Antidromic Conditioning Research Articles

The slow afterhyperpolarization modulates high pH‐induced changes in the excitability of rat CA1 pyramidal neurons

Extra- and intracellular recordings from the CA1 region of rat hippocampal slices were employed to examine the role of the slow afterhyperpolarization (sAHP) in modulating the increases in neuronal excitability observed on increasing extracellular pH (pHo) from 7.4 to 7.7. In the majority of experiments, an antidromic conditioning stimulus applied in the presence of D(-)-2-amino-5-phosphonopentanoic acid (D-APV), 6-cyano-7-nitroquinoxaline-2,3-dione disodium salt (CNQX) and bicuculline was employed to elicit a sAHP, and an antidromic test stimulus was applied during the sAHP. At pHo 7.4, a single conditioning stimulus elicited an action potential followed by a sAHP, which in turn inhibited the response to the test stimulus compared with the conditioning stimulus. Increasing the number of action potentials in the conditioning stimulus augmented the sAHP and further inhibited the test response, whereas isoproterenol inhibited the sAHP and prevented the relative inhibition of the test response. At pHo 7.7, a single conditioning stimulus elicited a burst of action potentials followed by a large sAHP, which in turn prevented the test stimulus from eliciting a burst of action potentials and, in extracellular recordings, further increased the inhibition of the test response. The latter effect did not solely reflect a high pHo-induced increase in the conditioning response (and, thus, the subsequent sAHP), but rather involved a more direct effect of high pHo to augment the sAHP. The results indicate that increasing pHo increases the excitability of CA1 neurons to an initial stimulus; however, a high pHo-dependent increase in the sAHP evoked by the initial stimulus limits the response to subsequent stimuli.

Functional alteration of inhibitory influences on spinal motor output in painful diabetic neuropathy in rats

Diabetes is frequently accompanied by painful polyneuropathies that are mediated by enhanced neuronal excitability in the spinal cord, partly because of decrease in spinal intrinsic inhibitory influences. Changes in spinal excitatory–inhibitory balance may alter spinal segmental motor output. In the study presented here, the mono- and disynaptic (the fastest polysynaptic) reflexes (MSR and DSR, respectively) were recorded from L5 ventral roots in response to stimulation of the ipsilateral L5 dorsal root in spinalized streptozotocin (STZ)-induced diabetic rats with a reduced withdrawal threshold to mechanical stimuli. The diabetic rats generally exhibited larger spinal reflex amplitudes, the DSR being influenced in particular. We addressed whether recurrent and presynaptic inhibition of the spinal reflexes were altered in STZ-treated animals. The recurrent inhibition of the MSR and DSR elicited by preceding antidromic conditioning stimulation delivered to the recorded L5 ventral root was markedly suppressed in diabetic rats. By contrast, the presynaptic inhibition of the MSR and DSR elicited by preceding conditioning stimulation to the ipsilateral L4 dorsal root was not impaired. Thus, in diabetic painful neuropathy, reduced spinal intrinsic inhibition in the ventral horn contributes to an enhanced spinal segmental motor output.

Inhibitory nature of tiagabine-augmented GABAA receptor-mediated depolarizing responses in hippocampal pyramidal cells.

