Group III and IV muscle afferent discharge patterns after repeated lengthening and shortening actions

2009 ◽  
Vol 40 (5) ◽  
pp. 827-837 ◽  
Author(s):  
Vincent Martin ◽  
Erick Dousset ◽  
J��r��me Laurin ◽  
Julien Gondin ◽  
Maxime Gautier ◽  
...  
1995 ◽  
Vol 73 (2) ◽  
pp. 651-661 ◽  
Author(s):  
R. D. Johnson ◽  
J. S. Taylor ◽  
L. M. Mendell ◽  
J. B. Munson

1. In this study we investigate the peripheral receptive field properties and spinal cord connections of low-threshold muscle afferent fibers cross-regenerated into the skin to determine whether a cutaneous target can rescue physiological functions lost after chronic axotomy. 2. In adult cats the medial gastrocnemius (MG) muscle nerve was coated with the distal cut end of either the caudal or lateral cutaneous sural nerves and allowed to regenerate into the hairy skin (postoperative period 6-30 mo). During terminal acute experiments we made recordings of single MG afferent fibers in dorsal root filaments and peripheral nerve. Conduction velocity and receptive field characteristics were determined for each fiber. In addition, the MG nerve was stimulated to elicit cord dorsum potentials and monosynaptic excitatory postsynaptic potentials (EPSPs) in heteronymous motoneurons. As controls, studies were carried out after MG nerve axotomy (postoperative period 2.5-12 mo). 3. After innervation of the skin, MG muscle afferent fibers exhibited firing characteristics and proximal segment conduction velocities like those of normal MG afferents. Responses to skin and hair stimulation consisted primarily of slowly adapting, stretch-sensitive, and steady discharge patterns, all common in normal muscle afferents but not in cutaneous afferents. These properties were observed despite the innervation of touch domes and single hairs, suggesting that the peripheral physiology of muscle afferents is a function of the axonal membrane and is not respecified by a cutaneous target and/or receptors. 4. Cord dorsum potentials were characteristic of those elicited by intact muscle afferents rather than skin afferents and showed recovery of configurations lost after chronic axotomy. 5. The monosynaptic EPSPs elicited in lateral gastrocnemius-soleus motoneurons also recovered from the reduction in amplitude observed after chronic axotomy. The configurations of these EPSPs were characteristic of muscle afferents rather than skin afferents. 6. These experiments demonstrate that the peripheral and central physiological properties of muscle afferents are rescued from the axotomy state if the afferents are allowed to reinnervate skin. We found no evidence that respecification had occurred to bring the function of muscle afferents into accord with the new cutaneous target.


1986 ◽  
Vol 55 (1) ◽  
pp. 13-22 ◽  
Author(s):  
H. Querfurth

The present experiments investigated the signal transfer in the isolated frog muscle spindle by using pseudorandom noise (PRN) as the analytical probe. In order to guarantee that the random stimulus covered the entire dynamic range of the receptor, PRN stimuli of different intensities were applied around a constant mean length, or PRN stimuli of the same intensity were used while varying the mean length of the spindle. Subthreshold receptor potentials, local responses, and propagated action potentials were recorded simultaneously from the first Ranvier node of the afferent stem fiber, thus providing detailed insight into the spike-initiating process within a sensory receptor. Relevant features of the PRN stimulus were evaluated by a preresponse averaging technique. Up to tau = 2 ms before each action potential the encoder selected a small set of steeply rising stretch transients. A second component of the preresponse stimulus ensemble (tau = 2-5 ms) opposed the overall stretch bias. Since each steeply rising stretch transient evoked a steeply rising receptor potential that guaranteed the critical slope condition of the encoding site, this stimulus profile was most effective in initiating action potentials. The dynamic range of the muscle spindle receptor extended from resting length, L0, to about L0 + 100 microns. At the lower limit (L0) the encoding membrane was depolarized to its firing level and discharged action potentials spontaneously. When random stretches larger than the upper region of the dynamic range were applied, the spindle discharged at the maximum impulse rate and displayed no depolarization block or "overstretch" phenomenon. Random stretches applied within the dynamic range evoked regular discharge patterns that were firmly coupled to the PRN. The afferent discharge rate increased, and the precision of phase-locking improved when the intensity of the PRN stimulus was increased around a constant mean stretch; or the mean prestretch level was raised to higher values while the intensity of the PRN stimulus was kept constant. In the case when the PRN stimulus covered the entire dynamic range, the temporal pattern of the afferent discharge remained constant for at least 10 consecutive sequences of PRN. A spectral analysis of the discharge patterns averaged over several sequences of PRN was employed. At the same stimulus intensity the response spectra displayed low-pass filter characteristics with a 10-dB bandwidth of 300 Hz and a high-frequency slope of -12 dB/oct. Increasing the mean intensity of the PRN stimulus or raising the prestretch level increased the response power.(ABSTRACT TRUNCATED AT 400 WORDS)


