scholarly journals Spinal Neuronal activity During the Pectoral Fin Reflex of the Dogfish: Pathways For Reflex Generation and Cerebellar Control

1990 ◽  
Vol 148 (1) ◽  
pp. 403-414
Author(s):  
D. H. PAUL ◽  
B. L. ROBERTS
Keyword(s):  
Spinal Cord ◽  
Primary Afferents ◽  
Intracellular Recordings ◽  
Pectoral Fin ◽  
Antidromic Activation ◽  
Primary Afferent ◽  
Pulse Trains ◽  
Scyliorhinus Canicula ◽  
Afferent Volley ◽  
Monosynaptic Excitation

ingle units were recorded from the spinal cord of decerebrate dogfish (Scyliorhinus canicula) during pectoral fin reflexes (PFR) evoked by electrical pulse trains to the fin. The units were classified as primary afferent neurones, motoneurones or interneurones. Motoneurones discharged for limited (and various) periods during the reflex at latencies of 20 ms or more. There was no evidence for monosynaptic activation by primary afferents. Short-latency (S) units received monosynaptic input from fast-conducting afferents at latencies (<20 ms) appropriate for pre-motor interneurones. However, excitation of individual S-units by intracellular current injection never evoked motoneurone discharges, suggesting that convergence is necessary for motoneurone activation. Intracellular recordings from S-units which discharged for periods longer than the duration of the afferent volley generated by the fin stimulus showed that they receive other inputs in addition to those from primary afferent fibres. Intermediate-latency (I) units had similar properties to S-units except for a longer latency (>30ms), which ruled out monosynaptic excitation by fast-conducting afferents. Antidromic activation of S- and I-units by high spinal stimulation was rarely seen and orthodromic driving was also uncommon. A significant number of interneurones with latencies greater than 60 ms (L-units) were antidromically activated by high spinal stimulation. Their discharges were often long-lasting (>1 s) and we suggest that they may provide input to the cerebellum during the PFR.

α5GABAA receptors mediate primary afferent fiber tonic excitability in the turtle spinal cord

2013 ◽  
Vol 110 (9) ◽  
pp. 2175-2184 ◽  
Author(s):  
Emanuel Loeza-Alcocer ◽  
Martha Canto-Bustos ◽  
Justo Aguilar ◽  
Ricardo González-Ramírez ◽  
Ricardo Felix ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Afferent Fiber ◽  
Primary Afferents ◽  
Equilibrium Potential ◽  
Primary Afferent Depolarization ◽  
Primary Afferent ◽  
Dorsal Root Reflex

γ-Amino butyric acid (GABA) plays a key role in the regulation of central nervous system by activating synaptic and extrasynaptic GABAA receptors. It is acknowledged that extrasynaptic GABAA receptors located in the soma, dendrites, and axons may be activated tonically by low extracellular GABA concentrations. The activation of these receptors produces a persistent conductance that can hyperpolarize or depolarize nerve cells depending on the Cl− equilibrium potential. In an in vitro preparation of the turtle spinal cord we show that extrasynaptic α5GABAA receptors mediate the tonic state of excitability of primary afferents independently of the phasic primary afferent depolarization mediated by synaptic GABAA receptors. Blockade of α5GABAA receptors with the inverse agonist L-655,708 depressed the dorsal root reflex (DRR) without affecting the phasic increase in excitability of primary afferents. Using RT-PCR and Western blotting, we corroborated the presence of the mRNA and the α5GABAA protein in the dorsal root ganglia of the turtle spinal cord. The receptors were localized in primary afferents in dorsal root, dorsal root ganglia, and peripheral nerve terminals using immunoconfocal microscopy. Considering the implications of the DRR in neurogenic inflammation, α5GABAA receptors may serve as potential pharmacological targets for the treatment of pain.

scholarly journals Muscle afferent excitability testing in spinal root-intact rats: dissociating peripheral afferent and efferent volleys generated by intraspinal microstimulation

2017 ◽  
Vol 117 (2) ◽  
pp. 796-807 ◽  
Author(s):  
Saeka Tomatsu ◽  
Geehee Kim ◽  
Joachim Confais ◽  
Kazuhiko Seki
Keyword(s):  
Spinal Cord ◽  
Presynaptic Inhibition ◽  
Muscle Afferents ◽  
Primary Afferents ◽  
Medial Gastrocnemius ◽  
Primary Afferent Depolarization ◽  
Spinal Root ◽  
Primary Afferent ◽  
Intraspinal Microstimulation ◽  
Spinal Roots

