Latency EPSPs Research Articles

Facilitation of nicotinic acetylcholine responses during the late slow EPSP in a subpopulation of bullfrog sympathetic neurons.

Facilitation of nicotinic acetylcholine responses during the late slow EPSP in a subpopulation of bullfrog sympathetic neurons.

Information processing at a central synapse suggests a noise filter in the auditory pathway of the noctuid moth.

1. The central projections of the A1 afferent were confirmed via intracellular recording and staining with Lucifer Yellow in the pterothoracic ganglion of the noctuid moths, Agrotis infusa and Apamea amputatrix (Fig. 1). Simultaneous recordings of the A1 afferent in the tympanal nerve (extracellularly) and in the pterothoracic ganglion (intracellularly) confirm the identity of the stained receptor as being the A1 cell. 2. The major postsynaptic arborizations of interneurone 501 in the pterothoracic ganglion were also demonstrated via intracellular recording and staining (Fig. 2). Simultaneous recordings of the A1 afferent (extracellularly) and neurone 501 (intracellularly) revealed that each A1 spike evokes a constant short latency EPSP in the interneurone (Fig. 2Bi). Neurone 501 receives only monaural input from the A1 afferent on its soma side as demonstrated by electrical stimulation of each afferent nerve (Fig. 2Bii). EPSPs evoked in neurone 501 by high frequency (100 Hz) electrical stimulation of the afferent nerve did not decrement (Fig. 2Biii). These data are consistent with a monosynaptic input to neurone 501 from the A1 afferent. 3. The response of neurone 501 to a sound stimulus presented at an intensity near the upper limit of its linear response range (30 ms, 16 kHz, 80 dB SPL) was a plateau-like depolarization, with tonic spiking activity which continued beyond the end of the tone. The instantaneous spike frequency of the response was as high as 800 Hz, and was maintained at above 600 Hz for the duration of the tone (Fig. 3). 4. The relationship between the instantaneous spike frequency in the A1 afferent and that recorded simultaneously in neurone 501 is linear over the entire range of A1 spike frequencies evoked by white noise sound stimuli (Fig. 4). Similarly, the relationship between instantaneous spike frequency in the A1 afferent and the mean depolarization evoked in neurone 501 is also linear for all A1 spike frequencies tested (Fig. 5). No summation of EPSPs occurred for A1 spike frequencies below 100 Hz.(ABSTRACT TRUNCATED AT 250 WORDS)

Distribution of potentiation following short high frequency bursts to motoneurons of different rheobase

Potentiation of composite EPSPs has been studied at group Ia fiber/alpha motoneuron connections using a short burst of conditioning stimuli [32 shocks with 6 ms interstimulus interval (ISI)]. Potentiation reached its peak (range 1.2-2.0 X control value) 100-150 ms following the burst. Potentiation decayed slowly and was still present 2 s after the burst. High frequency burst stimulation of a nerve to a synergist muscle did not potentiate the response to stimulation of the homonymous nerve. Three independent sets of measurements suggest that the time course of decline of potentiation depends on the amount of transmission during the potentiated state. First, connections on high rheobase motoneurons exhibited more peak potentiation than those on low rheobase motoneurons but potentiation decayed more rapidly in the former than in the latter. Second, increasing the frequency of the conditioning burst enhanced peak potentiation but the rate of decay of this potentiation also increased. Third, potentiated EPSPs exhibited more low frequency depression than unpotentiated ones at the same connection suggesting that low frequency stimulation during the potentiated state could elevate the rate of decay of potentiation. The short burst paradigm could cause peak potentiation similar in magnitude to that evoked by long, high frequency trains (studied here at the same connection) but with much less of an increase in latency and rise time of the potentiated EPSP. The magnitude of potentiation was unrelated to changes in EPSP latency and rise time. These findings indicate that potentiation can act to modulate EPSP amplitude under conditions of normal motor behaviour when spindle afferents fire in patterns similar in duration and frequency to those used in the present experiments.

