Segmental inhibitory response in the frog spinal cord during orthodromic motoneuron activation

Different types of reflex discharges were produced in various preparations by stimulating the dorsal root of isolated frog spinal cord. These ranged from multiphasic low-amplitude waves to distinctly synchronized monosynaptic response. The discharges were followed by facilitation in the former and deep, protracted inhibition of response to test dorsal root stimulation in the latter. When interstimulus intervals measured 40–50 msec, inhibitory action was less pronounced than at shorter (15–30 msec) or longer (60–100 msec) intervals, thus indicating that at least two types of inhibition were at work, one at an earlier and the other at a later stage. Strychnine at a concentration of 10^–5 M effectively reinforced the former and blocked the latter, while 10^–4 M d-tubocurarine attenuated both types of inhibition substantially. It is concluded that inhibition of response occurs mainly as a result of recurrent activation of inhibitory systems via recurrent motoneuron axon collaterals when frog spinal cord afferents are excited. Intensity of the later (presynaptic) and earlier (postsynaptic) inhibition of reflex transmission is determined by the degree of synchrony in motoneuronal discharge in response to orthodromic stimulation.Institute of Medical Radiology, Academy of Medical Sciences of the USSR, Obninsk, Kaluga Oblast. Translated from Neirofiziologiya, Vol. 19, No. 3, pp. 343–350, May–June, 1987.     

Corticofugal influences on segmental responses of lumbar spinal ventral horn interneurons in cats

Experiments on cats using extra- and intracellular recording methods showed that stimulation of the motor cortex of both hemispheres leads to considerable modulation of responses to stimulation of cutaneous and muscular lower limb afferents in spinal ventral horn interneurons in segments L6, 7. Three types of conditioning corticofugal effect were observed: facilitation, inhibition, and facilitation followed by inhibition (biphasic effect), and inhibitory effects predominated. The duration of facilitation of responses did not exceed 30–40 msec. The characteristics of the time course of inhibition varied: in some cases it began with relatively short intervals (8–15 msec), in other cases with an interval of 30–40 msec; its duration was 125–500 msec, or sometimes more. The effect of cortical stimulation on responses to stimulation of various afferent inputs of the same interneuron was shown to differ. The character of the conditioning corticofugal effect correlated with the latent period of segmental responses: facilitation was observed only in responses with a relatively short latent period (under 5 msec); responses with a longer latent period were mainly inhibited. The type of cortical effect also depended on the function performed by the activated afferent input. It is suggested that differential descending control of segmental polysynaptic responses recorded in ventral horn interneurons with wide convergence of afferent influences takes place in the initial stages of the reflex are. The mechanism of this control is discussed.I. P. Pavlov Institute of Physiology, Academy of Sciences of the USSR, Leningrad. Translated from Neiorofizologiya, Vol. 14, No. 6, pp. 563–571, November–December, 1982.     

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.     

Mechanisms of bioelectric activity in electric tissue. I. The response to indirect and direct stimulation of electroplaques of Electrophorus electricus

1. A preparation is described consisting of one or several layers of innervated cells of the electric organ of Electrophorus electricus. 2. Each plaque is multiply innervated and only at its caudal face. The nerve fibers may derive from two or more different nerve trunks. 3. During activity the innervated face becomes negative relative to the non-innervated. 4. The first electrical response of the cell to an increasing neural volley is graded and has the character of a prepotential. At a critical size of the prepotential the cell discharges with an all-or-nothing spike. 5. Both responses have durations of about 2 msec. 6. A neural volley which does not cause the spike discharge facilitates the discharge of the cell by a second subsequent volley in the same nerve (temporal facilitation). 7. The period of facilitation lasts ca. 900 msec. During the first 100 msec., the facilitation is large enough to cause a spike. In the later portion only the prepotential is facilitated. No electrical concomitant has been detected. 8. Neural volleys reaching the plaque from different trunks interact at the cell to produce a period of facilitation lasting only about 2 msec. This interaction is interpreted as spatial summation. 9. In a population of cells, simultaneous stimulation of 2 nerves causes a smaller discharge than the sum of the two isolated responses (occlusion). 10. Cells denervated for 7 weeks or more can be excited directly, but only by a current flow outward through the caudal face. 11. Weak direct stimulation causes a prepotential in the denervated plaque. On increasing the stimulus the prepotential increases to a critical size when a spike develops. The duration of both responses is about 2 msec. 12. The absolutely refractory period of the denervated cell is about 1.5 msec. and relative refractoriness lasts about 15 msec. 13. Direct stimulation causes slight facilitation lasting as long as 200 msec. 14. Repetitive stimulation of the nerve at low frequencies (2 to 3 per second) causes rapid "fatigue" of transmission. The denervated plaque, however, responds for several minutes to repetitive direct stimulation at high frequencies (25 per second).     

