Integration in descending motor pathways controlling the forelimb in the cat

A further analysis has been made of inhibitory pathways to motoneurones via C3-C4 propriospinal neurones (PNs). Intracellular recording was made from triceps brachi motoneurones and effects from higher centres and forelimb afferents on corticospinal IPSPs were investigated after transection of the corticospinal tract at the C5/C6 border. The shortest latencies of the IPSPs evoked by stimulation of the pyramid were as brief as those of the pyramidal EPSPs (Illert et al. 1977). It is postulated that the minimal linkage of the pyramidal IPSPs is disynaptic via inhibitory C3-C4 PNs projecting directly to motoneurones. It was confirmed that pyramidal IPSPs usually are depressed by volleys in forelimb motor axon collaterals (Illert and Tanaka 1978). A quantitative comparison was made of the recurrent depression of pyramidal IPSPs and of IPSPs caused by activation of the Ia inhibitory interneurones. The result support the hypothesis of two parallel inhibitory cortico-motoneuronal pathways via C3-C4 PNs, one disynaptic via the inhibitory PNs and the other trisynaptic via excitatory PNs and Ia inhibitory interneurones. Pyramidal volleys also evoked late IPSPs which in some cases were not depressed from forelimb motor axon collaterals. It is postulated that the late IPSPs are partly due to activation of inhibitory C3-C4 PNs. Disynaptic pyramidal IPSPs were effectively facilitated by volleys in rubro-, tecto- and reticulospinal fibres - but not from vestibulospinal fibres - showing a convergence from the former descending tracts on common inhibitory C3-C4 PNs. Projection from forelimb afferents and corticospinal fibres on common inhibitory C3-C4 PNs was revealed by strong facilitation of disynaptic pyramidal IPSPs from cutaneous forelimb afferents. No corresponding effect was evoked from C2 neck afferents. Stimulation in the lateral reticular nucleus (LRN) evoked monosynaptic IPSPs in some motoneurones. The results of threshold mapping in and around the LRN suggest that the IPSPs are caused by antidromic stimulation of ascending collaterals of inhibitory neurones also projecting to motoneurones, possibly the inhibitory C3-C4 PNs.     

Commissural and perforant path interactions in the rat hippocampus

Summary The interaction of the commissural and perforant path systems was studied by recording extracellular field potentials and single unit activity in the dentate gyrus in urethane-anesthetized rats. Conditioning commissural volleys suppressed extracellular synaptic potentials, population spikes and single unit discharges evoked by perforant path stimulation. Commissural stimulation (single or repetitive) failed to induce a population spike, however strong the stimulation. About half of the cells fired monosynaptically to perforant path volleys and 20% to commissural volleys. Half of the commissurally driven units fired before or coincided with field potential onset. The antidromic mechanism of these short latency unitary spikes was shown by the collision test. Commisural activation reduced spontaneous cell firing without previous excitation in 25% of the neurons. Less than 6% of the cells responded to stimulation of both inputs, indicating little convergence between the two pathways. We contend that a simple form of recurrent inhibition fails to explain the above findings, and the possibility of feed-forward inhibition by commissural activation has been raised.     

Responses of mitral/tufted cells to orthodromic and antidromic electrical stimulation in the olfactory bulb of the tiger salamander

1. Responses evoked by electrical stimulation of the olfactory nerve and olfactory tracts were analyzed in 46 output cells of the salamander olfactory bulb, in vivo. Labeling of several cells with horseradish peroxidase indicated that they were mitral and/or tufted neurons. The responses contained reproducible sequences of depolarizing and hyperpolarizing potentials, which changed with increases in stimulus intensity. 2. Stimulation of the nerve with intensities subthreshold for evoking spikes in the recorded cell resulted in a small depolarization followed by a period of hyperpolarization, during which spontaneous spikes were suppressed. With suprathreshold stimulus intensities, a single spike or often a burst of spikes was evoked, followed by a complex prolonged hyperpolarization. When full spikes were blocked by injecting hyperpolarizing current through the recording electrode, an excitatory postsynaptic potential (EPSP) with two major components and sometimes a fast prepotential were observed at the beginning of the response. Amplitudes of the EPSP and hyperpolarization increased with graded increases in stimulus intensity. In tests with paired stimulus volleys, spike generation was inhibited for at least 1 s and often for several seconds during the hyperpolarization. 3. Stimulation of the tracts with intensities subthreshold for evoking spikes in the recorded cell resulted in a complex prolonged hyperpolarization. With suprathreshold stimulus intensities, a single spike was evoked, followed by a similar period of hyperpolarization. When full spikes were blocked by injecting hyperpolarizing current through the recording electrode, a small antidromic spike, presumably generated in the axon or initial segment, was often observed. Amplitude of the hyperpolarization increased with graded increases in stimulus intensity. In tests with paired volleys, generation of a full antidromic spike was inhibited for a period that usually began 20-30 ms, following the spike evoked by the conditioning stimulus and lasted 100-500 ms. Full antidromic spikes were evoked prior to the period of inhibition and small antidromic spikes were evoked during the period. 4. The mean latencies of single evoked spikes or the first spikes of bursts decreased from 22 to 17 ms with increases in the intensity of nerve stimulation and from 7 to 6 ms with increases in the intensity of tract stimulation. Only decreases in orthodromic latency were significant at P less than or equal to 0.05, as determined by one-sided t tests between the means of responses subdivided according to response pattern and relative stimulus intensity.(ABSTRACT TRUNCATED AT 400 WORDS)     

