Modulation of incisor eruption in rats by sympathetic efferents

2018 ◽  
Vol 89 ◽  
pp. 31-36 ◽  
Author(s):  
José Johann Chidiac ◽  
Ammar Kassab ◽  
Khaldoun Rifai ◽  
Nayef E. Saadé ◽  
Elie D. Al Chaer
Keyword(s):  
Sympathetic Efferents

Adrenoreceptor subtype mediating sympathetic-sensory coupling in injured sensory neurons

1996 ◽  
Vol 76 (6) ◽  
pp. 3721-3730 ◽  
Author(s):  
Y. Chen ◽  
M. Michaelis ◽  
W. Janig ◽  
M. Devor
Keyword(s):  
Sciatic Nerve ◽  
Nerve Injury ◽  
Expression Profiles ◽  
Functional Results ◽  
Firing Frequency ◽  
Receptor Type ◽  
Afferent Neurons ◽  
Sympathetic Efferents ◽  
Frequency Excitation

1. Teased axon recordings were made from 167 spontaneously active A beta- and A delta-afferents that ended in sciatic nerve end neuromas of 6-12 days standing. When challenged with a standard bolus of systemically applied adrenaline, 100 (60%) responded, either with an increase in baseline firing frequency (excitation, 96/100) or with a decrease (suppression, 4/100). 2. Experiments using receptor type-selective antagonists indicated that the adreno-sensitivity was mediated by alpha 2 adrenoreceptors in 65% of the afferents sampled, by alpha 1 adrenoreceptors in 13%, and about equally by alpha 1 and alpha 2 adrenoreceptors in approximately 10%. In the remaining 13%, neither type of antagonist blocked adrenaline-evoked excitation, at least not at the doses used. Both excitatory and suppressive responses were primarily sensitive to alpha 2 antagonists. 3. Experiments using receptor type-selective agonists substantiated the conclusion that sympathetic-sensory coupling at sites of nerve injury is mediated primarily by alpha 2 adrenoreceptors. 4. Recordings were also made from 14 afferent neurons with spontaneous ectopic discharge originating in dorsal root ganglia (DRGs) L4 and L5. The rats had undergone transection of the ipsilateral sciatic nerve 8–93 days previously. All neurons responded to systemic adrenaline and/or trains of activity evoked in postganglionic sympathetic efferents with either excitation or suppression. As in the neuroma endings, responses in the large majority of cases were blocked by alpha 2-selective, but not by alpha 1-selective adrenoreceptor antagonists. 5. The results indicate that sympathetic-sensory coupling, both at nerve injury sites and in axotomized DRG neurons, is mediated primarily by alpha 2 adrenoreceptors. In a minority of afferent neurons, however, it appears to be mediated by alpha 1 adreno-receptors or by both alpha 1 and alpha 2 adrenoreceptors. These functional results are consistent with receptor-type expression profiles from studies based on in situ hybridization and immunocytochemistry.

The role of the sympathetic efferents in endotoxin-induced localized inflammatory hyperalgesia and cytokine upregulation

2002 ◽  
Vol 42 (6) ◽  
pp. 864-872 ◽  
Author(s):  
B. Safieh-Garabedian ◽  
S Poole ◽  
J.J. Haddad ◽  
C.A. Massaad ◽  
S.J. Jabbur ◽  
...  
Keyword(s):  
Inflammatory Hyperalgesia ◽  
Sympathetic Efferents

Central command, but not muscle reflex, stimulates cutaneous sympathetic efferents of cats

1998 ◽  
Vol 274 (5) ◽  
pp. H1552-H1559 ◽  
Author(s):  
Janeen M. Hill ◽  
Marc P. Kaufman
Keyword(s):  
Electrical Stimulation ◽  
Blocking Agent ◽  
Muscle Afferents ◽  
Group Iii ◽  
Hairy Skin ◽  
Sympathetic Efferents ◽  
Muscle Reflex ◽  
Decerebrate Cats ◽  
Sympathetic Discharge ◽  
Stimulation Of