Postsynaptic potentials of neurons of the cat auditory cortex

The electrical reactions of 294 neurons of the auditory cortex to a click were recorded in experiments on cats immobilized with tubocurarine (174 intra- and 120 extracellularly). The value of the membrane potential varied from 30 to 70 mV with intracellular leads. The following types of reactions were obtained (the number of neurons is given in parentheses): a peak without slow oscillations in the membrane potential (4), EPSP (3), EPSP-peak (6), EPSP-peak-IPSP (17), EPSP-IPSP (9), primary IPSP (114, including 23 with an after-discharge). Twenty one neurons did not react to a click. The amplitude of the sub-threshold EPSP was 1–1.5 mV, the duration of the ascending part was about 10 and of the descending part 20–30 msec. The peak potential on the ascending part of the EPSP developed at the critical level of 3–4 mV. The amplitude of the peaks varied from several millivolts to 50–60. In 17 neurons prolonged hyperpolarization having all the properties of an IPSP, developed after the peak. The amplitude of these IPSP varied in different neurons from 1 to 10 mV and the duration varied from 20 to 80 msec. IPSP without preceding excitation of the given neuron were the predominant types of reaction. The latent period of these primary IPSP varied from 7 to 20 msec and the amplitude from 1 to 15 msec with a duration of 30–200, more frequently 80–100 msec. It is suggested that two types of inhibition develop in neurons of the auditory cortex in response to a click: recurrent and afferent. The functional significance of the first consists in limiting the duration of the discharge in the reacting neurons, the second prevents the development of excitation in adjacent neurons, thereby limiting the area of neuronal activity.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSSR, Kiev. Translated from Neirofiziologiya, Vol. 3, No. 4, pp. 339–349, July–August, 1971.     

Neuronal and synaptic mechanisms of cortical inhibition

The latent periods, amplitude, and duration of IPSPs arising in neurons in different parts of the cat cortex in response to afferent stimuli, stimulation of thalamocortical fibers, and intracortical microstimulation are described. The duration of IPSPs evoked in cortical neurons in response to single afferent stimuli varied from 20 to 250 msec (most common frequency 30–60 msec). During intracortical microstimulation of the auditory cortex, IPSPs with a duration of 5–10 msec also appeared. Barbiturates and chloralose increased the duration of the IPSPs to 300–500 msec. The latent period of 73% of IPSPs arising in auditory cortical neurons in response to stimulation of thalamocortical fibers was 1.2 msec longer than the latent period of monosynaptic EPSPs evoked in the same way. It is concluded from these data that inhibition arising in most neurons of cortical projection areas as a result of the arrival of corresponding afferent impulsation is direct afferent inhibition involving the participation of cortical inhibitory interneurons. A mechanism of recurrent inhibition takes part in the development of inhibition in a certain proportion of neurons. IPSPs arise monosynaptically in 2% of cells. A study of responses of cortical neurons to intracortical microstimulation showed that synaptic delay of IPSPs in these cells is 0.3–0.4 msec. The length of axons of inhibitory neurons in layer IV of the auditory cortex reaches 1.5 mm. The velocity of spread of excitation along these axons is 1.6–2.8 msec (mean 2.2 msec).A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 16, No. 3, pp. 394–403, May–June, 1984.     