Responses of rat lateral hypothalamic neuron activity to vestibular nuclei stimulation

Effects of lateral vestibular nucleus (LVN) stimulation on neuronal activity in the rat lateral hypothalamic area (LHA), including specific glucose-sensitive neurons, were investigated by extracellular and intracellular recordings in vivo. Stimulation of the contralateral LVN evoked 3 types of response in 46% (111/240) of the neurons recorded extracellularly: long latency (38.1 ± 23.6ms) excitation (62/111, 56%), short latency (6.9 ± 3.1ms) excitation-inhibition (33/111, 30%), and inhibition with20.1 ± 11.1ms latency (16/111, 14%). Glucose-sensitive neurons, which were identified by electrophoretic application of glucose, did not respond specificaly to such stimulation. Neuronal activity was recorded intracellularly from 31 LHA neurons, of which 13 responded to LVN stimulation. Seven of the 13 neurons showed a long latency EPSP (10.4 ± 5.5ms) and the remaining 6 exhibited an EPSP-IPSP sequence with shorter latency (4.5 ± 3.0ms). The amplitude of these responses was graded with a change in stimulus intensity. The EPSPs of both types of response were considered to be polysynaptic because of shortening of latencies by higher current stimulation. Since the LHA is implicated in the regulation of autonomic nerve activity, the present results showing polysynaptic pathways from the LVN to the LHA suggest functional involvement of the LHA in vestibulo-autonomic responses.

Slow synaptic transmission in frog sympathetic ganglia.

Bullfrog ganglia contain two classes of neurone, B and C cells, which receive different inputs and exhibit different slow synaptic potentials. B cells, to which most effort has been directed, possess slow and late slow EPSPs. The sEPSP reflects a muscarinic action of acetylcholine released from boutons on B cells, whereas the late sEPSP is caused by a peptide (similar to teleost LHRH) released from boutons on C cells. During either sEPSP there is a selective reduction in two slow potassium conductances, designated 'M' and 'AHP'. The M conductance is voltage dependent and the AHP conductance is calcium dependent. Normally they act synergistically to prevent repetitive firing of action potentials during maintained stimuli. Computer stimulation of the interactions of these conductances with the other five voltage-dependent conductances present in the membrane allows a complete reconstruction of the effects of slow synaptic transmission on electrical behaviour.

Connections between pericruciate cortex and the medullary reticulospinal neurons in cat: an electrophysiological study

The connections between the pericruciate cortex and the medullary reticulospinal (RS) neurons were studied in anesthetized cat. Intracellular recordings were made from reticulospinal neurons and the effects of stimulating different areas of the pericruciate cortex were compared. EPSPs were elicited in all the 93 neurons studied which were antidromically activated by spinal stimulation and had an IS-SD notch on the ascending limb of their antidromic spikes. According to the conduction velocity (c.v.) of the axon and the minimal EPSP latency to cortical stimulation, the neurons could be divided into two groups, i.e. fast-conducting RS neurons (FRS neurons, c.v. greater than 45 m/s) and slow-conducting RS neurons (SRS neurons, c.v. less than 45 m/s). The minimal latencies of FRS neurons were equal to or shorter than 2 ms whereas those of SRS neurons were longer than 2 ms. EPSPs with short latency (less than 2 ms) could be evoked in FRS neurons by stimulating a relatively wide cortical area including the major part of precruciate area 4 and area 6, with a central area of strongest excitatory effect located in area 4 slightly medial to the tip of the cruciate sulcus. Stimulation of the postcruciate area 4 only produced long latency EPSPs. By extrapolation from the cortical and peduncular latencies and the conducting distances it was revealed that the earliest part of the minimal latency EPSPs were monosynaptically evoked in FRS neurons and were mediated by fast-conducting corticobulbar fibers. FRS neurons could be excited by stimuli applied to both ipsilateral and contralateral pericruciate cortex. The influence from the contralateral cortex was slightly stronger.

Integration in descending motor pathways controlling the forelimb in the cat. 13. Corticospinal effects in shoulder, elbow, wrist, and digit motoneurones