2019 ◽  
Vol 117 (1) ◽  
pp. 698-707 ◽  
Author(s):  
Luis F. Queme ◽  
Alex A. Weyler ◽  
Elysia R. Cohen ◽  
Renita C. Hudgins ◽  
Michael P. Jankowski

Group III/IV muscle afferents transduce nociceptive signals and modulate exercise pressor reflexes (EPRs). However, the mechanisms governing afferent responsiveness to dually modulate these processes are not well characterized. We and others have shown that ischemic injury can induce both nociception-related behaviors and exacerbated EPRs in the same mice. This correlated with primary muscle afferent sensitization and increased expression of glial cell line-derived neurotrophic factor (GDNF) in injured muscle and increased expression of GDNF family receptor α1 (GFRα1) in dorsal root ganglia (DRG). Here, we report that increased GDNF/GFRα1 signaling to sensory neurons from ischemia/reperfusion-affected muscle directly modulated nociceptive-like behaviors and increased exercise-mediated reflexes and group III/IV muscle afferent sensitization. This appeared to have taken effect through increased cyclic adenosine monophosphate (cAMP) response element binding (CREB)/CREB binding protein-mediated expression of the purinergic receptor P2X5 in the DRGs. Muscle GDNF signaling to neurons may, therefore, play an important dual role in nociception and sympathetic reflexes and could provide a therapeutic target for treating complications from ischemic injuries.


1967 ◽  
Vol 45 (2) ◽  
pp. 319-327 ◽  
Author(s):  
M. Banet ◽  
J. J. Séguin

Muscle receptors in the mouse were shown to discharge in response to cooling of the muscle. Afferent activity was recorded in vitro from the whole nerve of the soleus muscle of 20 male white mice. These animals were maintained at a constant temperature of 22 °C for at least 15 days. In muscles cooled from 37 °C, receptors first showed activity at 32.9 ± 0.89 °C. With further cooling, there was an increase in the number of receptors firing and in the frequency of their discharge. The temperature at which maximum afferent response to cooling (TMA) occurred was 26.6 ± 0.83 °C. Similar experiments were carried out on 61 mice which had been exposed to a constant temperature of 6 °C for periods ranging from 6 hours to 32 days. Sensitivity of the receptors to cooling was significantly decreased following 24 hours' cold exposure (TMA 22.5 ± 1.02 °C) and was lowest after 12 hours' exposure. In animals exposed to cold for 3 days, sensitivity returned to a norma! level (TMA 25.4 ± 1.02 °C), but there was again a decrease in the sensitivity of the receptors to cooling in mice exposed for 5 to 6 days (TMA 22.1 ± 1.13 °C) and in those exposed for 8 to 10 days (TMA 22.4 ± 0.94 °C). Following exposure for 14 to 20 and 30 to 32 days, the sensitivity of the receptors returned to normal levels (TMA 26.3 ± 1.48 °C and 24.6 ± 2.04 °C respectively). At present the mechanisms underlying these changes in sensitivity of muscle receptors to cooling are not known.


2002 ◽  
Vol 93 (1) ◽  
pp. 92-98 ◽  
Author(s):  
Alexandr M. Degtyarenko ◽  
Marc P. Kaufman

In decerebrate paralyzed cats, we examined the responses of 18 spinoreticular neurons to electrical stimulation of the mesencephalic locomotor region. The activity of each of the spinoreticular neurons was recorded extracellularly from laminae IV through VI of the L7 and S1 spinal cord. In addition, each of the 18 spinoreticular neurons received group III afferent input from the tibial nerve. Spinoreticular projections were established for each of 18 neurons by antidromic invasion of the ventro lateral medulla at the P11 though P14 levels. The onset latencies and current thresholds for antidromic invasion from the ventro lateral medulla averaged 15.0 ± 3.8 ms and 117 ± 11 μA, respectively. Electrical stimulation of the mesencephalic locomotor region attenuated the spontaneous activity or the responses of each of the spinoreticular neurons to tibial nerve stimulation at currents that recruited group III afferents. Our data support the notion that thin-fiber muscle afferent input to the ventrolateral medulla is gated by a central command to exercise.