The effect of DOPA on the reciprocal inhibition of the innervation centers of antagonistic muscles in newborn rat pups]

In experiments on 5--7- and 16-day rat puppies with acute lesion of the spinal cord, by means of monosynaptic tests, studies have been made of the effect of DOPA on reciprocal inhibition of antagonist muscles. Test stimuli were applied to n. tibialis, conditioned ones--to n. peroneus. It was shown that the pattern of the effects depends on the action of the drug on the magnitude of the initial monosynaptic reflex used as a test. It the latter was initially inhibited, the conditioned stimulation resulted within the first 1-8 msec not in the development of postsynaptic inhibition, but in evident facilitation, which was longer in 5--7-day animals. The level of presynaptic inhibition was somewhat lower than the initial one, but exhibited longer duration. In case of facilitation of a control test after DOPA injection, configuration of reciprocal inhibition curves did not significantly differ from that obtained before administration of the drug.     

EPSPs of masseter motoneurons evoked by stimulation of low-threshold infraorbital nerve afferents in cat

Stimulation of the infraorbital nerve at strengths 1.4–2.5 times higer than the threshold of excitation of A fibers in cats anesthetized with chloralose and pentobarbital evoked EPSPs with an amplitude up to 3.0 mV and a duration of 9–15 msec in 69% of masseter motoneurons after 1.5–3.0 msec. These EPSPs were complex and formed by summation of simpler short-latency and long-latency EPSPs. The short-latency EPSPs appeared in response to infraorbital nerve stimulation at 1.1–1.5 thresholds and had a slow rate of rise (2.5–4.5 msec, mean 3.7±0.4 msec), low amplitude (under 2.0 mV), and short duration (5–6 msec). Their latent period varied from 1.5 to 3.0 msec (mean 2.1±0.2 msec). The shortness of the latent period and its constancy during stimulation of the nerve at increasing strength, and also the character of development of facilitation and inhibition of the EPSP during high-frequency stimulation suggests that these EPSPs are monosynaptic. The slow rate of rise suggested that these EPSPs arise on distal dendrites of the motoneurons. Long-latency EPSPs appeared 7–9 msec after stimulation of the infraorbital nerve at 1.1–1.5 thresholds. Their amplitude reached 1.5–2.0 mV and their duration 7–9 msec. The long duration of the latent period combined with low ability to reproduce high-frequency stimulation (up to 30/sec) points to the polysynaptic origin of these EPSPs.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 9, No. 6, pp. 583–591, November–December, 1977.     

Long-lasting H-reflex inhibition evoked by stimulation of a nerve to the antagonist muscles and vibrational stimulation of the muscle receptors in humans

In testing of healthy subjects, we studied the influence of conditioning stimulation of then.peroneus communis on the H-reflex EMG discharge recorded from them. soleus. Two waves of inhibition separated by a period of relative facilitation of the reflex were observed. The first wave,D ₁, was not longer than 50 msec. The intensity of later inhibition (D ₂ wave) within a 500 to 4000 msec time segment linearly depended on the logarithm of the interval between the conditioning and test stimuli. Extrapolation showed that the duration of this wave could be evaluated as equal to 6.3 msec, on average. We also studied the temporal course of H-reflex inhibition after conditioning vibrational stimulation of the receptors of them. tibialis ant. andm. biceps femori. Within a 500 to 4000 msec test interval, it could also be fitted with a logarithmic dependence similar to that observed after electrical stimulation of then. peroneus comm. The duration of inhibition after vibrational stimulation of them. tibialis ant. andm. biceps femori was 6.2 and 8.9 sec, respectively. Inhibition evoked by both conditioning influences was not removed after a voluntary plantar flexion of the foot. Our observations support the statement that in humans stimulation of the afferent fibers from the antagonist muscles, as well of the muscle receptors, evokes in two-neuron reflex arcs presynaptic inhibition, whose duration reaches several seconds; this phenomenon can play a significant role in the control of muscle tone in the course of muscle performance.     

Detection of red and green flashes: evidence for cancellation and facilitation.