Short-term reduction of intracortical inhibition in the human motor cortex induced by repetitive transcranial magnetic stimulation

Ten healthy subjects and two patients who had an electrode implanted into the cervical epidural space underwent repetitive transcranial magnetic stimulation (rTMS; 50 stimuli at 5 Hz at active motor threshold intensity) of the hand motor area. We evaluated intracortical inhibition before and after rTMS. In healthy subjects, we also evaluated threshold and amplitude of motor evoked potentials (MEPs), duration of cortical silent period and short-latency intracortical facilitation. rTMS led to a short-lasting reduction in the amount of intracortical inhibition in control subjects with a high interindividual variability. There was no significant effect on other measures of motor cortex excitability. Direct recordings of descending corticospinal volleys from the patients were consistent with the idea that the effect of rTMS on intracortical inhibition occurred at the cortical level. Since the level of intracortical inhibition can be influenced by drugs that act on GABAergic systems, this may mean that low-intensity repetitive magnetic stimulation at 5 Hz can selectively modify the excitability of GABAergic networks in the human motor cortex. Electronic Publication     

Ascending spinal tracts of the spino-bulbo-spinal reflex in cats.

Twenty-six chloralosed cats were employed in order to determine spinal ascending pathways of the spino-bulbo-spinal (SBS) reflex evoked by stimulation of the sural nerve. 1. Partial spinal transection of the dorsal part of the lateral funiculus abolished the SBS reflex ipsilateral to sural nerve stimulation. 2. By recording spinal cord potentials in response to sural nerve stimulation two pathways were established in the dorsolateral funiculus as the spinal ascending tracts of the SBS reflex; one is the direct pathway to the bulbar reticular-formation (direct spino-reticular tract) and the other one (indirect spino-reticular tract) is the relayed by the lateral cervical nucleus. Direct stimulation of the dorsolateral funiculus at the lumbar level elicited the SBS reflex. 3. Short-latency unit discharges were recorded from axons of the direct spino-reticular tract by sural nerve stimulation. These axons were discharged antidromically by stimulation of the bulbar reticular formation. 4. Intracellular recordings from the neurons of the lateral cervical nucleus revealed that spike potentials, riding on EPSPs, were induced by sural nerve stimulation and antidromic firings were obtained by stimulation of the bulbar reticular formation. 5. Neurons originating the spino-reticular tract, direct and indirect, were located in the Rexed V-VII laminae in the lower lumbar segments. They were fired monosynaptically by sural nerve stimulation and antidromically by stimulating the dorsolateral funiculus of the lumbar segments. Among them, some were activated antidromically by stimulating the bulbar reticular formation.     

Coupling between feline cerebellum (fastigial neurons) and motoneurons innervating hindlimb muscles

The aims of the study were twofold: (1) to verify the hypothesis that neurons in the fastigial nucleus excite and inhibit hindlimb alpha-motoneurons and (2) to determine both the supraspinal and spinal relays of these actions. Axons of fastigial neurons were stimulated at the level of their decussation in the cerebellum, within the hook bundle of Russell, in deeply anesthetized cats with only the right side of the spinal cord intact. The resulting excitatory postsynaptic potentials and inhibitory postsynaptic potentials were analyzed in motoneurons on the left side of the lumbar enlargement. Postsynaptic potentials evoked by the first effective stimulus were induced at latencies <2 ms from descending volleys and <1 ms from interneuronally relayed volleys, indicating a trisynaptic coupling between the fastigial neurons and alpha-motoneurons, via commissural interneurons on the right side. Cerebellar stimulation facilitated the synaptic actions of both vestibulospinal and reticulospinal tract fibers. However, the study leads to the conclusion that trisynaptic fastigial actions are mediated via vestibulospinal rather than reticulospinal tract fibers [stimulated within the lateral vestibular nucleus (LVN) and the medial longitudinal fascicle (MLF), respectively]. This is indicated firstly by collision between descending volleys induced by cerebellar stimulation and volleys evoked by LVN stimuli but not by MLF stimuli. Second, similar cerebellar actions were evoked before and after a transection of MLF. Mutual facilitation between the fastigial and reticulospinal, as well as between the fastigial and vestibulospinal actions, could be due to the previously reported integration of descending vestibulospinal and reticulospinal commands by spinal commissural interneurons.     