We determined the effects of stimulation of the mesencephalic locomotor region (MLR) and the muscle reflex, each evoked separately, on the discharge of cutaneous sympathetic fibers innervating the hairy skin of decerebrate cats. Electrical stimulation of the MLR was performed while the cats were paralyzed with vecuronium bromide. The muscle reflex was evoked while the cats were not paralyzed by electrical stimulation of the tibial nerve at current intensities that did not activate directly group III and IV muscle afferents. MLR stimulation increased, on average, the discharge of the 23 cutaneous sympathetic fibers tested ( P < 0.05). The muscle reflex, in contrast, had no overall effect on the discharge of 21 sympathetic fibers tested ( P > 0.05). Both maneuvers markedly increased mean arterial pressure and heart rate ( P < 0.05). Prevention of the baroreceptor reflex with the α-adrenergic blocking agent phentolamine did not reveal a stimulatory effect of the muscle reflex on cutaneous sympathetic discharge. We conclude that the MLR is a more important mechanism than is the muscle reflex in controlling sympathetic discharge to hairy skin during dynamic exercise.

Reflex sympathetic changes in aortic diastolic pressure-diameter relationship

1975 ◽  
Vol 229 (2) ◽  
pp. 286-290 ◽  
Author(s):  
M Pagani ◽  
PJ Schwartz ◽  
VS Bishop ◽  
A Malliani
Keyword(s):  
Thoracic Aorta ◽  
Carotid Arteries ◽  
Diastolic Pressure ◽  
External Diameter ◽  
Ultrasound Technique ◽  
Sinusoidal Oscillations ◽  
Aortic Blood Pressure ◽  
Sympathetic Efferents ◽  
Inferior Cardiac Nerve ◽  
Stimulation Of

In anesthetized vagotomized cats with the chest opened and artificially ventilated, aortic blood pressure (AP) and external diameter (AD; ultrasound technique) were measured in the proximal third of the descending thoracic aorta. Slow sinusoidal oscillations (0.2-0.3 Hz in aortic volume were produced by a piston pump connected to a femoral artery. Diastolic pressure-diameter relationship (PDR) curves were obtained during control conditions and during stimulation of either the cut central end of the left inferior cardiac nerve (ICN) or the decentralized thoracic sympathetic chain (SC). In six cats with both carotid arteries occluded ICN stimulation reflexly shifted the PDR curves to lower diameters for any given pressure (mean deltaAD 3.2% at control AP). A smaller response to ICN stimulation was obtained in five cats with one patent carotid artery (mean deltaAD 2.3% at control AP). Stimulation of sympathetic efferents to the aorta (SC) caused similar responses in five animals (mean deltaAD 3.4% at control AP). This reflex control of the thoracic aorta may be involved in cardioaortic coupling and may influence the sensitivity of aortic mechanoreceptors.

Neural control of vascular permeability: interactions between primary afferents, mast cells, and sympathetic efferents

1989 ◽  
Vol 62 (1) ◽  
pp. 48-58 ◽  
Author(s):  
T. J. Coderre ◽  
A. I. Basbaum ◽  
J. D. Levine
Keyword(s):  
Blood Pressure ◽  
Mast Cells ◽  
Vascular Permeability ◽  
Neural Control ◽  
Primary Afferents ◽  
Sympathetic Chain ◽  
Blue Dye ◽  
Base Line ◽  
Plasma Extravasation ◽  
Sympathetic Efferents

