Excitability of primary afferents in feline spinal cord: taurine, homotaurine, and γ-aminobutyric acid compared

1982 ◽  
Vol 60 (6) ◽  
pp. 850-855 ◽  
Author(s):  
Radan Čapek ◽  
Barbara Esplin
Keyword(s):  
Primary Afferents ◽  
Aminobutyric Acid ◽  
Primary Afferent Depolarization ◽  
Conditioning Stimulation ◽  
Primary Afferent ◽  
Antagonistic Muscle ◽  
Consistent Change ◽  
Muscle Nerve ◽  
Gaba Synthesis ◽  
Stimulation Of

Effects of taurine and homotaurine (3-aminopropancsuIfonic acid), on excitability of primary afferents were compared with effects of γ-aminobutyric acid (GABA) in spinal unanaesthesized cats. Homotaurine and GABA, administered intravenously or topically, produced a marked increase in afferent excitability. Homotaurine was about 10 times more potent than GABA. Taurine (up to 2 mmol/kg i.v., or 10 mM topically) did not produce a consistent change in afferent excitability. The effect of homotaurine was antagonized by bicuculline or picrotoxin in doses which suppressed the primary afferent depolarization, as indicated by an increase of afferent excitability, evoked by conditioning stimulation of an antagonistic muscle nerve. Semicarbazidc, an inhibitor of GABA synthesis, did not attenuate the homotaurine-induced excitability changes of afferents while suppressing entirely the primary afferent depolarization. These findings suggest that homotaurine exerts a direct GABA-like action on feline primary afferents.

Baclofen-induced decrease of excitability of primary afferents and depression of monosynaptic transmission in cat spinal cord

1982 ◽  
Vol 60 (2) ◽  
pp. 160-166 ◽  
Author(s):  
Radan Čapek ◽  
Barbara Esplin
Keyword(s):  
Spinal Cord ◽  
Primary Afferents ◽  
Spinal Reflex ◽  
Primary Afferent Depolarization ◽  
Antagonistic Muscle ◽  
Muscle Nerve ◽  
Relationship Of ◽  
The Relationship ◽  
Excitatory Transmitter ◽  
Terminal Excitability

The relationship of the depressant effect of baclofen on spinal monosynaptic transmission and its effect on the excitability of primary afferents was examined in spinal unanesthetized cats. Baclofen (1.0 mg/kg, i.v.) produced a deep and long-lasting depression of spinal reflex responses with a concomitant decrease of terminal excitability. Primary afferent depolarization, as indicated by an increase of terminal excitability, evoked by conditioning of an antagonistic muscle nerve, was greatly reduced by this drug. Depression of monosynaptic transmission induced by baclofen was temporarily reversed by posttetanic potentiation. However, the same high frequency orthodromic stimulation further reduced excitability of terminals. It is therefore unlikely that block of terminal invasion is responsible for baclofen-induced depression of spinal monosynaptic transmission. These results are compatible with the suggestion that baclofen causes a reduction of transmitter release. In the spinal cord, this action is probably limited to the excitatory transmitter of primary afferents.

Inhibition Evoked From Primary Afferents in the Electrosensory Lateral Line Lobe of the Weakly Electric Fish (Apteronotus leptorhynchus)

1998 ◽  
Vol 80 (6) ◽  
pp. 3173-3196 ◽  
Author(s):  
Neil J. Berman ◽  
Leonard Maler
Keyword(s):  
Lateral Line ◽  
Granule Cell ◽  
Electric Fish ◽  
Inhibitory Response ◽  
Primary Afferents ◽  
Weakly Electric Fish ◽  
Apteronotus Leptorhynchus ◽  
Primary Afferent ◽  
Weakly Electric ◽  
Stimulation Of