Tiagabine is a potent GABA uptake inhibitor with demonstrated anticonvulsant activity. GABA uptake inhibitors are believed to produce their anticonvulsant effects by prolonging the postsynaptic actions of GABA, released during episodes of neuronal hyperexcitability. However, tiagabine has recently been reported to facilitate the depolarizing actions of GABA in the CNS of adult rats following the stimulation of inhibitory pathways at a frequency (100 Hz) intended to mimic interneuronal activation during epileptiform activity. In the present study, we performed extracellular and whole cell recordings from CA1 pyramidal neurons in rat hippocampal slices to examine the functional consequences of tiagabine-augmented GABA-mediated depolarizing responses. Orthodromic population spikes (PSs), elicited from the stratum radiatum, were inhibited following the activation of recurrent inhibitory pathways by antidromic conditioning stimulation of the alveus, which consisted of either a single stimulus or a train of stimuli delivered at high-frequency (100 Hz, 200 ms). The inhibition of orthodromic PSs produced by high-frequency conditioning stimulation (HFS), which was always of much greater strength and duration than that produced by a single conditioning stimulus, was greatly enhanced following the bath application of tiagabine (2-100 microM). Thus, in the presence of tiagabine (20 microM), orthodromic PSs, evoked 200 and 800 ms following HFS, were inhibited to 7.8 +/- 2.6% (mean +/- SE) and 34.4 +/- 18.5% of their unconditioned amplitudes compared with only 35.4 +/- 12.7% and 98.8 +/- 12.4% in control. Whole cell recordings revealed that the bath application of tiagabine (20 microM) either caused the appearance or greatly enhanced the amplitude of GABA-mediated depolarizing responses (DR). Excitatory postsynaptic potentials (EPSPs) evoked from stratum radiatum at time points that coincided with the DR were inhibited to below the threshold for action-potential firing. Independently of the stimulus intensity with which they were evoked, the charge transferred to the soma by excitatory postsynaptic currents (EPSCs), elicited in the presence of tiagabine (20 microM) during the large (1,428 +/- 331 pA) inward currents that underlie the DRs, was decreased on the average by 90.8 +/- 1.7%. Such inhibition occurred despite the presence of the GABAB receptor antagonist, CGP 52 432 (10 microM), indicating that GABAB heteroreceptors, located on glutamatergic terminals, do not mediate the observed reduction in the amplitude of excitatory postsynaptic responses. The present results suggest that despite facilitating the induction of GABA-mediated depolarizations, tiagabine application may nevertheless increase the effectiveness of synaptic inhibition during the synchronous high-frequency activation of inhibitory interneurons by enhanced shunting.

Increased Acetylcholine Content Induced by Antidromic Stimulation of a Sympathetic Ganglion: A Possible Retrograde Action of Adenosine

Prolonged high-frequency orthodromic stimulation of superior cervical ganglia is known to result in increased acetylcholine (ACh) synthesis and ACh content after the period of stimulation. In a previous study, we provided evidence to suggest that adenosine acts as an extracellular signal to activate this increased ACh synthesis and we proposed that the source of that adenosine might be postsynaptic. Thus, the purpose of the present study was to test whether direct stimulation of the post-ganglionic nerves could affect ganglionic ACh content. Antidromic conditioning of ganglia (15 Hz, 45 min) did not affect significantly their ACh content. However, if ganglia were allowed a 15-min rest period after this antidromic conditioning, their ACh stores were increased by 20%; a similar increase was induced by 4-Hz stimulation before the rest period. During the 15-Hz antidromic stimulation, ACh release was not clearly increased above the basal level, suggesting that preganglionic nerve endings were not stimulated to an extent that could explain the increased ACh content. Orthodromic stimulation (5 Hz) of ganglia 15 min after they had been subjected to antidromic conditioning (15 Hz, 45 min) showed increased ACh release in comparison with that from control unconditioned ganglia. Moreover, the extra ACh released by the conditioned ganglia was quantitatively similar to the increase in the ACh stores, as if most, or all, of the additional ACh was released by preganglionic stimulation. If the antidromic conditioning and the rest period were done during perfusion with Ca(2+)-free medium, the ganglia did not accumulate extra ACh.(ABSTRACT TRUNCATED AT 250 WORDS)

Associative EPSP--spike potentiation induced by pairing orthodromic and antidromic stimulation in rat hippocampal slices.