Presynaptic inhibition of the sensory input from the periphery to the spinal cord can be evaluated directly by intra-axonal recording of primary afferent depolarization (PAD) or indirectly by intraspinal microstimulation (excitability testing). Excitability testing is superior for use in normal behaving animals, because this methodology bypasses the technically challenging intra-axonal recording. However, use of excitability testing on the muscle or joint afferent in intact animals presents its own technical challenges. Because these afferents, in many cases, are mixed with motor axons in the peripheral nervous system, it is crucial to dissociate antidromic volleys in the primary afferents from orthodromic volleys in the motor axon, both of which are evoked by intraspinal microstimulation. We have demonstrated in rats that application of a paired stimulation protocol with a short interstimulus interval (ISI) successfully dissociated the antidromic volley in the nerve innervating the medial gastrocnemius muscle. By using a 2-ms ISI, the amplitude of the volleys evoked by the second stimulation was decreased in dorsal root-sectioned rats, but the amplitude did not change or was slightly increased in ventral root-sectioned rats. Excitability testing in rats with intact spinal roots indicated that the putative antidromic volleys exhibited dominant primary afferent depolarization, which was reasonably induced from the more dorsal side of the spinal cord. We concluded that excitability testing with a paired-pulse protocol can be used for studying presynaptic inhibition of somatosensory afferents in animals with intact spinal roots. NEW & NOTEWORTHY Excitability testing of primary afferents has been used to evaluate presynaptic modulation of synaptic transmission in experiments conducted in vivo. However, to apply this method to muscle afferents of animals with intact spinal roots, it is crucial to dissociate antidromic and orthodromic volleys induced by spinal microstimulation. We propose a new method to make this dissociation possible without cutting spinal roots and demonstrate that it facilitates excitability testing of muscle afferents.

γ-Aminobutyric acid and primary afferent depolarization in feline spinal cord

1979 ◽  
Vol 57 (10) ◽  
pp. 1157-1167 ◽  
Author(s):  
B. R. Sastry
Keyword(s):  
Spinal Cord ◽  
Nerve Stimulation ◽  
Muscle Afferents ◽  
Aminobutyric Acid ◽  
Primary Afferent Depolarization ◽  
Antidromic Activation ◽  
Primary Afferent ◽  
Afferent Terminal ◽  
Group I ◽  
Terminal Excitability

The effects of iontophoretically applied γ-aminobutyric acid (GABA), (−)-nipecotic acid (NCA), 2,4-diaminobutyric acid (DABA), and pentobarbital were examined on the thresholds for antidromic activation of single group I muscle afferents, in decerebrated spinal cats. GABA decreased the threshold for antidromic activation of the majority of the afferents. During this decrease in the threshold, the preterminal axons were depolarized. This depolarization was decreased by a prior depolarization, but increased by a hyperpolarization, of the afferent. During the depolarization of the afferent produced by GABA, the size of the orthodromic action potential was decreased. Iontophoretically applied bicuculline antagonized the effect of GABA on the threshold for antidromic activation of the afferents. NCA, DABA, and pentobarbital potentiated the action of GABA on the afferent terminal excitability. Pre-treatment of the animals with semicarbazide, which reportedly depletes spinal GABA, resulted in a reduction in the threshold produced by a conditioning stimulation of other group I afferents. GABA decreased the threshold for antidromic activation of the nonterminal regions of the afferents when applied near the stimulation sites. The amounts of GABA required to produce a decrease in the threshold of the nonterminal afferents were greater than those required to produce a comparable effect on the terminal regions of the fibres. Iontophoretically applied NCA and bicuculline, in amounts that were adequate to alter the effects of applied GABA, failed to affect the nerve stimulation-induced decrease in the threshold for antidromic activation of the fibres. Intravenously injected bicuculline, however, antagonized the actions of GABA as well as of the reduction in the threshold produced by nerve stimulation.These results indicate that (1) GABA-induced increase in the excitability of group I afferent terminals is associated with a depolarization of the afferent, (2) the uptake of iontophoretically applied amino acid into the spinal cord tissue appears to limit its action on the afferent terminal excitability, (3) GABA has a preterminal depolarizing action on group I muscle afferents, and (4) primary afferent depolarization produced by nerve stimulation may be of diffuse origin and, hence, cannot be significantly affected by iontophoretically applied NCA and bicuculline.

