scholarly journals Electrical stimulation over muscle tendons in humans. Evidence favouring presynaptic inhibition of Ia fibres due to the activation of group III tendon afferents

Brain ◽  
1998 ◽  
Vol 121 (2) ◽  
pp. 373-380 ◽  
Author(s):  
A Priori
Keyword(s):  
Electrical Stimulation ◽  
Presynaptic Inhibition ◽  
Group Iii ◽  
Ia Fibres

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.

Distinct Mechanisms of Presynaptic Inhibition at GABAergic Synapses of the Rat Substantia Nigra Pars Compacta

2005 ◽  
Vol 94 (3) ◽  
pp. 1992-2003 ◽  
Author(s):  
Michela Giustizieri ◽  
Giorgio Bernardi ◽  
Nicola B. Mercuri ◽  
Nicola Berretta
Keyword(s):  
Substantia Nigra ◽  
Presynaptic Inhibition ◽  
Metabotropic Glutamate Receptors ◽  
Calcium Ionophore ◽  
Gaba Release ◽  
Substantia Nigra Pars Compacta ◽  
Gabaergic Neurotransmission ◽  
Group Iii ◽  
Metabotropic Glutamate ◽  
Voltage Dependent

We investigated the mechanisms of presynaptic inhibition of GABAergic neurotransmission by group III metabotropic glutamate receptors (mGluRs) and GABAB receptors, in dopamine (DA) neurons of the substantia nigra pars compacta (SNc). Both the group III mGluRs agonist l-(+)-2-amino-4-phosphonobutyric acid (AP4, 100 μM) and the GABAB receptor agonist baclofen (10 μM) reversibly depressed the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) to 48.5 ± 2.7 and 79.3 ± 1.6% (means ± SE) of control, respectively. On the contrary, the frequency of action potential-independent miniature IPSCs (mIPSCs), recorded in tetrodotoxin (TTX, 1 μM) and cadmium (100 μM) were insensitive to AP4 but were reduced by baclofen to 49.7 ± 8.6% of control. When the contribution of voltage-dependent calcium channels (VDCCs) to synaptic transmission was boosted with external barium (1 mM), AP4 became effective in reducing TTX-resistant mIPSCs to 65.4 ± 3.9% of control, thus confirming a mechanism of presynaptic inhibition involving modulation of VDCCs. Differently from AP4, baclofen inhibited to 58.5 ± 6.7% of control the frequency mIPSCs recorded in TTX and the calcium ionophore ionomycin (2 μM), which promotes Ca2+-dependent, but VDCC-independent, transmitter release. Moreover, in the presence of α-latrotoxin (0.3 nM), to promote a Ca2+-independent vesicular release of GABA, baclofen reduced mIPSC frequency to 48.1 ± 3.2% of control, while AP4 was ineffective. These results indicate that group III mGluRs depress GABA release to DA neurons of the SNc through inhibition of presynaptic VDCCs, while presynaptic GABAB receptors directly impair transmitter exocytosis.

Functional outcomes of botulinum neurotoxin-A injection followed by reciprocal electrical stimulation in children with cerebral palsy: A randomized controlled trial

2020 ◽  
pp. 1-11
Author(s):  
Ragab K. Elnaggar ◽  
Bader A. Alqahtani ◽  
Mohammed F. Elbanna
Keyword(s):  
Cerebral Palsy ◽  
Electrical Stimulation ◽  
Botulinum Neurotoxin ◽  
Hand Function ◽  
Botulinum Neurotoxin A ◽  
Group Iii ◽  
Children With Cerebral Palsy ◽  
Spastic Hemiplegia ◽  
Upper Extremity Function

Background: The integration of therapeutic approaches is increasingly recommended for children with cerebral palsy, to enhance outcomes. Nevertheless, clinicians still opt for separate or combined therapies based on little credible knowledge. Objective: This study endeavored to evaluate the effect of botulinum neurotoxin-A (BoNT-A) injection and reciprocal neuromuscular electrical stimulation (rNMES) and their combination on the upper extremity function in children with spastic hemiplegia. Methods: Sixty-four children with spastic hemiplegia (aged 6– 10 years) were randomly assigned to four treatment-based groups [group I (BoNT-A), group II (rNMES), group III (combined BoNT-A and rNMES), and group IV (Control)]. All children received a physical rehabilitation program, thrice/week over three months. Unilateral upper-limb function, bimanual hand function, and real-time arm-hand function were assessed using Melbourne Assessment (MA), Assisting Hand Assessment (AHA), and Pediatric Motor Activity Log (PMAL) scales respectively pre-treatment, post-treatment, and at 6 months follow-up. Results: Post-treatment, group III achieved greater improvement in MA, AHA, and PMAL compared to other groups (all P <  0.05), and the difference remained in favor of group III at the follow-up (all P <  0.05). Conclusions: This study suggests that BoNT-A and rNMES combined are more effective than either of them alone to enhance upper-extremity function in children with spastic hemiplegia.