1. This study addressed the contribution of primary afferents, mast cells, and sympathetic efferents to the control of vascular permeability in synovial joints. Extravasation of Evans blue dye into the synovial space was measured by perfusion of the knee joint in the adult rat. Plasma extravasation (PE) was evoked by pharmacologic activation of either unmyelinated primary afferents, mast cells, or sympathetic postganglionic nerve (SPGN) terminals with acute injection of either capsaicin, compound 48/80, or 6-hydroxydopamine (6-OHDA), respectively. In otherwise untreated control rats, acute infusion of capsaicin or compound 48/80 produced a brief increase in vascular permeability; infusion of 6-OHDA produced a larger and more prolonged increase. 2. To evaluate the contribution of an interaction of different cellular elements in the joint to PE, we repeated these experiments in rats pretreated with capsaicin, compound 48/80, or 6-OHDA; administered quercetin; or surgically sympathectomized by excision of the lumbar sympathetic chain. Eliminating unmyelinated afferent nerve terminals by neonatal treatment with capsaicin only reduced the increase in PE produced by acute infusion of capsaicin. Degranulating mast cells by pretreatment with compound 48/80, or preventing the degranulation of mast cells by treatment with quercetin, reduced the increase in PE evoked by infusion of either capsaicin or compound 48/80. Finally, sympathectomy, produced by excision of the lumbar sympathetic chain or by pretreatment with 6-OHDA, significantly reduced PE elicited by acute infusion of capsaicin, compound 48/80, or 6-OHDA. 3. Neither infusing substances normally localized to sympathetic efferents nor inducing changes in blood pressure could mimic the profound increase in PE evoked by activation of sympathetic postganglionic neurons with acute infusion of 6-OHDA. Thus norepinephrine produced a significant decrease in PE, adenosine triphosphate produced only a brief increase, neuropeptide Y had no effect, and manipulating blood pressure (either up or down) had no effect on either base-line or 6-OHDA-induced PE. 4. Indomethacin treatment significantly reduced the increase in PE produced by 6-OHDA. This effect of indomethacin was reversed by the addition of prostaglandin E2 (PGE2) to the 6-OHDA in the perfusion fluid. This finding implicates prostaglandins (i.e., cyclooxygenase products of arachidonic acid metabolism) in SPGN-dependent generation of PE.(ABSTRACT TRUNCATED AT 400 WORDS)

Involvement of sympathetic efferents but not capsaicin-sensitive afferents in nociceptin-mediated dual control of rat synovial blood flow

2003 ◽  
Vol 284 (6) ◽  
pp. R1477-R1485 ◽  
Author(s):  
Jason J. McDougall
Keyword(s):  
Blood Flow ◽  
Direct Action ◽  
Knee Joints ◽  
Opioid Antagonist ◽  
High Dose ◽  
Adrenoceptor Antagonist ◽  
Anaesthetized Rats ◽  
Unmyelinated Nerve ◽  
Sympathetic Efferents ◽  
Constrictor Response

This study set out to examine the vasomotor effects of the opioid-like peptide nociceptin on knee joint capsular blood flow in urethane-anaesthetized rats. Topical application of nociceptin (10−15–10−8 mol) caused a progressive fall in joint perfusion that was significantly inhibited by the specific nociceptin receptor antagonist [Phe1-(CH2-NH)-Gly2] Nociceptin(1–13)-NH2 as well as the nonspecific opioid antagonist naloxone. To test whether this constrictor response was sympathetically mediated, we administered nociceptin in animals treated with guanethidine to produce sympathetic blockade or in the presence of the α-adrenoceptor antagonist phentolamine. Both guanethidine treatment and phentolamine coadministration attenuated the constrictor response to nociceptin. Inhibition of nociceptin-mediated vasoconstriction revealed a supplementary hyperemic response that persisted in animals whose knee joints were treated with 1% capsaicin to destroy the articular unmyelinated nerve supply. These results show that, in the rat knee, peripheral administration of nociceptin primarily causes a sympathetically mediated vasoconstriction. In addition, high-dose nociceptin produces a vasodilatatory response that is likely due to the direct action of nociceptin on vascular smooth muscle and not by a neurogenic mechanism.

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