1. Pairing low-frequency orthodromic stimulation with high-frequency antidromic conditioning of pyramidal cells in area CA1 of the rat hippocampus resulted in long-lasting potentiation of the extracellular population spike of the cells, without an accompanying increase in the extracellular excitatory postsynaptic potential (EPSP), indicating an increase in EPSP-spike (E-S) coupling, also called E-S potentiation. 2. The amplitude of the antidromically conditioned E-S potentiation took up to 60 min to reach its peak, much longer than synaptic long-term potentiation (LTP) induced by orthodromic tetanic stimulation. 3. The population spike amplitude of a control orthodromic input, which stimulated a separate set of fibres and which was inactive during the pairing, was also increased in over half the slices tested. That it can affect a silent pathway suggests that antidromically conditioned E-S potentiation is not generated locally at tetanized synapses. 4. Bath application of 50 microM D,L-2-amino-5-phosphonovaleric acid (AP5) blocked induction of antidromically conditioned E-S potentiation. After washing out the AP5, the same stimulation resulted in population spike increases. This suggests that activation of the NMDA subtype of glutamate receptor is necessary for the induction of this form of E-S potentiation. 5. Application of 10 microM picrotoxin and/or 10 microM bicuculline, which block inhibition mediated by gamma-aminobutyric acid A (GABAA) receptors, did not reduce antidromically conditioned E-S potentiation. Thus, plasticity in GABAA-mediated inhibition cannot account for the increased population spike amplitude. 6. E-S potentiation did not increase the amplitude of either extracellular or intracellular EPSPs recorded at the cell body.

Long-term depression at synapses in slices of rat hippocampus can be induced by bursts of postsynaptic activity

In slices of rat hippocampus, a train of conditioning pulses that would produce long-term potentiation (LTP) if applied to afferent inputs was found to produce a long-lasting depression of Schaffer collateral/commissural synapses on CA1 cells when instead it was applied to the CA1 axons. The depression lasted undiminished for up to 2 h (the maximum duration of recording). Intracellular recording showed that long-term depression (LTD) of e.p.s.p. amplitude occurred in 66% of cells when this antidromic conditioning stimulation was delivered in normal medium, and in 100% of cells when the antidromic stimulation was delivered in medium containing sufficient Mg++ to block all synaptic transmission. We infer that the difference is because conditioning stimuli sometimes activated test synapses in normal Mg++ but could not in high Mg++. The fact that LTD could be induced in high Mg++ eliminates enhanced inhibitory feedback as a possible mechanism of the long lasting synaptic depression and demonstrates that the mechanism is probably postsynaptic. Resting membrane potential and cell input resistance were the same before and after conditioning, so persisting changes in these postsynaptic parameters can not be the explanation for LTD. LTD of the sort described in this paper could have significant implications for models of learning and memory.

Disinhibitory effect of phencyclidine in the hippocampus in vitro: PCP receptors implicated

The effects of phencyclidine (PCP) and two dioxolane stereoisomers, dexoxadrol and levoxadrol, on hippocampal inhibition were compared. Field potentials were recorded in the CA1 pyramidal cell layer in the rat hippocampal slices in vitro. Recurrent inhibition of the population spikes evoked orthodromically by stimulation of the Schaffer collaterals was induced by antidromic conditioning stimulation at appropriate time intervals before the orthodromic stimulation. The drug were applied by micropressure ejection in concentrations which did not affect the unconditioned population spike. After PCP or dexoxadrol administration, the orthodromically evoked population spike was much less reduced by the antidromic conditioning stimulation than before, suggesting that the recurrent inhibition was diminished. Levoxadrol had only negligible effect. Since dexoxadrol has many PCP-like pharmacological properties but levoxadrol does not, we concluded that PCP attenuates hippocampal recurrent inhibition by activating the PCP receptors. It is suggested that this action results in depression of excitatory synaptic transmission from axon collaterals to the inhibitory interneuron with possible involvement of the N-methyl-D-aspartate (NMDA) subtype of excitatory amino acid receptor.

Evidence of functional mossy fiber sprouting in hippocampal formation of kainic acid-treated rats

