Depressive effect of morphine on the sympathetic reflex elicited by stimulation of unmyelinated hindlimb afferent nerve fibers in anesthetized cats

1983 ◽  
Vol 39 (2) ◽  
pp. 169-173 ◽  
Author(s):  
Kenichi Ito ◽  
Harue Nakamura ◽  
Akio Sato ◽  
Yuko Sato
Keyword(s):  
Nerve Fibers ◽  
Afferent Nerve ◽  
Depressive Effect ◽  
Afferent Nerve Fibers ◽  
Stimulation Of

Depression of Nociceptive Sensory Activity in the Rat Spinal Cord Due to the Intrathecal Administration of Drugs: Effect of Diazepam

Neurosurgery ◽  
1984 ◽  
Vol 15 (6) ◽  
pp. 917-920 ◽  
Author(s):  
Ilmar Jurna
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Nerve Fibers ◽  
Afferent Nerve ◽  
Spinal Reflexes ◽  
Sensory Response ◽  
Motor Responses ◽  
Afferent Nerve Fibers ◽  
C Fiber ◽  
Stimulation Of

Abstract The intrathecal (i.t.) administration of morphine inhibits nociceptive motor responses and activity in ascending axons evoked by stimulation of nociceptive afferent nerve fibers (nociceptive sensory response) in the rat. The i.t. administration of cholecystokinin octapeptide and ceruletide inhibits nociceptive motor responses, but does not affect ascending nociceptive activity. This shows that drug-induced depression of nociceptive motor responses is not always associated with depression of the nociceptive sensory response of the spinal cord. The microiontophoretic application of substance P excites single dorsal horn neurons that respond to noxious stimulation, whereas the i.t. administration of substance P inhibits both nociceptive motor and sensory responses. Thus, the results obtained from the i.t. administration of a drug may differ from those obtained from its application to single spinal neurons. Diazepam inhibits spinal reflexes and may reduce pain sensation in humans. To assess whether a spinal action is involved in the pain-relieving effect of diazepam, experiments were carried out on spinalized rats in which activity evoked by the stimulation of nociceptive and nonnociceptive afferent nerve fibers of the sural nerve was recorded from single ascending axons below the site of spinal cord transection. Diazepam, 20 ųg i.t., reduced activity evoked by afferent A delta and C fiber stimulation and by stimulation of afferent A beta fibers. The depressant effect caused by diazepam, 2 mg/kg i.v., on C fiber-evoked ascending activity was reduced by the i.t. injection of the benzodiazepine antagonist, Ro 15-1788 (40 ųg), an imidazodiazepine. It is concluded that the depression by diazepam of C fiber-evoked ascending activity contributes to pain relief caused by the drug.

Spontaneous action potential generation due to persistent sodium channel currents in simulated carotid body afferent fibers

2008 ◽  
Vol 104 (5) ◽  
pp. 1394-1401 ◽  
Author(s):  
David F. Donnelly
Keyword(s):  
Carotid Body ◽  
High Sensitivity ◽  
Nerve Fibers ◽  
Afferent Nerve ◽  
Random Pattern ◽  
Nerve Terminals ◽  
Discharge Rates ◽  
Afferent Nerve Fibers ◽  
Axonal Diameter ◽  
Spontaneous Action

The mechanism by which action potentials (APs) are generated in afferent nerve fibers in the carotid body is unknown, but it is generally speculated to be release of an excitatory transmitter and synaptic depolarizing events. However, previous results suggested that Na+ channels in the afferent nerve fibers play an important role in this process. To better understand the potential mechanism by which Na+ channels may generate APs, a mathematical model of chemoreceptor nerve fibers that incorporated Hodgkin-Huxley-type Na+ channels with kinetics of activation and inactivation, as determined previously from recordings of petrosal chemoreceptor neurons, was constructed. While the density of Na+ channels was kept constant, spontaneous APs arose in nerve terminals as the axonal diameter was reduced to that in rat carotid body. AP excitability and pattern were similar to those observed in chemoreceptor recordings: 1) a random pattern at low- and high-frequency discharge rates, 2) a high sensitivity to reductions in extracellular Na+ concentration, and 3) a variation in excitability that increased with AP generation rate. Taken together, the results suggest that an endogenous process in chemoreceptor nerve terminals may underlie AP generation, a process independent of synaptic depolarizing events.

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