The effect of corticospinal volleys evoked by stimulation of the contralateral pyramid was investigated using intracellular recordings from alpha-motoneurones to forelimb muscles. Confirming and extending previous observations (Illert et al. 1977, Illert and Wiedemann 1984), short latency EPSPs within a disynaptic range were evoked by a train of pyramidal volleys in all varieties of shoulder, elbow, wrist and digit motoneurones. The amplitude of pyramidal EPSPs was sensitive to the stimulus repetition rate. Maximal amplitudes were observed around 2-4 Hz, while at 10 Hz the early EPSP was markedly reduced and the long latency EPSP abolished. The persistence of disynaptic EPSPs after a corticospinal transection in C5/C6 suggested that, for all types of forelimb motor nuclei, disynaptic EPSPs are relayed by C3-C4 propiospinal neurones (PNs) (c.f. Illert et al. 1977). The transection, however, caused a clear reduction in the EPSP of all motoneurone types. After a ventral lesion of the lateral funicle in C5/C6 interrupting the axons of the C3-C4 PNs, disynaptic (and possibly trisynaptic) EPSPs were evoked by a short train of pyramidal volleys. It is postulated that intercalated neurones in a disynaptic cortico-motoneuronal pathway also exist in the forelimb segments. Disynaptic pyramidal IPSPs were observed in most types of forelimb motor nuclei both before and after a corticospinal transection in C5/C6. At all joints, pyramidal excitation dominated in motoneurones to physiological flexors, while in extensor motoneurones mixed excitation and inhibition or dominant inhibition was common. Comparison of pyramidal effects in slow motoneurones (classified according to the after-hyperpolarization duration) to the long head of the triceps and anconeus revealed dominant excitation in the former and inhibition in the latter. It is suggested that the slow motor units in these muscles differ in their function although both muscles are elbow extensors.

Responses of cat motor cortex neurons to cortico-cortical and somatosensory inputs.

Intracellular techniques were used to investigate a cortico-cortical path from sensory cortex to motor cortex of cats. Cortico-cortical epsps were evoked in motor cortex neurons by microstimulation of area 3a. Epsps with latencies between 1.2 and 2.4 ms were identified as monosynaptic. These short latency cortico-cortical effects were recorded in layers II through VI of the motor cortex. Neurons with monosynaptic cortico-cortical epsps also received excitatory inputs from forelimb nerves, usually from both muscle and cutaneous afferent fibers. The epsps evoked from forelimb nerves in motor cortex neurons were preceded by neural activity in somatosensory cortex. Time delays between arrival of inputs in sensory cortex and in motor cortex were compared to the latencies of cortico-cortical epsps in the same motor cortex neurons. It was apparent that the timing was appropriate for the identified cortico-cortical path to have relayed some sensory inputs to motor cortex.

Neuronal and synaptic mechanisms of cortical inhibition

Data are presented concerning the latencies, amplitude and durations of IPSPs evoked in neurons of different cortical regions by peripheral and thalamocortical fibre stimulations and intracortical microstimulation in cat. The duration of IPSPs developing due to single afferent stimulus ranged between 20 and 250 ms (60-80 ms as a rule). In response to intracortical microstimulation monosynaptic IPSPs of 5-10 ms duration arose parallel with IPSPs of 20-100 ms duration. Barbiturates and chloralose increased the duration of IPSP up to 300-500 ms. The latencies of 73% of IPSPs evoked in the auditory cortex neurons by thalamocortical fibres stimulation exceed the latencies of monosynaptic EPSPs evoked by the same kind of stimuli not more than by 1.2 ms. Conclusion is made that inhibition developing in neurons of the cortical projection areas in response to afferent volley is a direct one and is produced by cortical inhibitory interneurons. Some cortical neurons were inhibited by a recurrent mechanism. Only 2% of IPSPs developed monosynaptically. The synaptic delay of IPSP evoked by intracortical microstimulation ranged between 0.3-0.4 ms. The length of the inhibitory neuron axons in layer IV of the auditory cortex reached 1.5 mm. The excitation conduction velocity in these axons was calculated to be 1.6-2.8 m/s (2.2 m/s on the average).

Lateral spread of neuronal activity within the motor cortex investigated with intracellular responses to distant epicortical stimulation.

Lateral spread of activity within the motor cortex was examined by means of analyses of the direct cortical responses (DCRs) and intracellular responses to distant epicortical stimulation (EPICS) using cat encéphale isolé preparations. DCRs to the EPICS at a distance of 1.5-6.5 mm consisted of initial small positive (Pd) and subsequent negative waves (Nd). The reversal of polarity in depths occurred at 400-550 microns for Pd and at 150-250 microns for Nd as well as for the initial negative wave elicited by near EPICS. Intracellular responses to distant EPICS consisted of excitatory (EPSP) and inhibitory postsynaptic potentials (IPSP), disfacilitation (DF), and disinhibition (DI). Depth distributions of cells with EPSPs at two peaks in laminae II and V-VI, with IPSPs mainly in lamina III, and with DF or DI in laminae V-VI were the same with those by near EPICS. The inhibitory effects of distant EPICS on middle layer cells were much greater than those by near EPICS. No linear relations of the latency of EPSPs or IPSPs to the depth were seen for distant EPICS. Instead, the latency increased in proportion to the lateral distance in EPSPs at a slower rate than in IPSPs compared in superficial and middle layer cells. Several routes for lateral spread of activity were postulated. Most conspicuous are the excitatory route via horizontal axons in lamina I and the inhibitory route via laterally running axons in laminae II-III, which produce overall excitation of superficial layer cells and depression of middle and deep layer cells. Their possible role in phasic cortical arousal was discussed.