In the rat hippocampal formation, degeneration of CA4-derived afferent fibers provokes the growth of mossy fiber collaterals into the fascia dentata. These aberrant fibers subsequently form granule cell-granule cell synapses. The hippocampal slice preparation was employed to determine whether these recurrent connections are electrophysiologically functional. Hippocampal slices were prepared 12 to 21 days after the bilateral destruction of CA4 neurons with either intracerebroventricular or intravenous kainic acid (KA). In slices from control rats, antidromic stimulation of the mossy fibers elicited a single population spike in the granular layer of the fascia dentata. In contrast, when slices from some KA-treated rats were similarly tested, antidromic stimulation elicited multiple population spikes. This effect was not reproduced by blocking inhibitory transmission with bicuculline methiodide. Slices from other KA-treated rats fired a single population spike, but an antidromic conditioning volley increased the amplitude of a subsequent antidromic population spike by 5 to 15%. In slices from control rats, on the other hand, an antidromic conditioning volley always either decreased or failed to alter the amplitude of an antidromic test response. Superfusion with Ca2+-free medium containing 3.8 mM Mg2+ reversibly abolished all effects of KA administration. Abnormal responses to antidromic stimulation correlated with the loss of CA4 neurons and the growth of supragranular mossy fiber collaterals in the same animals. These results suggest that supragranular mossy fiber collateral sprouts form a functional recurrent excitatory circuit. These aberrant connections may further compromise hippocampal function already disrupted by neuronal degeneration, such as by facilitating seizure activity.

Actions of picrotoxinin and related compounds on the frog spinal cord: the role of a hydroxyl‐group at the 6‐position in antagonizing the actions of amino acids and presynaptic inhibition

The frog spinal cord has been used to test the effects of naturally occurring picrotoxane compounds (picrotoxinin, picrotin, tutin and coriamyrtin) and semisynthetic ones (6-acetylpicrotoxinin and anhydropicrotin) on the electrical activities of dorsal and ventral roots and on amino acid-induced depolarizations of primary afferent terminals. Picrotoxinin, tutin and coriamyrtin (10(-5)-3 X 10(-5)M), which have a free hydroxyl group at the 6-position, caused a gradual depolarization in both ventral and dorsal roots. The depolarizations were accompanied by a reduction in the size of the dorsal root potential (DR-DRP), dorsal root reflex (DR-DRR) and ventral root potential (DR-VRP) and by an augmentation of the first spike potential and polysynaptic components in the ventral root reflex (DR-VRR). 6-Acetylpicrotoxinin (10(-5)-3 X 10(-5)M) caused a slight hyperpolarization in both roots, and this hyperpolarization was accompanied by the augmentation of DR-DRP, DR-VRP and DR-VRR. The DR-DRR was reduced or abolished by the compound. Picrotoxinin, tutin and coriamyrtin reduced gamma-aminobutyric acid (GABA)-, beta-alanine- and taurine-induced depolarizations of primary afferent terminals. 6-Acetylpicrotoxinin showed almost the same degree of inhibition of beta-alanine and taurine as did picrotoxinin, but the GABA- antagonizing action of the compound was significantly weaker than was that of picrotoxinin. Picrotoxinin, tutin, coriamyrtin and 6-acetylpicrotoxinin all blocked presynaptic inhibition of the first spike potential caused by antidromic conditioning stimulation. 6 The present results suggest that the hydroxyl group at the 6-position of picrotoxane compounds are important for antagonism of the effects of GABA, but not of beta-alanine and taurine and for the blocking action of the presynaptic inhibition in the frog spinal cord.

Dendrobine, an antagonist of beta-alanine, taurine and of presynaptic inhibition in the frog spinal cord.

1 The effects of dendrobine and nobiline, alkaloids isolated from Dendrobium nobile, on the electrical activity and on amino acid-induced depolarizations of primary afferent terminals were tested on the frog isolated spinal cord and were compared with those of picrotoxinin and strychnine. 2 Dendrobine (3 X 10(-5) M) caused a slight hyperpolarization in both dorsal and ventral roots and this hyperpolarization was accompanied by the augmentation of the dorsal root potential (DR-DRP) and the ventral root potential and reflex (DR-VRP and DR-VRR). The amplitude of the dorsal root reflex (DR-DRR) however, was reduced significantly. Nobiline (3 X 10(-5) M) had no significant effect on either the root potentials or the reflexes. 3 Dendrobine (3 X 10(-5) M) reduced the dorsal root potential induced by repetitive antidromic stimulation of ventral root (VR-DRP) as well as diminishing the maximum rate of rise of the dorsal root potential induced by the stimulation of adjacent dorsal roots (DR-DRP), during which time the amplitude of the DR-DRP was seen to be augmented. 4 Dendrobine (3 X 10(-5) M) reduced the beta-alanine- and taurine-induced depolarizations of primary afferent terminals, while having little effect upon GABA- and glycine-induced depolarizations. 5 Dendrobine (10(-5) M) reversibly blocked the presynaptic inhibition caused by antidromic conditioning stimulation of the ventral root. 6 These effects of dendrobine were qualitatively similar to those of strychnine but were somewhat different from those of picrotoxinin, a molecule having the same picrotoxane skeleton. 7 The present results are discussed with reference to the likely neurotransmitters involved in presynaptic inhibition in the frog spinal cord, and with respect to the structure-activity relationship of picrotoxane compounds as amino acid antagonists.

