scholarly journals A transcortical loop demonstrated by stimulation of low-threshold muscle afferents in the awake monkey

1982 ◽  
Vol 323 (1) ◽  
pp. 393-402 ◽  
Author(s):  
M. Chofflon ◽  
J.-M. Lachat ◽  
D. G. Rüegg
1984 ◽  
Vol 51 (5) ◽  
pp. 986-997 ◽  
Author(s):  
S. J. Shefchyk ◽  
R. B. Stein ◽  
L. M. Jordan

Modulation of synaptic potentials produced by electrical stimulation of low-threshold muscle afferents in lumbar alpha-motoneurons innervating knee and ankle muscles was studied by intracellular recording during "fictive locomotion" induced by stimulating the mesencephalic locomotor region (MLR) in paralyzed, mesencephalic cats. Averaging postsynaptic potentials in different phases of the fictive step cycle indicated that relatively little amplitude modulation occurred. In nearly half of the 38 motoneurons analyzed, there was a statistically significant tendency for excitatory postsynaptic potentials (EPSPs) to increase in amplitude during the depolarized phase of the oscillation in the membrane potential produced during fictive locomotion (locomotor-drive potential). In 8% the EPSPs decreased under the same conditions, while the rest displayed a constant amplitude during all phases of the fictive step cycle. Only three cells showed a distinct second peak in the EPSP at a latency consistent with transmission in a di- or trisynaptic pathway. Late inhibitory postsynaptic potentials (IPSPs) were also rarely observed. Thus oligosynaptic pathways from muscle afferents to the motoneuron groups studied are not prominent during the locomotor cycle in this preparation. We suggest that the marked modulation of monosynaptic reflex amplitude observed in mesencephalic cats (1) arises mainly from the effects of the locomotor-drive potential in bringing the cells closer to threshold during some phases of locomotion. Specific modulation during fictive locomotion of transmission in pathways from muscle afferents, which has been demonstrated for cutaneous pathways (28), was not observed. The implications of these results for the control of locomotion are discussed briefly.


2009 ◽  
Vol 101 (6) ◽  
pp. 2741-2750 ◽  
Author(s):  
Li Zhang ◽  
Leo P. Renaud ◽  
Miloslav Kolaj

Burst firing mediated by a low-threshold spike (LTS) is the hallmark of many thalamic neurons. However, postburst afterhyperpolarizations (AHPs) are relatively uncommon in thalamus. We now report data from patch-clamp recordings in rat brain slice preparations that reveal an LTS-induced slow AHP (sAHP) in thalamic paraventricular (PVT) and other midline neurons, but not in ventrobasal or reticular thalamic neurons. The LTS-induced sAHP lasts 8.9 ± 0.4 s and has a novel pharmacology, with resistance to tetrodotoxin and cadmium and reduction by Ni2+ or nominally zero extracellular calcium concentration, which also attenuate both the LTS and sAHP. The sAHP is inhibited by 10 mM intracellular EGTA or by equimolar replacement of extracellular Ca2+ with Sr2+, consistent with select activation of LVA T-type Ca2+ channels and subsequent Ca2+ influx. In control media, the sAHP reverses near EK+, shifting to −78 mV in 10.1 mM [K+]o and is reduced by Ba2+ or tetraethylammonium. Although these data are consistent with opening of Ca2+-activated K+ channels, this sAHP lacks sensitivity to specific Ca2+-activated K+ channel blockers apamin, iberiotoxin, charybdotoxin, and UCL-2077. The LTS-induced sAHP is suppressed by a β-adrenoceptor agonist isoproterenol, a serotonin 5-HT7 receptor agonist 5-CT, a neuropeptide orexin-A, and by stimulation of the cAMP/protein kinase A pathway with 8-Br-cAMP and forskolin. The data suggest that PVT and certain midline thalamic neurons possess an LTS-induced sAHP that is pharmacologically distinct and may be important for information transfer in thalamic–limbic circuitry during states of attentiveness and motivation.