Studies of antidromically identified neurosecretory cells of the hypothalamus by intracellular and extracellular recordings

1. Neurosecretory neurones in supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus of cats, anaesthetized with chloralose, and dogs, anaesthetized with Nembutal, were studied. These neurosecretory neurones were identified by action potentials evoked antidromically following stimulation of the posterior lobe of the pituitary gland. Reactions of 158 such neurones in cats and 228 in dogs were analysed.2. The latencies of antidromic potentials evoked in neurosecretory neurones by posterior lobe stimulation were between 10 and 22 msec for SON and between 14 and 28 msec for PVN cells. Approximate speed of conduction in the axons was 0.4-0.9 m/sec. The absolute refractory period for the soma-dendritic (SD) spike was 5-10 msec. These cells followed repetitive stimulation up to a rate of 100/sec.A notch was generally present on the rising phase of antidromic potentials and when the antidromically conducted signal fell in the relative refractory period of the preceding response, a complete separation between this first small A-spike and later large B-spikes, probably soma-dendritic spike, frequently occurred. Thus, two responses, a small and a large, sometimes appeared with more than 10 msec intervening. When the second antidromic response fell in the absolute refractory period of the first, the B-spike was blocked and only the A-spike appeared.3. Intracellular recordings from neurosecretory cells, mainly from SON in the dog, showed that these neurones possess resting membrane potentials of 50-80 mV, and action potentials of the same magnitude.In spontaneously firing neurosecretory cells separate A- and B-spikes also occurred and could be recorded intracellularly.4. Neurosecretory cells were excited by current injected intracellularly through a micro-electrode. The rheobase was 1-10 nA. A low intensity of stimulation only induced a small A-spike, but as the current was increased the full sized spike was evoked. Application of suprathreshold depolarizing current produced repetitive discharges. The intervals between spikes shortened with an increase in applied current intensity.5. There were a few neurones excited by stimulation of the posterior pituitary whose potentials did not meet the adopted criteria of antidromic potentials. These units were not classified as neurosecretory cells. The characteristics of cells giving the atypical ;antidromic potentials' were: the neurones discharged repetitively to antidromic stimulation, but with fluctuating and very long latencies.6. Neurosecretory cells in both SON and PVN were orthodromically excited by single pulse stimulations of the septal area, mid-brain reticular formation (RF), central gray, anterior commissure and hippocampus. The orthodromic responses generally consisted of two to three spikes with latencies of 10-30 msec. Excitation was followed by an inhibition, of ;spontaneous' discharges as well as of subsequent antidromic excitation, lasting 100-500 msec. Intracellular recordings from neurosecretory cells showed that stimulations of the septal area and RF produced action potentials or EPSPs of short duration followed by long lasting IPSPs. Hyperpolarization was always longer than the preceding EPSP, and its duration was generally 80 msec. Large IPSPs of 20 mV could be recorded occasionally.7. Antidromic excitation of neurosecretory cells by stimulation of the posterior pituitary was followed by the inhibition of ;spontaneous' discharges of the cells. This inhibition usually lasted for 100 msec. A corresponding IPSP was recorded during this inhibitory phase. These findings indicate the existence of recurrent collaterals in neurosecretory cells.8. This conclusion that recurrent collaterals exist was also supported by other evidence, namely, that certain neurones were found in the SON and PVN which responded to a single pulse antidromic stimulation of the posterior pituitary with five to seven discharges at a rate of between 500 and 800/sec. Weaker stimuli produced fewer spikes. Such cells resembled in their behaviour ;Renshaw cells' of the spinal cord. RF stimulation had an inhibitory effect on some of these neurones and an excitatory effect on others.9. Neurosecretory cells in the SON and PVN were excited by osmotic stimulation. Other neurones in close proximity were also found to be osmosensitive but they were either interneurones or neurosecretory cells whose axons ended in areas other than the posterior pituitary since they were not antidromically excitable.     

Projections of pyramidal tract cells to alpha-motoneurones innervating hind-limb muscles in the monkey.