Long-term potentiation of excitatory synaptic transmission in the rat hippocampus: the role of inhibitory processes.

1. The possibility that changes in inhibitory processes are responsible for long-term potentiation (l.t.p.) was examined using the rat hippocampal slice preparation.2. Inhibitory pathways were characterized using both extra- and intracellular recordings from the CA1 pyramidal cell layer. Stimulating electrodes were placed in either stratum radiatum or the alveus to allow orthodromic or antidromic activation of the pyramidal cells.3. Using extracellular recordings, inhibition was studied by applying paired pulses at interstimulus intervals of 20-500 msec through either the same or different stimulating electrodes, and quantifying the reduction in the population spike. An antidromic conditioning pulse was least effective in influencing the test response, while paired stimuli delivered through separate stimulators in stratum radiatum revealed the longest duration effects. Inhibition was either reduced or enhanced, depending upon the stimulation paradigm, with increasing stimulus intensity.4. With l.t.p., alterations in paired-pulse inhibition were observed corresponding to the changes in conditioning pulse amplitude. Reducing stimulus intensity to restore the initial conditioning pulse amplitude eliminated these effects.5. Using intracellular recordings, the effects of l.t.p. on inhibition were studied by examining changes in e.p.s.p.-i.p.s.p. sequences, i.p.s.p.s evoked by antidromic stimulation, and spontaneous depolarizing i.p.s.p.s observed with KCl-filled electrodes.6. Following l.t.p. enhanced e.p.s.p.s and slightly reduced, but prolonged, i.p.s.p.s were observed in response to orthodromic stimulation. Antidromically evoked, as well as spontaneous, i.p.s.p.s were unaffected.7 It is concluded that alterations in inhibitory processes are not responsible for l.t.p. in hippocampal subfield CA1. However, changes in the strength of inhibitory synapses as a consequence of long-term potentiation may modify the functional character of the hippocampal connexions.

Prolonged changes in excitability of pyramidal tract neurones in the cat: a post‐synaptic mechanism.

1. Prolonged changes in the excitability of cortical neurones can be produced by altering their firing rates for brief periods. In the anaesthetized cat, increased firing of pyramidal tract cells induced by trains of antidromic conditioning shocks led to increases in cell excitability, as measured by the size of the mass response at the medullary pyramid to test shocks applied to the cortical surface. We have shown in two ways that post-synaptic mechanisms could be responsible. 2. In one experimental design, MgCl2 solution (1 mole/l.) was applied to the cortical surface in order to block synaptic activity throughout the cortical depth. Following antidromic conditioning trains, cell excitability was increased; the size of the mass response was up to 30% larger than the control values. This persisted undiminished for up to 3 hr. 3. In the second experimental design, synaptic activity was not blocked, but we compared the effects of antidromic plus synaptic activation of pyramidal tract cells with the effects of synaptic activation alone. Antidromic plus synaptic activation was obtained by applying conditioning trains to the pyramidal tract at the medulla ipsilateral to the cortical test shock; prolonged increases in the ipsilateral response to the test shock were produced. Synaptic activation alone was obtained by the same conditioning trains, but in those cells whose axons projected into the contralateral pyramidal tract; prolonged increases in the contralateral response to the cortical test shock were never seen. In many instances prolonged decreases in excitability were found. 4. We conclude that prolonged increases in excitability of pyramidal tract cells can occur in the absence of any synaptic input, demonstrating that the underlying mechanism is post-synaptic; this does not preclude the action of synaptic mechanisms when synaptic transmission is not blocked.