Berman, Neil J. and Leonard Maler. Inhibition evoked from primary afferents in the electrosensory lateral line lobe of the weakly electric fish ( Apteronotus leptorhynchus). J. Neurophysiol. 80: 3173–3196, 1998. The responses of two types of projection neurons of the electrosensory lateral line lobe, basilar (BP) and nonbasilar (NBP) pyramidal cells, to stimulation of primary electrosensory afferents were determined in the weakly electric fish, Apteronotus leptorhynchus. Using dyes to identify cell type, the response of NBP cells to stimulation of primary afferents was inhibitory, whereas the response of BP cells was excitation followed by inhibition. γ-Aminobutyric acid (GABA) applications produced biphasic (depolarization then hyperpolarization) responses in most cells. GABAA antagonists blocked the depolarizing effect of GABA and reduced the hyperpolarizing effect. The GABAB antagonists weakly antagonized the hyperpolarizing effect. The early depolarization had a larger increase in cell conductance than the late hyperpolarization. The conductance changes were voltage dependent, increasing with depolarization. In both cell types, baclofen produced a slow small hyperpolarization and reduced the inhibitory postsynaptic potentials (IPSPs) evoked by primary afferent stimulation. Tetanic stimulation of primary afferents at physiological rates (100–200 Hz) produced strongly summating compound IPSPs (∼500-ms duration) in NBP cells, which were usually sensitive to GABAA but not GABAB antagonists; in some cells there remained a slow IPSP that was unaffected by GABAB antagonists. BP cells responded with excitatory or mixed excitatory + inhibitory responses. The inhibitory response had both a fast (∼30 ms, GABAA) and long-lasting slow phase (∼800 ms, mostly blocked by GABAA antagonists). In some cells there was a GABAA antagonist-insensitive slow IPSP (∼500 ms) that was sensitive to GABAB antagonists. Application of glutamate ionotropic receptor antagonists blocked the inhibitory response of NBP cells to primary afferent stimulation and the excitatory response of BP cells but enhanced the BP cell slow IPSP; this remaining slow IPSP was reduced by GABAB antagonists. Unit recordings in the granule cell layer and computer simulations of pyramidal cell inhibition suggested that the duration of the slow GABAA inhibition reflects the prolonged firing of GABAergic granule cell interneurons to primary afferent input. Correlation of the results with known GABAergic circuitry in the electrosensory lobe suggests that the GABAergic type 2 granule cell input to both pyramidal cell types is via GABAA receptors. The properties of the GC2 GABAA input are well suited to their putative role in gain control, regulation of phasicness, and coincidence detection. The slow GABAB IPSP evoked in BP cells is likely due to ovoid cell input to their basal dendrites.

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.

Primary afferent depolarization of muscle afferents elicited by stimulation of joint afferents in cats with intact neuraxis and during reversible spinalization

1993 ◽  
Vol 70 (5) ◽  
pp. 1899-1910 ◽  
Author(s):  
J. Quevedo ◽  
J. R. Eguibar ◽  
I. Jimenez ◽  
R. F. Schmidt ◽  
P. Rudomin
Keyword(s):  
Spinal Cord ◽  
Knee Joint ◽  
High Threshold ◽  
Primary Afferent Depolarization ◽  
Delayed Response ◽  
Primary Afferent ◽  
Myelinated Fibers ◽  
Group I ◽  
Posterior Knee ◽  
Stimulation Of