Green and red flashes of light will differentially stimulate the middle- and long-wavelength sensitive cones. Interaction of cone signals was studied by measuring increment thresholds for combinations of green and red flashes on a yellow adapting field. When the yellow adapting field was at 10.000 trolands (td), green and red incremental flashes (1 degree, 200-msec duration) produced cancellation when presented simultaneously and facilitation when presented sequentially. A green incremental flash (1.15 degrees, 200 msec, 5000-td adaptation field) and red decremental flash, or vice versa, produced facilitation when presented simultaneously. The results can be explained by color-differencing, opponent-mechanisms. The cancellation effect for the simultaneous incremental flashes largely disappeared when the flashes were exposed briefly (10 msec) or reduced in size (0.04 degrees). It is unlikely that the stimuli were exclusively detected by achromatic, luminance channels, as suggested by previous work, since observers could partially distinguish the hue of threshold flashes of 570- and 590-nm light (0.04 degrees, 10 msec) on a bright yellow field.     

Paired pulse facilitation of summated intracellular synaptic potentials in single retinotectal fibers in the frog

Facilitation of the second of two consecutive test EEG quanta (the summated monosynaptic potentials of the synapses of one axon arborizing in layer F of the frog tectum) was investigated in the normal and under conditions of raised extracellular Ca²⁺ and Mg²⁺ concentration. Intensification of paired-pulse facilitation (×1.4–2.4) was observed at the shortest interstimulus intervals (of 2.5–5 msec). The distribution of maximum levels for facilitation of EEG quanta was bimodal at levels 1.95 and 1.65, on the basis of which two groups were identified, one potentiating EEG quanta more than the other. The time course of paired-pulse facilitation of both groups of EEG quanta can be broken down into two exponential components with time constants of 5–6, 140–150 and 6–8, 60–70 msec respectively. Bimodal distribution of maximum paired-pulse levels in the normal, together with findings from experiments involving raised Ca²⁺ and Mg²⁺ concentrations would indicate that facilitation of frog retinotectal synapses is dependent on the quantal release of transmitter; it may thus be postulated that this release reaches near-saturation point in the normal. It is suggested that two types of axonal terminal arborizations whose synapses differ in the quantal content of transmitter release are present in layer F of the frog tectum. These axonal arbors could well originate from different class 3 and 5 retinal detectors.Z. Yanushkevichyus Institute of Physiology and Pathology of the Cardiovascular System of the Kaunas Medical Institute. Translated from Neirofiziologiya, Vol. 18, No. 1, pp. 45–55, January–February, 1986.     

Neurotransmitter release: Facilitation and three-dimensional diffusion of intracellular calcium

In order to account for the time courses of both evoked release and facilitation, in the framework of the Ca²⁺ hypothesis, Fogelson and Zucker (1985,Biophys. J. 48, 1003–1017) suggested treating diffusion of Ca²⁺, once it enters through the Ca²⁺ channels, as a three-dimensional process (three-dimensional diffusion model). This model is examined here as a refined version of the “Ca²⁺-theory” for neurotransmitter release. The three-dimensional model was suggested to account for both the time course of release and that of facilitation. As such, it has been examined here as to its ability to predict the dependence of the amplitude and time course of facilitation under various experimental conditions. It is demonstrated that the three-dimensional diffusion model predicts the time course of facilitation to be insensitive to temperature. It also predicts the amplitude and time course of facilitation to be independent of extracellular Ca²⁺ concentration. Moreover, it predicts that inhibition of the [Na⁺]_o↔[Ca²⁺]_i exchange does not alter facilitation. These predictions are not upheld by the experimental results. Facilitation is prolonged upon reduction in temperature. The amplitude of facilitation declines and its duration is prolonged upon increase in extracellular Ca²⁺ concentration. Finally, inhibition of the [Na⁺]_o↔[Ca²⁺]_i exchange prolongs facilitation but does not alter the time course of evoked release after an impulse.     

Comparison of the electrophysiological effect of amiodarone, lidocaine and quinidine on rat ventricular cells.