1. We have investigated the spatial organization of monosynaptic corticospinal projections to hind-limb motoneurones, using near threshold stimulation of the surface of the precentral gyrus to activate pyramidal tract (PT) cells and intracellular recording from motoneurones to detect the resulting e.p.s.p.s. 2. Monosynaptic e.p.s.p.s. of cortical origin were seen in all motoneurone species investigated, those of distal as well as of proximal hind-limb muscles. The proportion of motoneurones in which the e.s.p.s. were evoked and the amplitudes of the latter indicated a more extensive cortical projection to motor nuclei for distal than for proximal muscles, as previously found for forelimb motoneurones. 3. Cortical areas from which monosynaptic e.p.s.p.s. were evoked in individual motoneurones were remarkably large, most often between 3 and 7 mm2. Several motoneurones appeared to have two or three separate areas within the hind-limb division of the motor cortex. 4. Areas of location of pyramidal tract cells projecting to various motoneurones innervating one muscle were usually not identical. They overlapped often only partially or did not overlap at all. 5. Areas of location of pyramidal tract cells projecting to motor nuclei for different muscles often showed an extensive overlap. When it occurred, various motoneurones of a given motor nucleus had common cortical projection areas with motoneurones of other motor nuclei, either to synergistic or to antagonistic muscles. Our results give further evidence for overlapping of areas of cortical projections to motoneurones and speak against a mosaic-like organization of pyramidal tract cells projecting to different motor nuclei. 6. The rise times of cortically evoked e.p.s.p.s. indicate that the corticospinal tract fibres terminate on motoneurones at approximately similar distances from the soma as group Ia afferents. The small amplitudes of the majority of e.p.s.p.s. evoked by near threshold cortical stimulation therefore suggest that unitary e.p.s.p.s of cortical origin are small and that the density of pyramidal tract cells projecting to individual motoneurones is usually low, even in the centrum of projection areas. 7. Effects of intracortical stimulation depended on the stimulus strength. With currents of 2-3 muA, e.p.s.p.s were usually evoked in one motoneurone species or in close synergists. With currents of 5-10 muA, largest e.p.s.p.s a number of other motoneurones. Latencies of descending volleys in the lumbar corticospinal tract indicated that intracortical stimuli activated pyramidal tract cells indirectly; the effects of these stimuli could thus not be used to indicate the location of pyramidal tract cells responsible for them.     

Convergence of skin reflex and corticospinal effects in segmental and propriospinal pathways to forelimb motoneurones in the cat

The organization of facilitatory convergence from cutaneous afferents (Skin) and the corticospinal tract (pyramidal tract, Pyr) in pathways to forelimb motoneurones of mainly distal muscles was studied in anaesthetized cats by analysing postsynaptic potentials (PSPs), which were spatially facilitated by combinations of stimuli to the two sources at different time intervals. Conditioning Pyr volleys facilitated Skin-evoked PSPs of fixed (1.2–3.6 ms) central latencies (Skin PSPs), suggesting that disynaptic and polysynaptic skin reflex pathways are facilitated from the pyramidal tract. The shortest latencies (1.2–1.7 ms) of pyramidal facilitation suggested direct connection of pyramidal fibres with last order neurones of skin reflex pathways. Conditioning Skin volleys facilitated Pyr-evoked PSPs of fixed, mostly disynaptic latencies (1.0–2.5 ms; Pyr PSPs), suggesting that pyramido-motoneuronal pathways are facilitated from Skin at a premotoneuronal level. The shortest pathway from skin afferents to the premotor neurones appeared to be monosynaptic. Although Pyr and Skin volleys were mutually facilitating, the facilitation curve of Pyr PSPs and that of Skin PSPs were discontinuous to each other, with the peak facilitation at different Skin-Pyr volley intervals. Transection of the dorsal column (DC) at the C5/C6 border had little effect on the latencies or amplitudes evoked by maximal stimulation and the pyramidal facilitation of Skin PSPs. In contrast, the facilitation of Pyr PSPs by Skin stimulation was greatly decreased after the DC transection, and the facilitation curve of Pyr PSPs was continuous to that of Skin PSPs, with no separate peak. Latencies of Pyr PSPs ranged similarly to those in DC intact preparations. More rostral DC transection (C4/C5 border) reduced Skin-facilitated Pyr excitatory PSPs (EPSPs) less than C5/C6 lesions, suggesting that the C5 segment also contains neurones mediating Skin-facilitated Pyr EPSPs. The results show that convergence from skin afferents and the corticospinal tract occurs at premotor pathways of different cervical segments. We suggest that corticospinal facilitation of skin reflex occurs mostly in the brachial segments and Skin facilitation of cortico-motoneuronal effects takes place largely in the rostral cervical segments and partly in the brachial segments.     

A reanalysis of the ventrolateral input in slow and fast pyramidal tract neurons of the cat motor cortex

In deeply anesthetized cats the temporal characteristics of ventro-lateral (thalamic) excitatory postsynaptic potentials (EPSPs) induced in pyramidal tract cells were studied with an averaging technique. Stimulation of the ventrolateral thalamus induced EPSPs in all pyramidal tract neurons at latencies of 1–5 ms. It was found that there was a positive relationship between the latency and rise time of stimulation-induced EPSPs and the latency of antidromic invasions of pyramidal tract neurons. In response to two closely spaced shocks the second EPSP had the same latency and amplitude as the first one in both slow and fast pyramidal tract neurons. Moreover, the span of antidromic latencies of ventrolateral thalamic relay cells to motor cortex stimulation showed that these thalamic neurons had the necessary conduction velocities to account for the distribution of EPSP latencies recorded in pyramidal tract neurons. From these electrophysiological results, it has been concluded that slow and fast pyramidal tract neurons receive a monosynaptic input from neurons in the ventrolateral thalamus. We also report morphological evidence, obtained at the electron-microscopic level, supporting this conclusion. Terminal degeneration induced by a lesion in the ventrolateral thalamus was found on the apical dendrite of a slow pyramidal tract neuron that had been injected with horseradish peroxidase.It is proposed that the matching between the latencies of EPSPs evoked from the ventrolateral thalamus and the latencies of antidromic invasions of pyramidal tract neurons may reflect a matching between the conduction velocity of thalamocortical and cortico-spinal neurons and/or it may be due to the electrotonic properties of the apical dendrites.     