1. In the anesthetized and artificially ventilated cat, stimulation of the posterior articular nerve (PAN) with low strengths (1.2-1.4 x T) produced a small negative response (N1) in the cord dorsum of the lumbosacral spinal cord with a mean onset latency of 5.2 ms. Stronger stimuli (> 1.4 x T) produced two additional components (N2 and N3) with longer latencies (mean latencies 7.5 and 15.7 ms, respectively), usually followed by a slow positivity lasting 100-150 ms. With stimulus strengths above 10 x T there was in some experiments a delayed response (N4; mean latency 32 ms). 2. Activation of posterior knee joint nerve with single pulses and intensities producing N1 responses only, usually produced no dorsal root potentials (DRPs), or these were rather small. Stimulation with strengths producing N2 and N3 responses produced distinct DRPs. Trains of pulses were clearly more effective than single pulses in producing DRPs, even in the low-intensity range. 3. Cooling the thoracic spinal cord to block impulse conduction, increased the DRPs and the N3 responses produced by PAN stimulation without significantly affecting the N2 responses. Reversible spinalization also increased the DRPs produced by stimulation of cutaneous nerves. In contrast, the DRPs produced by stimulation of group I afferents from flexors were reduced. 4. Conditioning electrical stimulation of intermediate and high-threshold myelinated fibers in the PAN depressed the DRPs produced by stimulation of group I muscle and of cutaneous nerves. 5. Analysis of the intraspinal threshold changes of single Ia and Ib fibers has provided evidence that stimulation of intermediate and high threshold myelinated fibers in the posterior knee joint nerve inhibits the primary afferent depolarization (PAD) of Ia fibers, and may either produce PAD or inhibit the PAD in Ib fibers, in the same manner as stimulation of cutaneous nerves. In 7/16 group I fibers the inhibition of the PAD was increased during reversible spinalization. 6. The results obtained suggest that intermediate and high-threshold myelinated fibers in the PAN have the same actions on Ia and Ib fibers as intermediate and high-threshold cutaneous afferents and may therefore be considered as belonging to the same functional system. They further indicate that in anesthetized preparations the pathways mediating the PAD of group I fibers, as well as the pathways mediating the inhibition of the PAD, may be subjected to a descending control that is removed by spinalization.

Modulation of synaptic effectiveness of Ia and descending fibers in cat spinal cord

1975 ◽  
Vol 38 (5) ◽  
pp. 1181-1195 ◽  
Author(s):  
P. Rudomin ◽  
R. Nunez ◽  
J. Madrid
Keyword(s):  
Spinal Cord ◽  
Time Course ◽  
Peak Amplitude ◽  
Primary Afferent Depolarization ◽  
Base Line ◽  
Conditioning Stimulation ◽  
Ia Epsp ◽  
Threshold Strength ◽  
Low Threshold ◽  
Stimulation Of

1. In the unanesthetized spinal cord, conditioning stimulation of low-threshold afferents (below 1.3 times threshold strength) in the biceps semitendinosus (BST) nerve often reduced the peak amplitude of the monosynaptic Ia EPSPs evoked in gastrocnemius motoneurons without affecting the monosynaptic component of the EPSPs evoked by stimulation of the ipsilateral ventral funiculus (VF) in the thoracic cord. 2. Volleys to the BST nerve comprising higher threshold afferents (usually above 1.4 times threshold strength) reduced the peak amplitude of the monosynaptic Ia and VF EPSPs and shortened their falling phase. 3. Conditioning volleys to low-threshold cutaneous afferents often increased the Ia-EPSP peak amplitude, sometimes without affecting the monosynaptic component of the VF EPSP. 4. In most cases the Ia nd VF monosynaptic EPSPs elicited in a given motoneuron summated nonlinearly. The amount of nonlinear summation between Ia and VF monosynaptic EPSPs was often reduced by low-threshold BST conditioning volleys. These observations suggest that in many instances, both species of fibers end in "electrotonically close" synaptic loci over the motoneuron surface. Therefore, amplitude changes of monosynaptic Ia EPSPs produced by conditioning afferent volleys without concomitant changes of monosynaptic VF EPSPs do not appear to result from postsynaptic remote conductance changes and may be attributed to a presynaptic mechanism. 5. At the time of occurrence of the Ia and VF monosynaptic EPSP the variance of the motoneuron membrane potential may be increased above base-line levels with a time course approximately matching the EPSP itself. Conditioning stimulation of BST afferents usually reduced Ia EPSP variance, often without affecting or even increasing the variance of the monosynaptic VF EPSPs. These observations provide additional evidence that Ia EPSP variability is introduced, at least in part, through the segmental pathways mediating primary afferent depolarization. 6. The possibility of a differential control of the information flow transmitted through two independent channels converging on a given cell ensemble is discussed.

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