3101-3105 ◽

Cited By ~ 32

Author(s):

Alan Randich ◽

D. Seth Spraggins ◽

James E. Cox ◽

Stephen T. Meller ◽

Gary R. Kelm

Keyword(s):

Portal Vein ◽

Afferent Activity ◽

Vagal Afferent

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Mechanoreceptor afferent activity compared with receptor field dimensions and pressure changes in feline urinary bladder

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y92-206 ◽

1992 ◽

Vol 70 (11) ◽

pp. 1457-1467 ◽

Cited By ~ 32

Author(s):

John W. Downie ◽

J. Andrew Armour

Keyword(s):

Contractile Activity ◽

Bladder Wall ◽

Afferent Activity ◽

Intravesical Pressure ◽

Receptor Field ◽

Precise Relationship ◽

Pressure Changes ◽

The Relationship ◽

Simple Fashion ◽

Pressure Receptor

The relationship between vesical mechanoreceptor field dimensions and afferent nerve activity recorded in pelvic plexus nerve filaments was examined in chloralose-anesthetized cats. Orthogonal receptor field dimensions were monitored with piezoelectric ultrasonic crystals. Reflexly generated bladder contractile activity made measurements difficult, therefore data were collected from cats subjected to actual sacral rhizotomy. Afferent activity was episodic and was initiated at different pressure and receptor field dimension thresholds. Maximum afferent activity did not correlate with maximum volume or pressure. Furthermore, activity was not linearly related to intravesical pressure, receptor field dimensions, or calculated wall tension. Pressure–length hysteresis of the receptor fields occurred. The responses of identified afferent units and their associated receptor field dimensions to brief contractions elicited by the ganglion stimulant 1,1-dimethyl-4-phenylpiperazinium iodide (2.5–20 μg i.a.), studied under constant volume or constant pressure conditions, are compatible with bladder mechanoreceptors behaving as tension receptors. Because activity generated by bladder mechanoreceptors did not correlate in a simple fashion with intravesical pressure or receptor field dimensions, it is concluded that such receptors are influenced by the viscoelastic properties of the bladder wall. Furthermore, as a result of the heterogeneity of the bladder wall, receptor field tension appears to offer a more precise relationship with the activity of bladder wall mechanoreceptors than does intravesical pressure.Key words: bladder distension, intravesical pressure, sacral rhizotomy, viscoelasticity.

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Rapid regulation of microtubule-associated protein 2 in dendrites of nucleus laminaris of the chick following deprivation of afferent activity

Neuroscience ◽

10.1016/j.neuroscience.2008.02.032 ◽

2008 ◽

Vol 154 (1) ◽

pp. 381-389 ◽

Cited By ~ 25

Author(s):

Y. Wang ◽

E.W. Rubel

Keyword(s):

Afferent Activity ◽

Nucleus Laminaris

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Different Profile in Ventilatory vs. Respiratory Sensation Responses to CO2 with Varying Po2

Advances in Experimental Medicine and Biology - Post-Genomic Perspectives in Modeling and Control of Breathing ◽

10.1007/0-387-27023-x_1 ◽

2004 ◽

pp. 3-7

Author(s):

Atsuko Masuda ◽

Yoshikazu Sakakibara ◽

Toshio Kobayashi ◽

Michiko Tanaka ◽

Yoshiyuki Honda

Keyword(s):

Respiratory Sensation

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Threshold for efferent bladder nerve firing in the rat

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.276.6.r1819 ◽

1999 ◽

Vol 276 (6) ◽

pp. R1819-R1824

Author(s):

Els van Asselt ◽

Joost le Feber ◽

Ron van Mastrigt

Keyword(s):

Theoretical Model ◽

Rise Time ◽

Afferent Nerve ◽

Bladder Pressure ◽

Afferent Activity ◽

Nerve Activity ◽

Efferent Activity ◽

Rat Bladder ◽

Bladder Contraction

In this study, the mechanism involved in the initiation of voiding was investigated. Bladder pressure and bladder and urethral nerve activity were recorded in the anesthetized rat. Bladder nerve activity was resolved into afferent and efferent activity by means of a theoretical model. The beginning of an active bladder contraction was defined as the onset of bladder efferent firing at a certain time ( t 0). From t 0 onward, bladder efferent activity increased linearly during δ t seconds (rise time) to a maximum. The pressure at t 0 was 1.0 ± 0.4 kPa, the afferent nerve activity at t 0 was 2.0 ± 0.6 μV (53 ± 15% of maximum total nerve activity), and δ t was 11 ± 13 s. Between contractions the afferent activity at t 0 was never exceeded. Urethral afferent nerve activity started at bladder pressures of 2.1 ± 1.1 kPa. Therefore, we concluded that urethral afferent nerve activity does not play a role in the initiation of bladder contractions; voiding contractions presumably are initiated by bladder afferent nerve activity exceeding a certain threshold.

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