Antidromic activation of sensory afferent fibres in sympathetic nerves of the cat by stimulation of collaterals within the dorsal medulla oblongata

Action potentials were evoked in the white ramus of the third thoracic segment by electrical stimulation in the dorsal medulla oblongata. The following findings indicate that these potentials are due to antidromic activation of collaterals of afferent fibres in sympathetic nerves rather than to orthodromic synaptic activation of preganglionic sympathetic neurones via bulbospinal sympatho-excitatory pathways: (i) they had short latencies yielding intraspinal conduction velocities of 13–43 m/sec; (ii) they followed short trains of stimuli at frequencies up to 600 Hz; and (iii) they were abolished by cutting the dorsal roots of the same spinal segment.     

Indications for coupling between feline spinocervical tract neurones and midlumbar interneurones

The possibility of collateral segmental actions of spinocervical tract (SCT) neurones upon interneurones with input from cutaneous and group II muscle afferents was investigated in deeply anaesthetized cats. To this end, intracellular and/or extracellular recordings were made from 35 dorsal horn and 15 intermediate zone interneurones in midlumbar segments of the spinal cord and effects of stimulation of the ipsilateral dorso-lateral funiculus (DLF) at C3 and C1 levels, i.e. below and above the lateral cervical nucleus where axons of SCT cells terminate, were compared. The stimuli applied at the C3 segment were within the range of stimuli (50–100 μA) required for antidromic activation of SCT neurones in the same experiment. Those applied at the C1 segment (200–500 μA) were at least 3 times stronger than C3 stimuli. Under the same experimental conditions, long ascending and descending tract neurones (dorsal spino-cerebellar and rubro-spinal tract neurones) with axons in the DLF were activated at similar thresholds from the C1 and C3 segments. Intracellular recordings were made from 29 interneurnoes of which 19 (65%) were dorsal horn and 10 (35%) were intermediate zone interneurones. Excitatory postsynaptic potentials (EPSPs) evoked by single stimuli applied at the C3 segment, but not the C1 segment, were found in 14 (48%) of those interneurones; their latencies (3.0–5.7 ms) and frequency following with only minimal temporal facilitation were as required for potentials being evoked monosynaptically by the fastest conducting SCT neurones. Extracellular recordings were made from 30 interneurones (24 dorsal horn and 6 intermediate zone interneurones), and in these neurones spike potentials induced from the C3, but not from the C1 segment, were evoked only by short trains of stimuli. However, their latencies from the first effective stimulus (4.3–5.4 ms) were compatible with mono- or oligosynaptically mediated collateral actions of SCT neurones. They were found in 10 (33%) of the 30 investigated interneurones. Similar effects of C3 stimuli were found in similar proportions of dorsal horn interneurones and intermediate zone interneurones. Indications were also found for synaptic actions evoked by C3 stimuli that could not be attributed to direct collateral actions of SCT neurones. In some intracellularly recorded dorsal horn interneurones, short-latency EPSPs were evoked from the C3 segment by the 2nd or 3rd stimulus in the train, but not by single stimuli. In other dorsal horn and intermediate zone interneurones, inhibitory postsynaptic potentials (IPSPs) were evoked from the C3 segment at minimal latencies (2.7–3.2 ms), which might be too short to allow their mediation via SCT neurones. We conclude that SCT neurones might be used to forward information from muscle group II and cutaneous afferents not only to neurones in the lateral cervical nucleus and via them to thalamus and cerebral cortex but also to interneurones in spinal reflex pathways. Thereby reflex actions evoked from group II and cutaneous afferents might be co-ordinated with responses mediated by supraspinal neurones. We conclude also that dorsal horn and intermediate zone mid-lumbar interneurones might contribute to the previously reported di-and poly-synaptic excitation or inhibition of postsynaptic dorsal column (PSDC), spinothalamic tract (STT) and spinomesencephalic tract (SMT) neurones by collateral actions of SCT cells. Thereby these interneurones might contribute to the co-ordination of responses mediated by various populations of supraspinal neurones. Received: 18 November 1996 / Accepted: 1 September 1997     

Inhibition of primate spinothalamic tract neurons by stimulation in periaqueductal gray or adjacent midbrain reticular formation

