Analyses of Ia — Afferent Discharge in Humans during Isotonic Position Holding and Load Perturbations

Modelling of Chaotic and Regular Ia Afferent Discharge During Fusimotor Stimulation

Alpha and Gamma Motor Systems ◽

10.1007/978-1-4615-1935-5_69 ◽

1995 ◽

pp. 325-327 ◽

Cited By ~ 1

Author(s):

K. A. Scheepstra ◽

E. Otten ◽

M. Hulliger ◽

R. W. Banks

Keyword(s):

Ia Afferent ◽

Afferent Discharge

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Permanent central synaptic disconnection of proprioceptors after nerve injury and regeneration. I. Loss of VGLUT1/IA synapses on motoneurons

Journal of Neurophysiology ◽

10.1152/jn.01095.2010 ◽

2011 ◽

Vol 106 (5) ◽

pp. 2450-2470 ◽

Cited By ~ 76

Author(s):

Francisco J. Alvarez ◽

Haley E. Titus-Mitchell ◽

Katie L. Bullinger ◽

Michal Kraszpulski ◽

Paul Nardelli ◽

...

Keyword(s):

Peripheral Nerve ◽

Nerve Injury ◽

Cell Body ◽

Peripheral Nerve Injury ◽

Motor Coordination ◽

Electrophysiological Study ◽

Peripheral Nerve Injuries ◽

Nerve Injuries ◽

Ia Afferent ◽

Axon Collaterals

Motor and sensory proprioceptive axons reinnervate muscles after peripheral nerve transections followed by microsurgical reattachment; nevertheless, motor coordination remains abnormal and stretch reflexes absent. We analyzed the possibility that permanent losses of central IA afferent synapses, as a consequence of peripheral nerve injury, are responsible for this deficit. VGLUT1 was used as a marker of proprioceptive synapses on rat motoneurons. After nerve injuries synapses are stripped from motoneurons, but while other excitatory and inhibitory inputs eventually recover, VGLUT1 synapses are permanently lost on the cell body (75–95% synaptic losses) and on the proximal 100 μm of dendrite (50% loss). Lost VGLUT1 synapses did not recover, even many months after muscle reinnervation. Interestingly, VGLUT1 density in more distal dendrites did not change. To investigate whether losses are due to VGLUT1 downregulation in injured IA afferents or to complete synaptic disassembly and regression of IA ventral projections, we studied the central trajectories and synaptic varicosities of axon collaterals from control and regenerated afferents with IA-like responses to stretch that were intracellularly filled with neurobiotin. VGLUT1 was present in all synaptic varicosities, identified with the synaptic marker SV2, of control and regenerated afferents. However, regenerated afferents lacked axon collaterals and synapses in lamina IX. In conjunction with the companion electrophysiological study [Bullinger KL, Nardelli P, Pinter MJ, Alvarez FJ, Cope TC. J Neurophysiol (August 10, 2011). doi:10.1152/jn.01097.2010], we conclude that peripheral nerve injuries cause a permanent retraction of IA afferent synaptic varicosities from lamina IX and disconnection with motoneurons that is not recovered after peripheral regeneration and reinnervation of muscle by sensory and motor axons.

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Saccade-Related Inhibitory Input to Pontine Omnipause Neurons: An Intracellular Study in Alert Cats

Journal of Neurophysiology ◽

10.1152/jn.1999.82.3.1198 ◽

1999 ◽

Vol 82 (3) ◽

pp. 1198-1208 ◽

Cited By ~ 41

Author(s):

Kaoru Yoshida ◽

Yoshiki Iwamoto ◽

Sohei Chimoto ◽

Hiroshi Shimazu

Keyword(s):

Initial Phase ◽

Time Course ◽

Inhibitory Input ◽

Peak Time ◽

Time Integral ◽

Intracellular Study ◽

Afferent Discharge ◽

Alert Cats ◽

Eye Velocity ◽

Omnipause Neurons

Omnipause neurons (OPNs) are midline pontine neurons that are thought to control a number of oculomotor behaviors, especially saccades. Intracellular recordings were made from OPNs in alert cats to elucidate saccade-associated postsynaptic events in OPNs and thereby determine what patterns of afferent discharge impinge on OPNs to cause their saccadic inhibition. The membrane potential of impaled OPNs exhibited steep hyperpolarization before each saccade that lasted for the whole period of the saccade. The hyperpolarization was reversed to depolarization by intracellular injection of Cl− ions, indicating it consisted of temporal summation of inhibitory postsynaptic potentials (IPSPs). The duration of the saccade-related hyperpolarization was almost equal to the duration of the concurrent saccades. The time course of the hyperpolarization was similar to that of the radial eye velocity except for the initial phase. During the falling phase of eye velocity, the correlation between the instantaneous amplitude of hyperpolarization and the instantaneous eye velocity was highly significant. The amplitude of hyperpolarization at the eye velocity peak was correlated significantly with the peak eye velocity. The time integral of the hyperpolarization was correlated with the radial amplitude of saccades. The initial phase disparity between the hyperpolarization and eye velocity was due to the relative constancy of peak time (∼20 ms) of the initial steep hyperpolarization regardless of the later potential profile that covaried with the eye velocity. The initial steep hyperpolarization led the beginning of saccades by 15.9 ± 3.8 (SD) ms, which is longer than the lead time for medium-lead burst neurons. These results demonstrate that the pause of activity in OPNs is caused by IPSPs initiated by an abrupt, intense input and maintained, for the whole duration of the saccade, by afferents conveying eye velocity signals. We suggest that the initial sudden inhibition originates from central structures such as the superior colliculus and frontal eye fields and that the eye velocity-related inhibition originates from the burst generator in the brain stem.