The effects of 20 microM each of amiodarone, lidocaine and quinidine on action potential and membrane currents were studied in rat ventricular cells. At a stimulation frequency of 0.1 Hz, quinidine prolonged the action potential duration (APD50) from 120 +/- 26 to 660 +/- 8 msec and increased the time to peak (Tp) amplitude from 7 +/- 1 msec to 32 +/- 6 msec. Lidocaine shortened APD50 from 123 +/- 15 to 83 +/- 6 msec without altering Tp. Amiodarone changed neither APD50 nor Tp. Voltage clamp study revealed that quinidine inhibited sodium inward current (INa) even when this current was elicited by depolarizing pulses at 0.1 Hz from a holding potential of -90 mV. For amiodarone and lidocaine, the inhibition was observed when INa was elicited from a holding potential of -70 mV. A frequency-dependent inhibition of INa by amiodarone and lidocaine was observed at frequencies higher than 1 Hz. Quinidine showed this inhibition even at 1 Hz. In correlation with the stronger frequency dependent inhibition of INa, a greater delay of the recovery and increase of the non-recovery fraction of INa was induced by quinidine. For lidocaine and amiodarone, only the recovery time constant was delayed. In cells treated with sea anemone toxin (ATX, 0.2 microM), APD50 was prolonged to 4-5 sec in 5 min. Quinidine, but not amiodarone, completely reversed the effect of ATX. Quinidine showed use-dependent inhibition of INa in these ATX-treated cells. Amiodarone, however, did not show this inhibition. It is likely that amiodarone suppresses INa by delaying the recovery of INa instead of blocking the open-state Na(+)-channels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Implications of G-Protein-Mediated Ca2+ Channel Inhibition for Neurotransmitter Release and Facilitation

G-protein-mediated inhibition of Ca²⁺ current is ubiquitous in neurons, and in synaptic terminals it can lead to a reduction in transmitter release (presynaptic inhibition). This type of Ca²⁺ current inhibition can often be relieved by prepulse depolarization, so the disinhibition of Ca²⁺ current can combine with Ca²⁺-dependent mechanisms for activity-induced synaptic facilitation to amplify this form of short-term plasticity. We combine a mathematical model of a G-protein-regulated Ca²⁺ channel with a model of transmitter secretion to study the potential effects of G-protein-mediated Ca²⁺ channel inhibition and disinhibition on transmitter release and facilitation. We investigate several scenarios, with the goal of observing a range of behaviors that may occur in different synapses. We find that the effects of Ca²⁺ channel disinhibition depend greatly on the location and distribution of inhibited channels. Facilitation can be greatly enhanced if all channels are subject to inhibition or if the subpopulation of channels subject to inhibition are located closer to release sites than those insensitive to inhibition, an arrangement that has been suggested by recent experiments (Stanley and Mirotznik, 1997). We also find that the effect of disinhibition on facilitation is greater for longer action potentials. Finally, in the case of homosynaptic inhibition, where Ca²⁺ channel inhibition occurs through the binding of transmitter molecules to presynaptic autoreceptors, there will be little reduction in transmitter release during the first of two successive bursts of impulses. The reduction of release during the second burst will be significantly greater, and if the unbinding rate of autoreceptors is relatively low, then the effects of G-protein-mediated channel inhibition become more pronounced as the duration of the interburst interval is increased up to a critical point, beyond which the inhibitory effects become less pronounced. This is in contrast to presynaptic depression due to the depletion of the releasable vesicle pool, where longer interburst intervals allow for a more complete replenishment of the pool. Thus, G-protein-mediated Ca²⁺ current inhibition leads to a reduction in transmitter release, while having a highly variable amplifying effect on synaptic facilitation. The dynamic properties of this form of presynaptic inhibition are very different from those of vesicle depletion.     

Early post-tetanic potentiation and low frequency depression of some group I reflex actions

Group I reflex functions, namely monosynaptic reflex transmission, facilitation of synergists, and direct and disynaptic inhibition, show early post-tetanic potentiation following conditioning with a brief, high frequency, tetanus. Of these reflex functions, monosynaptic transmission always shows low frequency depression. Direct inhibitory pathways, and therefore inhibitory junctions, are insensitive to low frequency depression. The fact that direct inhibition can be potentiated shows it to be sufficiently labile that a decrease in efficacy at inhibitory junctions during repetitive activity should be revealed. Disynaptic inhibition often shows low frequency depression. As it is likely that inhibitory junctions in the direct and disynaptic pathways are similar, the low frequency depression of disynaptic inhibition is probably due to the properties of the excitatory relay between afferent fibers and interneurons in that pathway. Facilitation between synergists is often more depressed when the conditioning and testing volleys are nearly simultaneous than when they are separated by 1 to 1.5 msec. This result indicates that an early and rapid phase of action, responsible for homonymous and heteronymous transmission, is more sensitive to low frequency depression than is residual facilitation. In general, reflex transmission is more sensitive than are other aspects of action by group I fibers to events concurrent with and following repetitive activation.     