Recordings were made from spinothalamic tract (STT) cells in the lumbosacral enlargement of anesthetized monkeys. The cells were identified by antidromic activation from the contralateral ventral posterior lateral nucleus of the thalamus. Electrical stimulation at sites within the periaqueductal gray, the adjacent midbrain reticular formation, or the deep layers of the tectum were found to inhibit the activity of STT cells. In general, midbrain stimulation inhibited the background discharges and the responses of wide dynamic range cells evoked by innocuous and noxious cutaneous stimulation (29 of 37 cases). However, for six cells, midbrain stimulation preferentially inhibited the responses to noxious stimulation. The evoked responses of all 10 high-threshold cells were inhibited. In only two cases was midbrain stimulation ineffective, and no excitatory effects were observed. The mean latency to onset of inhibition resulting from midbrain stimulation was 24.9 +/- 7.2 ms (n = 35). The amount of inhibition produced by midbrain stimulation was graded with stimulus intensity. For example, trains of stimuli (333 Hz) at 50 microA produced a mean inhibition to 81.7 +/- 16.6% of control, while 200 microA resulted in a mean inhibition to 36.3 +/- 21.7%. Not only was the inhibition increased by the use of stronger current intensities, but the duration of inhibition was prolonged. Midbrain stimulation inhibited the responses of STT cells to volleys in both the A-fibers and the C-fibers of the sural nerve. However, there was a selective action in that the responses to C-fiber volleys were more strongly inhibited than were the responses to A-fiber volleys. Lesions placed in the white matter of the upper cervical spinal cord reduced the inhibition produced by stimulation in either the midbrain or the nucleus raphe magnus. The extent to which the inhibition was reduced was proportional to the extent of the cord lesions. However, even when there was an interruption of the entire lateral funiculus on the side of an STT cell and of the dorsal quadrant of the contralateral side, there was still substantial inhibition following stimulation in either brain stem site. It is concluded that while part of the inhibition is mediated by pathways descending in the dorsal lateral funiculus (DLF), at least some depends on pathways coursing through the ventral spinal cord. Inhibition of STT cells may contribute to the neuronal mechanism of the analgesia that results from stimulation in the periaqueductal gray matter in awake, behaving animals.     

Input-output organization of reticulospinal neurones,with special reference to connexions with dorsal neck motoneurones in the cat

Summary Dorsal neck motoneurones receive disynaptic tectal and pyramidal EPSPs via common reticulospinal neurones (RSNs). This study was aimed at identification of the RSNs projecting directly to neck motoneurones and mediating these EPSPs. 1. Stimulation of the tectum and the cerebral peduncle evoked monosynaptic descending volleys in the spinal cord, which were chiefly mediated by reticulospinal neurones in the pons and the medulla. Systematic tracking of the C3 and C7 segments was made to locate descending volleys in the spinal funiculi. The tectal monosynaptic volley was largest in the medial part of the ventral funiculus and decreased gradually as the recording electrode was moved to the lateral part of the ventral funiculus and the lateral funiculus. In contrast, the peduncle-evoked monosynaptic volley was distributed rather evenly in the ventral funiculus and the ventral half of the lateral funiculus. 2. Differences in funicular distribution of the two descending volleys suggest the existence of subgroups of RSNs which differed in strength of inputs from the two descending fibre systems and in the funicular location of descending axons. 3. The RSNs were classified into the following four groups; (1) mRSNs which descended in the medial part of the ventral funiculus, (2) in RSNs which descended in the ventrolateral funiculus, (3) 1RSNs which descended in the dorsal 2/3 of the lateral funiculus and (4) coRSNs which descended in the contralateral funiculi. The mRSNs were located in a fairly localized region corresponding to the nucleus reticularis pontis caudalis (N.r.p.c.), while inRSNs, 1RSNs and coRSNs were mainly in the nucleus reticularis gigantocellularis (N.r.g.), in the nucleus reticularis magnocellularis (N.r.m.) and in the nucleus reticularis ventralis (N.r.v.). RSNs were further divided into three types depending on the levels of projection. L-RSNs projected to the lumbar spinal segments. C-RSNs descended to the C6–C7 spinal segment but not to the lumbar segments. N-RSNs projected to the C3 but not to the C6–C7 segments. 4. Stimulation of the tectum and the cerebral peduncle produced monosynaptic negative field potentials in the medial two thirds of the reticular formation in the pons and medulla. Tectal field potentials were largest in the N.r.p.c. and the rostral part of the N.r.g., while pyramidal field potentials were largest in the N.r.g. Correspondingly, RSNs in the N.r.p.c. (mRSNs) received larger monosynaptic EPSPs from tectal than from pyramidal volleys, while RSNs in the N.r.g. (in-, 1- and coRSNs) received stronger input from the peduncle than from the tectum. 5. Stimulation of the C7 ventral but not the lateral funiculus evoked monosynaptic EPSPs on all the dorsal neck motoneurones tested. Stimulation of the L1 segment only produced monosynaptic EPSPs in 35% of the motoneurones. The L1 evoked EPSPs were much smaller than C7 evoked EPSPs. 6. The C7 evoked EPSPs (C7 EPSP) showed complete occlusion (collision) with the tectal or pyramidal disynaptic EPSPs. Similar results were obtained with L1 EPSPs. These results indicate that tectal and pyramidal disynaptic EPSPs in dorsal neck motoneurones were mediated chiefly by C-mRSNs and C-inRSNs and partly by L-RSNs.     