Convergence of sensory inputs in somatosensory cortex: interactions from separate afferent sources.

Intracellular recording techniques were used to test for cross-modality and topographic convergence among inputs to area 3a of cerebral cortex. Recordings were made within the projection area of group I afferent fibers of the deep radial nerve in barbiturate-anesthetized cats. Epsps were evoked in 90% of neurons (81/90) by electrical stimulation of more than one nerve of the contralateral forelimb. The deep radial nerve evoked the shortest latency epsps within this region of cortex and the only ones likely to be mediated by a monosynaptic thalamocortical pathway. However, the epsps evoked from other forelimb nerves (of deep or cutaneous origin) had mean latencies only a few milliseconds (1.3-3.0 ms) longer. Furthermore, there were a variety of interactions among inputs from separate afferent sources. The observed interactions included spatial facilitation, occlusion and afferent inhibition. The consequence of these interactions was that neuronal responses were shaped by combinations of effects from different topographic regions of the forelimb or of different modalities. The findings are interpreted as indicating a sharing of neurons among pathways to cortical neurons from separate afferent sources. Interactions between ascending pathways by way of such shared neurons may contribute to the modulation or plasticity of somatosensory responsiveness during behavior or after deafferentation.

Integration in descending motor pathways controlling the forelimb in the cat. 12. Interneurones which may mediate descending feed-forward inhibition and feed-back inhibition from the forelimb to C3-C4 propriospinal neurones.

Extra- and intracellular recording was made from cells in the C3-C4 segments with the aim of finding interneurones of previously described inhibitory pathways to the C3-C4 propriospinal neurones, which may mediate descending feed-forward inhibition and feed-back inhibition from the forelimb, respectively. The lateral interneurones were found in the lateral part of lamina VII interspersed among the C3-C4 PNs and like them they receive convergent monosynaptic EPSPs and disynaptic IPSPs from the cortico-, rubro-, tecto- and reticulospinal tracts. Disynaptic IPSPs, but only rarely monosynaptic EPSPs, are evoked in them from forelimb nerves. The lateral interneurones do not project to the lateral reticular nucleus (LRN). The medial interneurones were found medially in laminae V and VI in a region where volleys in forelimb nerves evoke extracellular monosynaptic focal potentials (Rosén 1969). There is somatotopic organization of the projection from the forelimb to this region. Many neurones are strongly monosynaptically excited from group I muscle or/and cutaneous forelimb afferents. In addition, late discharges are evoked in many cells from cutaneous afferents and high threshold muscle afferents. Corticospinal volleys evoked monosynaptic excitation in the great majority of these cells and usually also late EPSPs or IPSPs. Typically, rubrospinal and tectospinal volleys evoked neither monosynaptic excitation nor late effects as those elicited from corticospinal fibres. In some of the interneurones, IPSPs were evoked from forelimb nerves. About 20% of the medial "interneurones" have an ascending projection to the caudal brain stem. Threshold mapping for antidromic stimulation revealed termination in the main cuneate nucleus, the external cuneate nucleus and/or the LRN and also a branch projecting to more rostral levels in the brain. A few of the neurones in the medial region are PNs projecting to the forelimb segments. It is postulated that interneurones both of the lateral and medial type are inhibitory and project to the C3-C4 PNs. It is further postulated that the former are intercalated in the descending feed-forward inhibitory pathway to the C3-C4 PNs and the latter in the feed-back inhibitory pathway from the forelimb to these PNs. The role of feed-forward and feed-back inhibition of transmission from the brain to forelimb motoneurones via the C3-C4 PNs is discussed.

An electrophysiological study of pathways mediating optokinetic responses to the vestibular nucleus in the rat.