2013 ◽  
Vol 110 (7) ◽  
pp. 1535-1543 ◽  
Author(s):  
Renuka Ramachandra ◽  
Bassil Hassan ◽  
Stephanie G. McGrew ◽  
James Dompor ◽  
Mohamed Farrag ◽  
...  

Cardiovascular adjustments to exercise are partially mediated by group III/IV (small to medium) muscle afferents comprising the exercise pressor reflex (EPR). However, this reflex can be inappropriately activated in disease states (e.g., peripheral vascular disease), leading to increased risk of myocardial infarction. Here we investigate the voltage-dependent calcium (CaV) channels expressed in small to medium muscle afferent neurons as a first step toward determining their potential role in controlling the EPR. Using specific blockers and 5 mM Ba2+ as the charge carrier, we found the major calcium channel types to be CaV2.2 (N-type) > CaV2.1 (P/Q-type) > CaV1.2 (L-type). Surprisingly, the CaV2.3 channel (R-type) blocker SNX482 was without effect. However, R-type currents are more prominent when recorded in Ca2+ ( Liang and Elmslie 2001 ). We reexamined the channel types using 10 mM Ca2+ as the charge carrier, but results were similar to those in Ba2+. SNX482 was without effect even though ∼27% of the current was blocker insensitive. Using multiple methods, we demonstrate that CaV2.3 channels are functionally expressed in muscle afferent neurons. Finally, ATP is an important modulator of the EPR, and we examined the effect on CaV currents. ATP reduced CaV current primarily via G protein βγ-mediated inhibition of CaV2.2 channels. We conclude that small to medium muscle afferent neurons primarily express CaV2.2 > CaV2.1 ≥ CaV2.3 > CaV1.2 channels. As with chronic pain, CaV2.2 channel blockers may be useful in controlling inappropriate activation of the EPR.


2018 ◽  
Vol 120 (3) ◽  
pp. 1032-1044 ◽  
Author(s):  
Tyler L. Marler ◽  
Andrew B. Wright ◽  
Kristina L. Elmslie ◽  
Ankeeta K. Heier ◽  
Ethan Remily ◽  
...  

The exercise pressor reflex (EPR) is activated by muscle contractions to increase heart rate and blood pressure during exercise. While this reflex is beneficial in healthy individuals, the reflex activity is exaggerated in patients with cardiovascular disease, which is associated with increased mortality. Group III and IV afferents mediate the EPR and have been shown to express both tetrodotoxin-sensitive (TTX-S, NaV1.6, and NaV1.7) and -resistant (TTX-R, NaV1.8, and NaV1.9) voltage-gated sodium (NaV) channels, but NaV1.9 current has not yet been demonstrated. Using a F−-containing internal solution, we found a NaV current in muscle afferent neurons that activates at around −70 mV with slow activation and inactivation kinetics, as expected from NaV1.9 current. However, this current ran down with time, which resulted, at least in part, from increased steady-state inactivation since it was slowed by both holding potential hyperpolarization and a depolarized shift of the gating properties. We further show that, following NaV1.9 current rundown (internal F−), application of the NaV1.8 channel blocker A803467 inhibited significantly more TTX-R current than we had previously observed (internal Cl−), which suggests that NaV1.9 current did not rundown with that internal solution. Using immunohistochemistry, we found that the majority of group IV somata and axons were NaV1.9 positive. The majority of small diameter myelinated afferent somata (putative group III) were also NaV1.9 positive, but myelinated muscle afferent axons were rarely labeled. The presence of NaV1.9 channels in muscle afferents supports a role for these channels in activation and maintenance of the EPR. NEW & NOTEWORTHY Small diameter muscle afferents signal pain and muscle activity levels. The muscle activity signals drive the cardiovascular system to increase muscle blood flow, but these signals can become exaggerated in cardiovascular disease to exacerbate cardiac damage. The voltage-dependent sodium channel NaV1.9 plays a unique role in controlling afferent excitability. We show that NaV1.9 channels are expressed in muscle afferents, which supports these channels as a target for drug development to control hyperactivity of these neurons.


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