Intracellular study of frog's vestibular neurons in relation to the labyrinth and spinal cord

Summary Field and intracellular potentials were recorded in the vestibular nuclei of the frog following stimulation of the anterior branch of the ipsilateral vestibular nerve and the spinal cord. The field potential induced by stimulation of the vestibular nerve consisted of an early positive-negative wave followed by a slow negativity and that recorded during spinal cord stimulation was composed of an antidromic potential followed by a slow negative wave. These potentials were most prominent in the ventral region of the stato-acoustic complex. Mono- and polysynaptic EPSPs were recorded from vestibular neurons following vestibular nerve stimulation. Short latency depolarizations of small amplitude preceded the monosynaptic EPSPs in some neurons. Spike-like partial responses were commonly superimposed on the EPSPs. These all-or-none depolarizations probably originated in the dendrites. In a group of vestibular neurons stimulation of the vestibular nerve evoked full action potentials with latencies ranging from 0.2 to 1.1 msec. They are presumably caused by antidromic activation of neurons which send their axons to the labyrinth. The presence of efferent neurons in the vestibular nuclei was confirmed by their successful staining with Procion Yellow following axonal electrophoresis.After stimulation of the spinal cord, antidromic spike potentials and EPSPs were recorded in vestibular neurons. In addition, short-latency depolarizing potentials (EDPs) were evoked by spinal stimulation, with latencies similar to those of antidromic potentials. The EDPs are suggested to be induced by electrotonic transmission from the neighboring cell and likely to be active spike potentials produced at some distance away from the soma.     

Effects of odor stimulation on antidromic spikes in olfactory sensory neurons

Spikes were evoked in rat olfactory sensory neuron (OSN) populations by electrical stimulation of the olfactory bulb nerve layer in pentobarbital anesthetized rats. The latencies and recording positions for these compound spikes showed that they originated in olfactory epithelium. Dual simultaneous recordings indicated conduction velocities in the C-fiber range, around 0.5 m/s. These spikes are concluded to arise from antidromically activated olfactory sensory neurons. Electrical stimulation at 5 Hz was used to track changes in the size and latency of the antidromic compound population spike during the odor response. Strong odorant stimuli suppressed the spike size and prolonged its latency. The latency was prolonged throughout long odor stimuli, indicating continued activation of olfactory receptor neuron axons. The amounts of spike suppression and latency change were strongly correlated with the electroolfactogram (EOG) peak size evoked at the same site across odorants and across stimulus intensities. We conclude that the curve of antidromic spike suppression gives a reasonable representation of spiking activity in olfactory sensory neurons driven by odorants and that the correlation of peak spike suppression with the peak EOG shows the accuracy of the EOG as an estimate of intracellular potential in the population of olfactory sensory neurons. In addition, these results have important implications about traffic in olfactory nerve bundles. We did not observe multiple peaks corresponding to stimulated and unstimulated receptor neurons. This suggests synchronization of spikes in olfactory nerve, perhaps by ephaptic interactions. The long-lasting effect on spike latency shows that action potentials continue in the nerve throughout the duration of an odor stimulus in spite of many reports of depolarization block in olfactory receptor neuron cell bodies. Finally, strong odor stimulation caused almost complete block of antidromic spikes. This indicates that a very large proportion of olfactory axons was activated by single strong odor stimuli.     

Synaptic organization in teleost spinal motoneurons.

Glass microelectrodes were inserted into motoneurons innervating pectoral fin muscles to record action and synaptic potentials, evoked by electrical stimulation of ventral and dorsal roots, and the medulla oblongata. Ventral root stimulation evoked a small depolarizing response which had properties compatible with those of the EPSP; its amplitude changes were graded, being increased by membrane hyperpolarization and decreased by high frequency repetitive stimulation. The latency of the response was sufficiently longer than that of the antidromic spike to allow for a monosynaptic delay. Stimulation of the dorsal root produced EPSPs with relatively long latencies, suggesting mediation by a polysynaptic pathway. EPSPs with short latencies were evoked by stimulation of the medulla oblongata, indicating the presence of a monosynaptic excitatory connection. Action potentials, recorded from peripheral nerve after stimulation of the medulla oblongata, were facilitated by conditioning volleys via ventral roots. This facilitation was blocked by dihydro-beta-erythroidine hydrobromide and atropine sulphate, indicating the cholinergic nature of the EPSP of ventral root origin. The conduction velocities of motor axons and of the ventral roots fibers responsible for production of EPSPs were about the same. The EPSP of ventral root origin had a slower rising time course and lesser sensitivity to shifts of membrane potential than the EPSP of medulla oblongata origin, suggesting that the sites of generation of the former EPSP were on the peripheral dendrites. From the above results, it was concluded that the EPSP of ventral root origin was mediated by recurrent axon collaterals of motoneurons.     