Intra- and extracellular responses of neurons in the pretectum (Pt), the nucleus reticularis tegmenti pontis (NRTP), the prepositus hypoglossal complex (NPH) and the vestibular nuclei (VN) were recorded during orthodromic/antidromic stimulation of their afferent/efferent fibers. In the Pt, many neurons were excited by stimulation of the contralateral optic nerve (ONc). Comparison of the latencies of evoked presynaptic action potentials and EPSPs yielded a time difference corresponding to one synaptic delay. Forty five per cent of these monosynaptically driven neurons were also excited antidromically from the ipsilateral NRTP. In the NRTP, ONc and Pt stimulations evoked disynaptic and monosynaptic EPSPs, respectively. Thirty six per cent of NRTP neurons orthodromically driven from ONc and/or ipsilateral Pt stimulation were also antidromically invaded from either the contralateral (67%) or the ipsilateral (33%) flocculus but never from both. In the NPH, both ipsilateral Pt and NRTP stimulations excited type II neurons monosynaptically. In addition, EPSPs evoked by Pt stimulation could be mediated to the NPH via a disynaptic route involving the NRTP. In the VN, type II neurons were excited by ipsilateral Pt stimulation. When comparing the latencies of action potentials and EPSPs evoked by Pt stimulation in the NPH and in VN type II neurons respectively, a short, possibly monosynaptic connection, may be postulated between the NPH and the VN. Our results suggest that vestibular neurons may be optokinetically driven from the contralateral eye both via Pt-NPH connections and Pt-NRTP-NPH paths. They also confirm the existence of a transcerebellar route from the Pt via the NRTP to the ipsior contralateral flocculi.

Activity in cortical cells after stimulation of tooth pulp afferents in the cat. Intracellular analysis

The projection of tooth pulp afferents to cortical cells was studied in intracellular recordings. In a small region of the coronal gyrus, cells in lamina IV were responding at stimulation of contralateral tooth pulp afferents with short latency, steeply rising EPSPs, and one or two action potentials followed by an IPSP. These cells received convergence from skin afferents. In a large cortical area in the coronal, anterior suprasylvian and anterior ectosylvian gyri, tooth pulp stimulation elicited long latency, long lasting EPSPs not succeeded by hyperpolarization mainly in superficial cortical cells. These EPSPs could elicit trains of spikes. A complex type of responses consisted of a short latency EPSP with one or two spikes followed by hyperpolarization which in part was counteracted by a second, long latency EPSP of long duration. Stimulation of low threshold contralateral skin afferents usually gave short latency EPSPs with spikes followed by long lasting hyperpolarization. A common feature of many cells was a high convergence from tooth pulp afferents and bilateral low threshold skin afferents. The response characteristics at tooth pulp stimulation compared to low threshold input are discussed in relation to cortical mechanisms of pain.

Distributions of EPSP latency at different group Ia-fiber-alpha-motoneuron connections.

Distributions of EPSP latency at different group Ia-fiber-alpha-motoneuron connections.T C Cope, and L M MendellT C Cope, and L M MendellPublished Online:01 Mar 1982https://doi.org/10.1152/jn.1982.47.3.469MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByIdentifying the components of a postsynaptic potential and their amplitude, latency and shape fluctuations: analysis by means of autocovariance functions and a stochastic infinite cable modelJournal of Neuroscience Methods, Vol. 124, No. 1The dynamics of synchronized neurotransmitter release determined from compound spontaneous IPSCs in rat dentate granule neurones in vitro22 September 2004 | The Journal of Physiology, Vol. 510, No. 2The exocytotic fusion pore and neurotransmitter releaseNeuron, Vol. 12, No. 4Non-uniform release at the frog neuromuscular junction: evidence of morphological and physiological plasticityBrain Research Reviews, Vol. 12, No. 1 More from this issue > Volume 47Issue 3March 1982Pages 469-78 https://doi.org/10.1152/jn.1982.47.3.469PubMed6279789History Published online 1 March 1982 Published in print 1 March 1982 Metrics

Monosynaptic excitation of principal cells in the lateral geniculate nucleus by corticofugal fibers

Electrical stimulation of the primary visual cortex evoked long latency EPSPs in X and Y principal cells of the cat's lateral geniculate nucleus. An extrapolation procedure was used to reveal that these EPSPs were mediated monosynaptically to principal cells by slowly conducting corticogeniculate fibers. A similar type of excitation was observed in intrageniculate interneurons.