Effect of stimulation of the nucleus entopeduncularis on neurons of thalamic motor nuclei under normal conditions and after injury of the nigrostriatal dopaminergic system by the neurotoxin mptp

In two series of acute experiments on cats anesthetized with ketamine and immobilized with succinylcholine chloride, we investigated the reactions of neurons of the ventral anterior (VA) and ventral lateral (VL) motor nuclei of the thalamus to stimulation of the nucleus entopeduncularis (nEp) in intact animals and in animals administered the neurotoxin N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). It was established that in intact animals 28.0% of the investigated VA-VL neurons reacted to stimulation of nEp by inhibition with a latent period of less than 7 msec. In half of the inhibited neurons the first phase of inhibition, lasting 18 ± 2 msec on average, was followed by a second inhibitory wave lasting 25 ± 4 msec. In cats treated with MPTP the number of neurons inhibited after stimulating nEp practically did not change (24.5%). A tendency toward shortening of the first phase of inhibition and a statistically significant increase of the duration of its second phase (50 ± 11 msec) were noted. The changes in inhibitory processes in VA-VL neurons receiving afferents from nEp in cats with injury of the nitrostriatal dopaminergic system are explained by the more pronounced hyperplarization of the membrane of these neurons than in intact animals due to intensification of pallidothalamic inhibitory influences, which leads to weakening of Cl^–-and strengthening of Ca²⁺-dependent K⁺ phase of postsynapic inhibition.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 23, No. 2, pp. 213–222, March–April, 1991.     

Measurements of human responses to short duration impact

Thirty human volunteers participated in 75 exposures to short duration impact (less than 10 msec). The tests were conducted to investigate the ability of the subjects to discriminate different pulse durations in the short duration region. Theoretical studies done previously imply that the subjects should only be sensitive to velocity change and not pulse duration below 10 msec duration. The tests were conducted on a free-fall facility with the subject in a seated position (G₂). The deceleration pulses were Gaussian in shape. Two durations (4 and 8 msec) were investigated at three velocity levels (2·6 m/sec, 3·5 m/sec, and 4·1 m/sec). The decelerations were accomplished with a coefficient of restitution from 0·4 to 0·6. The peak G ranged from 80 to 210. The tests were conducted in three phases. Phase I established the safety of the peak velocity level by proceeding in small increments from a known safe level. Phase II was conducted by exposing 9 subjects to each of the three velocity levels in a counterbalanced experimental design. The pulse duration was 8 msec. Phase III was a duplicate of Phase II, except that a 4 msec pulse was used. A physical or subjective tolerance level was not reached in these experiments, but the 4·1 m/sec velocity level prompted several subjects to discontinue participation in such exposures. A “Physical Symptom Survey” conducted by questionaire, which asked the subject to score severity of sensation by anatomic area, showed a correlation with velocity level and pulse duration. Symptomatology was diffuse but related primarily to the musculoskeletal system and central nervous system. The results of these tests and data derived are discussed relative to physical tolerance and injury potential.     

Participation of feed-forward and feed-backward inhibition in the "priming" effect in hippocampal sections