scholarly journals Normal Pain Transmission

2007 ◽  
Vol 1 (1) ◽  
pp. 2-6 ◽  
Author(s):  
Catherine Urch
Keyword(s):  
Spinal Cord ◽  
Linear Relationship ◽  
Dorsal Horn ◽  
Tissue Damage ◽  
Primary Afferents ◽  
Descending Pathways ◽  
Primary Afferent ◽  
Input Intensity ◽  
Pain Transmission

• Acute (normal) pain transmission is part of a survival response to prevent tissue damage and attend to and protect damaged tissue. • A cycle of afferent transmission, response to stimuli, followed by temporary hypersensitivity, then attenuation and resolution occurs. • Primary afferent, spinal cord ascending and descending pathways are fixed; however the response elicited is highly dynamic and not a linear relationship with input intensity. • Somatic inputs are topographically accurate, in contrast to diffuse visceral inputs. • Primary afferents code differentially for stimuli (heat, acid, pressure etc) and intensity. • The dorsal horn allows extensive modulation of initial inputs, either excitation or inhibition. • Higher CNS areas allow extensive modulation of inputs, account for the conscious recognition of pain: the intensity, location, emotional and memory aspects. • Descending pathways arising from midbrain regions can be inhibitory or excitatory.

Small-caliber afferent inputs produce a heterosynaptic facilitation of the synaptic responses evoked by primary afferent A-fibers in the neonatal rat spinal cord in vitro

1993 ◽  
Vol 69 (6) ◽  
pp. 2116-2128 ◽  
Author(s):  
S. W. Thompson ◽  
C. J. Woolf ◽  
L. G. Sivilotti
Keyword(s):  
Spinal Cord ◽  
Dorsal Root ◽  
Fiber Strength ◽  
Conditioning Stimulus ◽  
Neonatal Rat ◽  
Primary Afferent ◽  
Synaptic Potentials ◽  
C Fiber ◽  
Afferent Inputs

1. The effect of brief primary afferent inputs on the amplitude and duration of the synaptic potentials evoked in ventral horn (VH) neurons by the activation of other unconditioned primary afferents was studied by current-clamp intracellular recording in the neonatal rat hemisected spinal cord in vitro. Low-frequency (1 Hz) trains of stimulation were applied to a lumbar dorsal root (Conditioning root) for 20-30 s. Test excitatory synaptic potentials (EPSPs) were evoked by single electrical shocks applied to an adjacent Test dorsal root. 2. Test and Conditioning inputs were generated at stimulation strengths sufficient to activate A beta-, A delta- and C-afferent fibers successively. At A delta- and C-fiber strength the EPSPs lasted for 4-6 s, and, during the repetitive Conditioning inputs, these summated to produce a progressively incrementing cumulative depolarization that slowly decayed back to the control Vm over tens of seconds. 3. Dorsal root conditioning produced heterosynaptic facilitation, defined as an enhancement of Test EPSPs above their DC matched controls, in 7 out of 20 neurons. To facilitate the unconditioned afferent input, the intensity of conditioning stimulation had to exceed the threshold for the activation of thin myelinated (A delta) afferents: conditioning at A beta-fiber strength had no effect, whereas A delta- and C-fiber strength conditioning were equally effective. 4. Heterosynaptic facilitation of only A beta- or A delta-fiber-evoked Test EPSPs was observed, no enhancement of C-fiber strength Test EPSPs could be demonstrated. The facilitation manifested as increases in the EPSP peak amplitude, area or the number of action potentials evoked. 5. Conditioning trials that produced heterosynaptic facilitation generated cumulative depolarizations larger than those produced by ineffective conditioning trials (9.1 +/- 3.1 vs. 3.3 +/- 0.5 mV after 20 s conditioning at resting Vm, mean +/- SE, n = 6 and 13, respectively; P < 0.05). The slope of the Vm trajectory during the summation of the conditioning EPSPs was higher in trials resulting in heterosynaptic facilitation, at 0.31 +/- 0.10 mV/s in neurons with heterosynaptic facilitation and 0.06 +/- 0.02 mV/s in cells without heterosynaptic facilitation (P < 0.05). 5. Four of the 20 VH neurons in our sample responded to A delta/C-fiber conditioning with action-potential windup: all 4 also displayed heterosynaptic facilitation. 6. Heterosynaptic facilitation decayed after the completion of the conditioning stimulus with a time course that was parallel to but not superimposable on that of the slow Vm depolarization evoked by the conditioning.(ABSTRACT TRUNCATED AT 400 WORDS)

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