Firing of spinal motoneurones due to electrical interaction in the rat: An in vitro study

Summary The excitatory interaction between spinal motoneurones was investigated by means of electromyogram (EMG) recordings from hindlimb muscles as well as intracellular ones from their innervating motoneurones in the isolated preparation of immature rats.Stimulation of the muscle nerve to biceps femoris or medial gastrocnemius or of the L5 ventral root evoked early and late EMG responses in the muscle of the preparations with the dorsal roots cut. The early response was produced directly by volleys in the motor nerve. The late response was of spinal origin, since it disappeared after the severance of the ventral root. The thresholds and the conduction velocities of nerve fibres, which conducted the centripetal impulse causing the late response, were compatible with those of motor nerve fibres. The amplitude of the late response was 5–10% of that of the maximum early EMG response.Intracellular recordings from spinal motoneurones revealed that stimulation of the ventral root elicited the double discharge composed of antidromic and delayed spike potentials. The delayed spike was never evoked after the spike potential elicited directly by a short depolarizing pulse. The double discharge was observed in about 6% of the motoneurones examined. The threshold of the stimulus intensity evoking the double discharge was in the range of those of motor nerve fibres. The latencies of the delayed excitation were 7.0–9.0 ms, comparable to the intraspinal delays of the late EMG response.Stimulation of the ventral root at intensities subthreshold for antidromic activation was found to produce a small depolarizing potential in about 60% of the motoneurones examined. The amplitudes were 0.5–5.0 mV, and the onset and the peak latencies 2.0–7.0 ms and 5.0–8.0 ms, respectively. The potential was unaffected by the deficiency of calcium ions in the perfusing medium and persisted after the degeneration of the afferent fibres in the ventral root. It was thus concluded that the depolarizing potential was generated by electrical synapses between motoneurones.In a few motoneurones the electrical synaptic potential was found to elicit spike potentials. Latencies of these spikes were similar to those of the delayed excitation in motoneurones with the double discharge. The time course of changes in the excitability in these motoneurones showed that the delayed excitation, hence the late EMG response, was also caused by the electrical synaptic potential.     

Noninvasive stimulation of human corticospinal axons innervating leg muscles

These studies investigated whether a single electrical stimulus over the thoracic spine activates corticospinal axons projecting to human leg muscles. Transcranial magnetic stimulation of the motor cortex and electrical stimulation over the thoracic spine were paired at seven interstimulus intervals, and surface electromyographic responses were recorded from rectus femoris, tibialis anterior, and soleus. The interstimulus intervals (ISIs) were set so that the first descending volley evoked by cortical stimulation had not arrived at (positive ISIs), was at the same level as (0 ISI) or had passed (negative ISIs) the site of activation of descending axons by the thoracic stimulation at the moment of its delivery. Compared with the responses to motor cortical stimulation alone, responses to paired stimuli were larger at negative ISIs but reduced at positive ISIs in all three leg muscles. This depression of responses at positive ISIs is consistent with an occlusive interaction in which an antidromic volley evoked by the thoracic stimulation collides with descending volleys evoked by cortical stimulation. The cortical and spinal stimuli activate some of the same corticospinal axons. Thus it is possible to examine the excitability of lower limb motoneuron pools to corticospinal inputs without the confounding effects of changes occurring within the motor cortex.     

Action-potential discharge in hippocampal CA1 pyramidal neurons: current source-density analysis

1. The site of origin of evoked action-potential discharge in hippocampal CA1 pyramidal neurons was investigated using the in vitro rat hippocampal slice preparation. 2. Action-potential discharge in pyramidal cells was evoked by stimulation of efferent pyramidal cell fibers in the alveus (antidromic) or afferent synaptic inputs in stratum oriens (SO) or stratum radiatum (SR). Laminar profiles of evoked extracellular field potentials were recorded at 25-micron intervals along the entire dendrosomatic axis of the pyramidal cell and a one-dimensional current source-density analysis was applied. 3. Suprathreshold stimulation of the alveus evoked an antidromic population spike response and current sink with the shortest peak latency in stratum pyramidale or proximal stratum oriens. A biphasic positive/negative potential associated with a current source/sink was recorded in dendritic regions, with both components increasing in peak latency with distance from the border of stratum pyramidale. 4. Suprathreshold stimulation of SO or SR evoked a population spike response superimposed upon the underlying synaptic depolarization at all levels of the dendrosomatic axis. The shortest latency population spike and current sink were recorded in stratum pyramidale or proximal stratum oriens. In dendritic regions, a biphasic positive/negative potential and current source/sink conducted with increasing latency from the border of stratum pyramidale. 5. A direct comparison of alvear- and SR-evoked responses revealed a basic similarity in population spike potentials and associated sink/source relationships at both the somatic and dendritic level and a similar shift in peak latency of spike components along the pyramidal cell axis. 6. It is concluded that the initial site for generation of a spike along the dendrosomatic axis of the pyramidal cell following antidromic or orthodromic stimulation is in the region of the cell body layer (soma or axon hillock). Action-potential discharge in dendritic regions then occurs as the result of a subsequent retrograde spike invasion of basal and apical dendritic arborizations.