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Early postnatal development of GABAergic presynaptic inhibition of Ia proprioceptive afferent connections in mouse spinal cord

Journal of Neurophysiology ◽

10.1152/jn.00783.2012 ◽

2013 ◽

Vol 109 (8) ◽

pp. 2118-2128 ◽

Cited By ~ 9

Author(s):

Patrick M. Sonner ◽

David R. Ladle

Keyword(s):

Spinal Cord ◽

Postnatal Development ◽

Presynaptic Inhibition ◽

Dorsal Root ◽

Reciprocal Inhibition ◽

Afferent Feedback ◽

Early Postnatal Development ◽

Ia Afferent ◽

Ia Afferents ◽

Stimulation Of

Sensory feedback is critical for normal locomotion and adaptation to external perturbations during movement. Feedback provided by group Ia afferents influences motor output both directly through monosynaptic connections and indirectly through spinal interneuronal circuits. For example, the circuit responsible for reciprocal inhibition, which acts to prevent co-contraction of antagonist flexor and extensor muscles, is driven by Ia afferent feedback. Additionally, circuits mediating presynaptic inhibition can limit Ia afferent synaptic transmission onto central neuronal targets in a task-specific manner. These circuits can also be activated by stimulation of proprioceptive afferents. Rodent locomotion rapidly matures during postnatal development; therefore, we assayed the functional status of reciprocal and presynaptic inhibitory circuits of mice at birth and compared responses with observations made after 1 wk of postnatal development. Using extracellular physiological techniques from isolated and hemisected spinal cord preparations, we demonstrate that Ia afferent-evoked reciprocal inhibition is as effective at blocking antagonist motor neuron activation at birth as at 1 wk postnatally. In contrast, at birth conditioning stimulation of muscle nerve afferents failed to evoke presynaptic inhibition sufficient to block functional transmission at synapses between Ia afferents and motor neurons, even though dorsal root potentials could be evoked by stimulating the neighboring dorsal root. Presynaptic inhibition at this synapse was readily observed, however, at the end of the first postnatal week. These results indicate Ia afferent feedback from the periphery to central spinal circuits is only weakly gated at birth, which may provide enhanced sensitivity to peripheral feedback during early postnatal experiences.

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The Innervation of the Muscle-Spindle

Journal of Cell Science ◽

10.1242/jcs.s3-89.6.143 ◽

1948 ◽

Vol s3-89 (6) ◽

pp. 143-185

Author(s):

D. BARKER

Keyword(s):