Focal potentials (FP) elicited by stimulation of collateral-commissural fibers were recorded in the radial and pyramidal layers of the CA1 area in surviving mouse hippocampal slices. The influence of conditioning stimulation on responses in the tested neuronal pathway (the "priming" effect) at 50–1000 msec intervals between the conditioning and test stimuli and variable stimulation strengths was investigated. The relationship of the duration of the FP of the radial layer to the strength of the test stimulation at a 200 msec interval between the conditioning and test stimuli was studied in the first series of experiments. Three different regions of like relationship were distinguished. In region I (weak stimulation) the duration of the FP did not depend on the stimulus strength or on conditioning (i.e., the "priming" effect was not observed). In region II the duration of the FP in the control was shorter as compared with that observed in region I, which is associated with the triggering of the process of feed-forward inhibition. Conditioning led to the partial restoration of the duration of the FP (the "priming" effect, which evidently develops as the result of the suppression of feed-forward inhibition). In region III, by contrast with region II, the stimulation strength was sufficient for the suprathreshold excitation of the pyramidal neurons, which conditioned the development not only of feed-forward, but of feed-backward inhibition as well. The form of the FP in the radial layer is distorted in the process, and their duration cannot serve as an index of "priming." The influence of conditioning on the effect of paired-pulse depression of population peaks in the pyramidal layer was studied in the second series of experiments in order to identify possible changes in feed-backward inhibition. The principal effect consisted in a decrease in paired-pulse depression in the circuits tested; from this the conclusion was drawn of a suppression of feed-backward inhibition. It was concluded that both feed-forward and feed-backward inhibition are suppressed in "priming."Institute of the Brain, Russian Academy of Medical Sciences, Moscow. Translated from Neirofiziologiya, Vol. 24, No. 2, pp. 178–185, March–April, 1992.     

Multiple mechanisms shape selectivity for FM sweep rate and direction in the pallid bat inferior colliculus and auditory cortex

The inferior colliculus and auditory cortex of the pallid bat contain a large percentage of neurons that are highly selective for the direction and rate of the downward frequency modulated (FM) sweep of the bat’s echolocation pulse. Approximately 25% of neurons tuned to the echolocation pulse respond exclusively to downward FM sweeps. This review focuses on the finding that this selectivity is generated by multiple mechanisms that may act alone or in concert. In the inferior colliculus, selectivity for sweep rate is shaped by at least three mechanisms: shortpass or bandpass tuning for signal duration, delayed high-frequency inhibition that prevents responses to slow sweep rates, and asymmetrical facilitation that occurs only when two tones are presented at appropriate delays. When acting alone, the three mechanisms can produce essentially identical rate selectivity. Direction selectivity can be produced by two mechanisms: an early low-frequency inhibition that prevents responses to upward sweeps, and the same asymmetrical two-tone inhibition that shapes rate tuning. All mechanisms except duration tuning are also present in the auditory cortex. Discussion centers on whether these mechanisms are redundant or complementary.     

Electrical responses of the marine ciliate Euplotes vannus (Hypotrichia) to mechanical stimulation at the posterior cell end

Electrical responses upon mechanostimulation at the posterior cell end were investigated in the marine hypotrichous ciliate Euplotes vannus. A new mechanostimulator was developed to mimic stimuli that are identical with those involved in cell-cell collisions. The receptor potential hyperpolarized by 18–35 mV within 12–25 msec, reached a peak value of -62 mV with a delay of 4–9 msec after membrane deformation, and was deactivated after 50–70 msec. Cirri were stimulated to beat accelerated backward. The corresponding receptor current exerted a similar time course with a peak of 2.4 nA. The shift of the reversal potential by 57.6 mV at a tenfold increase of [K⁺] ₀ identifies potassium ions as current carriers within the development of the receptor potential. An intracellular K concentration of 355 mmol/liter was calculated for cells in a medium that was composed similar to sea-water. The mechanically activated potassium current was totally inhibited by extracellular TEA and intracellular Cs⁺, and partially inhibited by extracellular 4-AP. The total inhibition of the current by injected EGTA points to a Ca dependence of the posterior mechanosensitivity. It was confirmed by the increase of the peak current amplitude with rising [Ca²⁺] ₀ . Sodium presumably repolarizes the receptor potential because the repolarization was delayed and after-depolarizations were eliminated in media without sodium. Since deciliation did not affect mechano-sensitivity, the corresponding ion channels reside within the soma membrane.The authors wish to thank Mr. Norbert Spreckelmeier from the electronics workshop and Mr. Herbert Lutter from the fine-mechanical workshop of the department for their excellent work, Mrs. G. Key and Mr. H. Mikoleit for skillful technical assistance and for preparing the figures. This work was supported by Deutsche Forschungsgemeinschaft, SFB 171, C7.