Increased transneuronal excitation of the cat lateral geniculate nucleus after acute deafferentation

Single neurons and sum potentials were recorded from the cat optic tract (OT), the lateral geniculate nucleus (LGN) and the optic radiation (OR) before and after visual deafferentation obtained by locally restricted photocoagulation of the retina or by ‘total’ photocoagulation of the optic disc of ‘monocular’ cats. Immediately after deafferentation, the spontaneous activity of single LGN-neurons fell to a very low level ( ≪0.1impulses/sec). This nearly total depression of neuronal activity was followed by a slow but incomplete recovery of the spontaneous impulse rate which reached about 1–2 impulses/sec, 2–4 days after deafferentation. The ‘normal’ LGN neuron impulse rate was about 8–30 impulses/sec. After deafferentation the impulse pattern showed an increased occurrence of double discharges separated by very long intermittent intervals. The excitability of LGN principal cells activated by OT electrical stimuli increased immediately after deafferentation. Double and multiple discharges were then elicited by single optic tract stimuli. The deafferentation hyperexcitability was abolished temporarily by OT stimulus trains with a frequency range > 10stimuli/sec, and returned to the prestimulus level within 0.5–1 sec after the stimulus train was terminated. Antidromic conditioning stimuli did not influence the deafferentation hyperexcitability. The time course of the postdeafferentation hyperexcitability was separated into two parts: an immediate rise in excitability after deafferentation was followed by a further slow increase in excitability within the first 2 h after deafferentation. The hyperexcitability measurable at a single unit level was already maximal after locally restricted deafferentation and did not increase with the extension of the retinal lesion beyond 1–2 mm diameter, corresponding to 4–8° in the visual field. Intracellular recordings after deafferentation displayed no significant increase in the amplitude of subthreshold EPSPs, but additional slow, aperiodic, depolarizing waves were found to modify the resting membrane potential. From the multiple discharge pattern elicited by single OT electrical stimuli, one can conjecture that the suprathreshold EPSPs, however, increased considerably in their amplitude. The evoked potentials (OR-waves r 1, r 2) elicited by electrical OT stimuli increased in amplitude and the small waves r 3–r 6 became more prominent after deafferentation. All postsynaptic r-waves reached their maximum values about 1.5 h after interruption of the optic nerve signal flow and did not change further within the following 28 h.

Variations in conduction velocity and excitability following single and multiple impulses of visual callosal axons in the rabbit

The present study examined the conduction properties of 75 visual callosal axons of the awake rabbit. These axons were studied by measuring latency to antidromic activation of cell bodies following midline callosal and/or contralateral cortical stimulation. Seventy-three of 75 neurons (axon conduction velocities = 0.3 to 12.9 m/sec) demonstrated decreases in antidromic latency and threshold to a test stimulus which followed an antecedent conditioning stimulus at appropriate intervals. Control experiments indicated that (i) the latency and threshold variations resulted from prior impulse conduction along the axon, and (ii) the latency decrease reflected an increase in conduction velocity along the main axon trunk. The maximum magnitude of the latency decrease for different axons ranged from 3 to 22% of control values, and the duration ranged from 18 to 169 msec. The duration of the latency decrease was greater for slowly conducting axons than for fast conducting axons. Latency increases to an antidromic test stimulus occurred for up to several minutes following a train of antidromic conditioning pulses. Antidromic latency and threshold shifts were also observed in somatosensory callosal axons and in some corticotectal axons.

Antidromic conditioning of reciprocally inhibited monosynaptic extensor and flexor reflexes in decerebrate cats.