Muscle Spindles ◽

Muscle Fibres ◽

Gold Chloride ◽

Nerve Fibres ◽

Intrafusal Muscle ◽

Intrafusal Fibre ◽

Afferent Discharge ◽

Tendon Organ ◽

Nuclear Bag ◽

Secondary Fibre

A study of the morphology and innervation of muscle-spindles from the quadriceps of the rabbit and cat has shown that: 1. The intrafusal muscle-fibres do not subdivide in their course through the spindle, as is maintained in some descriptions, but retain their individuality from pole to pole. 2. There is no constant feature which is characteristic of one pole of a spindle and not the other. A distinction can be made between the proximal and distal ends only when it is possible to orientate the spindle according to the proximal and distal ends of the muscle. The extreme ends of the spindle are attached indifferently to extrafusal endomysium, tendon, or perimysial connective tissue. 3. In the equatorial region each muscle-fibre of the spindle contains a dense aggregation of spherical central nuclei (‘nuclear bag’). On either side of this aggregation oval nuclei are disposed in the form of a chain within a central core of protoplasm (‘myotube region’). The nuclear bag is devoid of cross-striations and presumably non-contractile. The two polar portions of the muscle-fibre on either side of the bag are striated and each receives a motor innervation; hence they are presumed to function as independent contractile units. 4. The number of end-plates possessed by a spindle is approximately double its number of intrafusal muscle-fibres, with half the total number of end-plates situated at each pole. The ratio is rarely exact, since one polar half of an intrafusal fibre frequently bears two end-plates; these are innervated by nerve-fibres which retain their individuality as far as they can be traced back from the spindle. Both small nerve-fibres (3-4 µ in gold chloride preparations) and relatively large nerve-fibres (6-7 µ in gold chloride preparations) take part in the motor innervation of muscle-spindles, as was deduced on physiological grounds by Leksell (1945). 5. An analysis of the sensory innervation has confirmed many of Ruffini's (1898) observations. Primary or ‘annulo-spiral’ and secondary or ‘flowerspray’ endings occur and they are innervated by independent nerve-fibres; it is suggested that Ruffini's terms ‘primary’ and ‘secondary’ be adopted since the descriptive terms cannot always be applied. In the rabbit the secondary ending is ‘annulo-spiral’ in form and differs little from the primary ending; in the cat it is more irregular and could be termed ‘flower-spray’. The primary ending is always present and is associated with the nuclear bags of the intrafusal muscle-fibres; in some instances its ramifications are more extensive and also entwine the myotube regions. The primary ending may be the only sensory termination present, or it may be accompanied by one or by two secondary endings. These are borne by the myotube regions of the musclefibres. In the rabbit's quadriceps and interossei, spindles with one primary and one secondary ending were the most frequent in the samples taken; in the cat's quadriceps spindles with one primary and two secondary endings were the most numerous. Both the primary and secondary nerve-fibres invariably ramify so as to innervate each intrafusal fibre in the muscle-bundle. The two sensory terminations are often closely intercalated but do not overlap with one another to any great extent. As estimated from measurements made on fresh, silver, and gold chloride preparations the total diameter of the primary fibre lies between 8 and 12 µ, that of the secondary fibre between 6 and 9 µ. 6. Apart from small sympathetic fibres innervating the vascular supply of the spindle, other finer fibres may occasionally be seen ramifying within the walls of the capsule and over the polar regions. It is possible that they are somatic sensory fibres subserving the sensation of pain. 7. The nature of the reflex effects of the afferent impulses discharged by the muscle-spindle and tendon-organ is considered, and it is concluded that the balance of evidence indicates that the afferent discharge from the spindle is excitatory and that from the tendon-organ inhibitory to the motor neurones of the same muscle. However, the identification of the spindle as the receptor which excites the stretch reflex is found to rest largely upon equivocal evidence, its acceptance depending ultimately upon Matthews's finding (1933) of a considerable difference-in threshold between the spindle and tendon-organ in response to stretch. It is suggested that the large primary fibre innervating the spindle should be identified as the ‘stretch afferent’ rather than the smaller secondary fibre specified by Matthews, for the rapid con duction rate of the afferent discharge exciting the stretch reflex (Lloyd, 1943) indicates that sensory fibres of the largest diameter are employed. The functional significance of the secondary fibres is obscure and the specific reflex functions of the sensory fibres innervating both the spindle and the tendon organ clearly require further elucidation.

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Mechanical stimulation is not responsible for activation of gastrointestinal afferents during ischemia

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.272.1.h99 ◽

1997 ◽

Vol 272 (1) ◽

pp. H99-H106 ◽

Cited By ~ 1

Author(s):

H. L. Pan ◽

Z. B. Zeisse ◽

J. C. Longhurst

Keyword(s):

Gastrointestinal Motility ◽

Mechanical Stimulation ◽

Single Unit ◽

Intraluminal Pressure ◽

Mechanical Activity ◽

Single Unit Activity ◽

C Fiber ◽

Afferent Discharge ◽

The Right

Abdominal ischemia reflexly excites the cardiovascular system through activation of visceral sympathetic afferents. Although a number of ischemic metabolites are known to stimulate sympathetic afferents, the contribution of mechanical stimulation to activation of afferents during abdominal ischemia remains uncertain. Thus the present study examined the role of changes in motility in activation of gastrointestinal afferents during ischemia. Single-unit activity of C fiber afferents located on the stomach, duodenum, jejunum, or colon was recorded from the right sympathetic chain of anesthetized cats during 15 min of ischemia. Intraluminal pressure, as a reflection of local mechanical activity, was measured by an open catheter placed in the lumen of the gastrointestinal tract. The results show that gastrointestinal motility was mainly inhibited during abdominal ischemia. Changes in intraluminal pressure did not correlate with afferent discharge activity during ischemia (r = -0.32, n = 10). Furthermore, discharge frequency of gastrointestinal afferents during ischemia was not altered significantly by topical application of 100 micrograms/ml of atropine (3.98 +/- 0.62 to 3.83 +/- 0.59 imp/s, n = 12), which profoundly inhibited local gastrointestinal motility. Collectively, these data indicate that gastrointestinal motility changes during abdominal ischemia do not contribute to activation of gastrointestinal sympathetic C fiber afferents.

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Encoder response of isolated frog muscle spindle elicited by pseudorandom noise stimuli

Journal of Neurophysiology ◽

10.1152/jn.1986.55.1.13 ◽

1986 ◽

Vol 55 (1) ◽

pp. 13-22 ◽

Cited By ~ 7

Author(s):

H. Querfurth

Keyword(s):

Muscle Spindle ◽

Action Potentials ◽

Dynamic Range ◽

Frog Muscle ◽

Pass Filter ◽

Low Pass Filter ◽

Pseudorandom Noise ◽

Afferent Discharge ◽

The Mean ◽

Discharge Patterns

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)

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