1992 ◽  
Vol 67 (5) ◽  
pp. 1375-1384 ◽  
Author(s):  
A. M. Aniss ◽  
S. C. Gandevia ◽  
D. Burke

1. Reflex responses were elicited in muscles that act at the ankle by electrical stimulation of low-threshold afferents from the foot in human subjects who were reclining supine. During steady voluntary contractions, stimulus trains (5 pulses at 300 Hz) were delivered at two intensities to the sural nerve (1.2-4.0 times sensory threshold) or to the posterior tibial nerve (1.1-3.0 times motor threshold for the intrinsic muscles of the foot). Electromyographic (EMG) recordings were made from tibialis anterior (TA), peroneus longus (PL), soleus (SOL), medial gastrocnemius (MG), and lateral gastrocnemius (LG) muscles by the use of intramuscular wire electrodes. 2. As assessed by averages of rectified EMG, stimulation of the sural or posterior tibial nerves at nonpainful levels evoked a complex oscillation with onset latencies as early as 40 ms and lasting up to 200 ms in each muscle. The most common initial responses in TA were a decrease in EMG activity at an onset latency of 54 ms for sural stimuli, and an increase at an onset latency of 49 ms for posterior tibial stimuli. The response of PL to stimulation of the two nerves began with a strong facilitation of 44 ms (sural) and 49 ms (posterior tibial). With SOL, stimulation of both nerves produced early inhibition beginning at 45 and 50 ms, respectively. With both LG and MG, sural stimuli produced an early facilitation at 52-53 ms. However, posterior tibial stimuli produced different initial responses in these two muscles: facilitation in LG at 50 ms and inhibition in MG at 51 ms. 3. Perstimulus time histograms of the discharge of 61 single motor units revealed generally similar reflex responses as in multiunit EMG. However, different reflex components were not equally apparent in the responses of different single motor units: an individual motor unit could respond slightly differently with a change in stimulus intensity or background contraction level. The multiunit EMG record represents a global average that does not necessarily depict the precise pattern of all motor units contributing to the average. 4. When subjects stood erect without support and with eyes closed, reflex patterns were seen only in active muscles, and the patterns were similar to those in the reclining posture. 5. It is concluded that afferents from mechanoreceptors in the sole of the foot have multisynaptic reflex connections with the motoneuron pools innervating the muscles that act at the ankle. When the muscles are active in standing or walking, cutaneous feedback may play a role in modulating motoneuron output and thereby contribute to stabilization of stance and gait.


1989 ◽  
Vol 143 (1) ◽  
pp. 419-434
Author(s):  
B. A. Bannatyne ◽  
S. E. Blackshaw ◽  
M. McGregor

1. New growth in cutaneous mechanosensory neurones elicited by axotomy or axon crush was studied using intracellular injection of horseradish peroxidase at different times after the lesion, ranging from a few days to over a year. 2. Cutting or crushing major, large-calibre axon branches of mechanosensory neurones elicits sprouting of new processes, either centrally within the ganglion neuropile or at the site of the lesion in the peripheral nerve. In contrast, cutting or crushing fine-calibre axon branches supplying accessory parts of the receptive field does not elicit sprouting of the main arbor or main axon branches. 3. Different modalities of mechanosensory neurone respond differently to lesions of their axons. Cutting the axons of high-threshold units responding to noxious stimulation of the skin elicits sprouting of additional processes from the axon hillock region within the central nervous system (CNS), whereas cutting or crushing the axons of low-threshold cells responding to light touch of the skin elicits sprouting at the site of the lesion only, and not within the CNS. 4. In addition to the new growth directed into the peripheral nerve, damaged nociceptive neurones also form new processes that wrap the somata of particular cells within the ganglion. 5. Sprouted processes of axotomized neurones are retained for long periods after the lesion (up to 425 days). 6. The electrical properties of touch and nociceptive cells were studied between 1 and 60 days after axotomy, by intracellular recording from the centrally located cell bodies. The amplitude, width and maximum dV/dt of the action potential and after-hyperpolarization, as well as the resting potential and input resistance, did not change significantly after axotomy, despite the considerable process sprouting known to occur during this time.


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