Origins of postsynaptic potentials evoked in identified rat neostriatal neurons by stimulation in substantia nigra.

Responses of striatal neurons to stimulation in substantia nigra were recorded intracellularly in intact rats and after acute or chronic unilateral lesions of cerebral cortex or after combined cortical lesions and unilateral thalamic transections. Spiny striatal efferent neurons were identified by intracellular injection of horseradish peroxidase. In intact animals substantia nigra stimulation evoked a complex response with both excitatory and inhibitory phases. Acute unilateral decortication abolished the inhibitory phase of the response and reduced the amplitude of the initial EPSP. Thus, part of the excitatory phase and most or all of the inhibitory phase of the response result from polysynaptic routes to striatum involving cerebral cortex. The remaining EPSP observed in acute decorticate animals exhibited two components distinguished on the basis of their time courses. The latter of these was abolished by thalamic transections. The earlier component was shown to be a monosynaptic EPSP evoked by axon collaterals of cortical efferent neurons projecting to brainstem and was not observed in animals subjected to chronic decortication. After removal of all of these non-nigral response components a small long latency EPSP could be evoked by nigral stimulation. The EPSP is probably due to activation of dopaminergic nigro-striatal axons.

Effect of L-glutamate on cyclic AMP levels in incubated slices of rat cerebral cortex with an iron-induced chronic focus : Y. Hattori, E. Uezu, K. Inaba and Y. Hori (Okayama, Japan)

Stimulation in the lateral reticular nucleus (LRN) antidromically activates neurones with cell bodies in C3–C4 which project to lower cervical segments. These neurones belong to the C3–C4 propriospinal system and are assumed to mediate disynaptic excitation from higher motor centres to forelimb motoneurones. Short latency EPSPs evoked in forelimb motoneurones by stimulation in the LRN are interpreted as being monosynaptically mediated via the bifurcating axons of the C3–C4 neurones. Stimulation in the LRN also evokes monosynaptic IPSPs in these C3–C4 neurones, possibly by antidromic activation of inhibitory neurones with a collateral projection to the propriospinal neurones. The collateral from the C3–C4 neurones to the LRN are assumed to provide the cerebellum with information of the activity reaching the forelimb motoneurones from the C3–C4 propriospinal system and to allow a feedback control of the activity in this system.

Inputs of the pulvinar and lateral posterior nucleus into the abducens nucleus of the cat

Intracellular potentials in anesthetized cats were recorded in abducens motoneurons after stimulation of the ipsilateral and contralateral pulvinar-lateral posterior nuclei (Pul-LPs). The contralateral superior colliculus was ablated to determine the dependence of the ocular input of the Pul-LP on this structure. Stimulation of the contralateral Pul-LP produced predominately excitatory responses in abducens motoneurons. The excitatory responses occurred as an early and/or late EPSP and demonstrated a variability of latency and amplitude characteristic of Pul-LP-evoked saccades. Stimulation of the ipsilateral Pul-LP produced inhibition more frequently than the contralateral Pul-LP. Stimulation of identical, bilateral sites in the Pul-LP suggests the ipsilateral and contralateral Pul-LP have reciprocal input into the abducens motoneurons. The polysynaptic pathway to the abducens nucleus is not dependent on the integrity of the superior colliculus. We conclude in agreement with Crommelinck et al. that although the Pul-LP definitely has an input into the oculomotor system, it is not closely linked to the final common pathway.

Collateral connections to the lateral reticular nucleus from cervical propriospinal neurones projecting to forelimb motoneurones in the cat

Stimulation in the lateral reticular nucleus (LRN) antidromically activates neurones with cell bodies in C3–C4 which project to lower cervical segments. These neurones belong to the C3–C4 propriospinal system and are assumed to mediate disynaptic excitation from higher motor centres to forelimb motoneurones. Short latency EPSPs evoked in forelimb motoneurones by stimulation in the LRN are interpreted as being monosynaptically mediated via the bifurcating axons of the C3–C4 neurones. Stimulation in the LRN also evokes monosynaptic IPSPs in these C3–C4 neurones, possibly by antidromic activation of inhibitory neurones with a collateral projection to the propriospinal neurones. The collateral from the C3–C4 neurones to the LRN are assumed to provide the cerebellum with information of the activity reaching the forelimb motoneurones from the C3–C4 propriospinal system and to allow a feedback control of the activity in this system.