Loss of Long-Lasting Potentiation Mediated by Group III mGluRs in Amygdala Neurons in Kindling-Induced Epileptogenesis

1997 ◽  
Vol 78 (6) ◽  
pp. 3475-3478 ◽  
Author(s):  
Volker Neugebauer ◽  
N. Bradley Keele ◽  
Patricia Shinnick-Gallagher
Keyword(s):  
Electrical Stimulation ◽  
Synaptic Transmission ◽  
Learning And Memory ◽  
Metabotropic Glutamate Receptors ◽  
Long Term Potentiation ◽  
Group Iii ◽  
Brain Functions ◽  
Group Ii ◽  
Mglur Antagonist

Neugebauer, Volker, N. Bradley Keele, and Patricia Shinnick-Gallagher. Loss of long-lasting potentiation mediated by group III mGluRs in amygdala neurons in kindling-induced epileptogenesis. J. Neurophysiol. 78: 3475–3478, 1997. Long-lasting modifications of synaptic transmission can be induced in the amygdala by electrical stimulation as done in the long-term potentiation (LTP) model of learning and memory and the kindling model of epilepsy. The present study reports for the first time a long-lasting potentiation (LLP) of synaptic transmission that is induced pharmacologically by the activation of group III metabotropic glutamate receptors (mGluRs) in basolateral amygdala (BLA) neurons. In whole cell voltage-clamp mode, BLA neurons were recorded in brain slices from control rats and rats with amygdala-kindled seizures. The group III mGluR agonist l-2-amino-4-phosphonobutyrate (l-AP4, 10 μM) induced LLP of monosynaptic excitatory postsynaptic currents (EPSCs) evoked by electrical stimulation in the lateral amygdala (maximum 258 ± 50% of predrug control; means ± SE) in control ( n = 7) but not in kindled neurons( n = 6). LLP was measured 15 min after the superfusion of l-AP4, lasted for >45 min, and was not accompanied by postsynaptic membrane changes. l-AP4 induced LLP was prevented by the group III mGluR antagonist (S)-2-methyl-2-amino-4-phosphonobutyrate (MAP4; 100 μM, n = 6) but not the group II mGluR antagonist (2S,3S,4S)-2-methyl-2-carboxycyclopropylglycine (MCCG; 100 μM, n = 3). LLP was not observed after superfusion of the group II mGluR agonist (2S,3S,4S)-2-(carboxycyclopropyl)glycine (l-CCG; 1.0 and 10 μM) in either control ( n = 13) or kindled ( n = 10) neurons. If the underlying mechanisms and the functional significance of pharmacologically induced LLP are similar to those of LTP, the loss of l-AP4 induced LLP in kindled neurons may be a neurobiological correlate of learning and memory deficits in kindled animals and long-term alterations of brain functions in patients with epilepsies.

Spinoreticular neurons that receive group III input are inhibited by MLR stimulation

2002 ◽  
Vol 93 (1) ◽  
pp. 92-98 ◽  
Author(s):  
Alexandr M. Degtyarenko ◽  
Marc P. Kaufman
Keyword(s):  
Electrical Stimulation ◽  
Tibial Nerve ◽  
Afferent Input ◽  
Ventrolateral Medulla ◽  
Central Command ◽  
Mesencephalic Locomotor Region ◽  
Group Iii ◽  
Tibial Nerve Stimulation ◽  
Muscle Afferent ◽  
Stimulation Of

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.