The effect of previous antidromic conditioning of reciprocally inhibited monosynaptic flexor and extensor reflexes was found to depend on the ventral root chosen. Use of a part of the root in which the test reflex was found led to increased inhibition, use of a neighboring root to disinhibition. It is suggested that Renshaw cells in the agonist pool inhibit only those Ia inhibitory interneurons which affect the antagonist. A model for the interconnection of Renshaw cells, Ia inhibitory interneurons and the antagonistic motoneuron pools is proposed which fits not only the results presented here, but also those on single units. The results indicate the presence of occlusion of inhibitory effects and support the assumption that these effects are distributed uniformly within a motoneuron pool.

Effects of antidromic conditioning on some motoneurons and interneurons.

ArticlesEFFECTS OF ANTIDROMIC CONDITIONING ON SOME MOTONEURONS AND INTERNEURONSVictor J. Wilson, and Paul R. BurgessVictor J. Wilson, and Paul R. BurgessPublished Online:01 Sep 1962https://doi.org/10.1152/jn.1962.25.5.636MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAction of nicotine on reflexes in spinal catsNeuropharmacology, Vol. 10, No. 4Recurrent inhibition and facilitation in the monkey, Macaca mulatta, in relation to spinal shockExperimental Neurology, Vol. 29, No. 1Effects of morphine on Renshaw cell activityNeuropharmacology, Vol. 9, No. 3Recurrent inhibition from motor axon collaterals in interneurones monosynaptically activated from la afferentsBrain Research, Vol. 9, No. 2Facilitatory and excitatory interaction between motoneurons of adjacent segments in the spinal cord of the frogExperimental Neurology, Vol. 20, No. 4Inhibition in Ia inhibitory pathway by impulses in recurrent motor axon collateralsLife Sciences, Vol. 7, No. 7Sensory neurons in the spinal ventral roots of the catBrain Research, Vol. 7, No. 3 More from this issue > Volume 25Issue 5September 1962Pages 636-650 https://doi.org/10.1152/jn.1962.25.5.636PubMed14007428History Published online 1 September 1962 Published in print 1 September 1962 Metrics

Recurrent conditioning in the cat spinal cord. Differential effect of meprobamate on recurrent facilitation and inhibition.

The action of cumulative doses of meprobamate on antidromic conditioning has been studied in spinal cats. Recurrent facilitation is greatly reduced or completely abolished by total doses ranging from 210 to 400 mg./kg. The depth of recurrent inhibition is not affected in a consistent manner by meprobamate, but the duration of inhibition is markedly increased in all experiments. This differential action of meprobamate on facilitation and inhibition can be utilized to study conditioning effects consisting of combined inhibition and facilitation. If conditioning starts with an inhibitory phase, variable in duration, followed by facilitation, meprobamate depresses the facilitation and reveals an extended inhibitory curve. Facilitation, however, is not always accompanied by inhibition, since in some cases facilitation is depressed and no inhibition is uncovered. The results of these experiments are discussed in relation to the various types of conditioning that have been produced by antidromic stimulation.

On the significance of post- and pre-synaptic events for facilitation and inhibition in the sympathetic ganglion of the cat.

Summary.Transmission of a test reflex through the stellate ganglion of the cat was examined 1) after antidromic conditioning, 2) after Conditioning the same preganglionic nerve as the one from which the test reflex was elicited, 3) after conditioning the other preganglionic nerve. There was less depression after 2 than 1 and, if there was a high degree of occlusion also less after 2 than after 3.When in the same preganglionic nerve as the one used for testing a volley was set up to excite the cells 2 msec. before they were reached by a maximal antidromic volley the depression of the test reflex was again less than after antidromic conditioning alone. If the combination of antidromic and orthodromic conditioning was made so that a preganglionic nerve other than the one used for testing was stimulated to excite the ganglion cells 2 msec. before they were reached by antidromic volley the depression was the same as after antidromic conditioning alone despite a high degree of occlusion. It is therefore concluded that following transmission of a single volley through the ganglion pre‐synaptic potentiation is a facilitatory factor along with post‐synaptic potentials in subliminally excited cells and the negative afterpotentials of excited cells. There is nor indication of a long‐lasting excitatory action from the pre‐synaptic terminals neither of inhibitory preganglionic fibres.In the last section are described conditions under which pre‐synaptic failure may occur.