Responses of neurons in VPL and VPL-VL region of the cat to algesic stimulation of muscle and tendon

1983 ◽  
Vol 49 (3) ◽  
pp. 649-661 ◽  
Author(s):  
K. D. Kniffki ◽  
K. Mizumura
Keyword(s):  
Electrical Stimulation ◽  
Mechanical Stimulation ◽  
Receptive Fields ◽  
Transitional Zone ◽  
The Other ◽  
Group Iii ◽  
Group I ◽  
Nociceptive Information ◽  
Noxious Mechanical Stimulation ◽  
Stimulation Of

1. The responses evoked by electrical stimulation of cutaneous and muscle nerves, by noxious and innocuous mechanical stimulation of muscle, tendon, and cutaneous tissues, and by intra-arterial (ia) injection of algesic substances (potassium, bradykinin) into arteries supplying the gastrocnemius-soleus muscle (GS) were studied in single neurons located in the ventroposterolateral nucleus (VPL) and in the transitional zone between VPL and the ventrolateral nucleus (VL) of cats lightly anesthetized with thiopenthal. Such chemical stimulation of the muscles has been shown to activate muscular groups III and IV axons specifically (43, 44) and presumably is nociceptive in character (14, 17, 31). 2. One hundred eight neurons were tested. Eighty-three of the units responded only to various types of cutaneous stimulation of the hindlimb. The other 25 responded to algesic stimulation of muscle and/or tendon. Of these latter 25, 7 had no apparent cutaneous receptive field although 4 of them responded to electrical stimulation of the common peroneal and/or sural nerve. Thus, only three neurons responded exclusively to algesic chemical and noxious mechanical stimulation of the muscle. Of the other 18 neurons, 14 had cutaneous receptive fields restricted to the hindlimb and often responded to non-noxious repetitive light stroking and to noxious pinching with a high-frequency discharge. Four cells (two of which had cutaneous input only from low-threshold mechanoreceptors) had complex and large receptive fields extending to more than one limb. 3. Potassium was a more potent muscle receptor stimulant than bradykinin, the latter only weakly exciting 3 neurons of 24 tested with both substances. The responses to potassium were rapid (approximately 4.0 s in latency) and tended to be greater (have higher response rates) for the units that responded to cutaneous as well as muscle/tendon stimulation. 4. Most neurons that responded to noxious deep stimulation had a threshold for the GS nerve volley in the group III fiber range. The few neurons with thresholds slightly below the group III range did not respond to activation of group I or II muscle spindle afferents by intra-arterial application of succinylcholine or by stretching the muscle. 5. Neurons with responses to any of the muscle, tendon, or cutaneous nociceptive stimuli were located at the ventral and dorsal periphery of VPL and in the VPL-VL transitional zone. 6. These results strongly suggest that there exist regions within the lateral diencephalon of cats that are capable of processing nociceptive information and that these regions are located at the periphery of VPL.

Group III muscle afferents evoke reflex depressor responses to repetitive muscle contractions in rabbits

2000 ◽  
Vol 278 (3) ◽  
pp. H871-H877 ◽  
Author(s):  
J. M. Legramante ◽  
G. Raimondi ◽  
C. M. Adreani ◽  
S. Sacco ◽  
F. Iellamo ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Muscle Twitch ◽  
Group Iii ◽  
Twitch Contraction ◽  
Depressor Response ◽  
Stimulation Of

Repetitive-twitch contraction of the hindlimb muscles in anesthetized rabbits consistently evokes a reflex depressor response, whereas this type of contraction in anesthetized cats evokes a reflex pressor response in about one-half of the preparations tested. Rapidly conducting group III fibers appear to comprise the afferent arm of the reflex arc, evoking the depressor response to twitch contraction in rabbits because electrical stimulation of their axons reflexly decreases arterial pressure. In contrast, electrical stimulation of the axons of slowly conducting group III and group IV afferents reflexly increases arterial pressure in rabbits. In the present study, we examined the discharge properties of group III and IV muscle afferents and found that the former (i.e., 13 of 20), but not the latter (i.e., 0 of 10), were stimulated by 5 min of repetitive-twitch contraction (1 Hz) of the rabbit triceps surae muscles. Moreover, most of the group III afferents responding to contraction appeared to be mechanically sensitive, discharging in synchrony with the muscle twitch. On average, rapidly conducting group III afferents responded for the 5-min duration of 1-Hz repetitive-twitch contraction, whereas slowly conducting group III afferents responded only for the first 2 min of contraction. We conclude that rapidly conducting group III afferents, which are mechanically sensitive, are primarily responsible for evoking the reflex depressor response to repetitive-twitch contractions in anesthetized rabbits.

Sign in / Sign up

Export Citation Format

Share Document