Indirect technique used to investigate convergence in interneurons of reflex pathways. Diagram exemplifies convergence from primary afferents (I, prim. aff.) and descending pathways (II, desc.) on common excitatory interneurons projecting to motoneurons. Neuronal circuits are illustrated on left. A: example of excitatory convergence from both sources. B: example of convergence of excitation from prim. aff. and inhibition from desc. pathways. Interneurons represent a population of interneurons with identical convergence. Traces on right give idealized intracellular records from a single motoneuron after the test stimulus (I, prim. aff.), the conditioning (cond.) stimulus (II, desc.), and combined stimulation (I+II). This example refers to convergence from descending fibers and primary afferents, but the technique can be used for convergence from any source. See text for explanation.

Relations between individual motoneurons and individual Renshaw cells. A: illustration of experimental arrangement and neuronal circuit. Excitatory effect on Renshaw cells (RC) by single impulses in motoneurons (Mn) and inhibitory effect of individual Renshaw cells onto individual motoneurons were investigated with the aid of 2 microelectrodes: 1 used for intracellular stimulation of and recording from motoneurons, and 1 used for extracellular recording from Renshaw cells. The 2nd electrode was filled with 3 M sodium glutamate, which allowed electrophoretic application of glutamate to induce repetitive firing of the recorded Renshaw cells. B: 2 samples of burst firing in a Renshaw cell (upper traces, large spikes) following single action potentials in the motoneuron (timing shown by lower trace). Stimulation frequency of motoneuron was 8.5 impulses/s. Time calibration in D applies also to records in B. C: graph showing rapid decrease of number of spikes in Renshaw cell burst firing following each motoneuronal spike with increasing stimulation frequency. Dots represent mean value of several trials (cf. records in B) at different stimulation frequencies. This example shows the most powerful excitatory coupling of 21 tested cases. D: slow repetitive firing of Renshaw cell (upper trace, large spike) with simultaneous recording of membrane potential of motoneuron (lower trace; voltage calibration applies to intracellular recording). Same motoneuron and Renshaw cell that was illustrated in B, C, E: averaged record of membrane potential in motoneuron following single discharges of the Renshaw cell (the Renshaw cell firing with “doublets” or “triplets” are excluded). Same motoneuron and Renshaw cell that was illustrated in B–D. Note remarkably long time course of this unitary IPSP. F: a more typical time course of a presumed unitary IPSP from a Renshaw cell in a different motoneuron. Pretriggered averaging was used in both E and F; zero on abscissa refers to a time 1 ms before occurrence of spike of Renshaw cell. (From L. Van Keulen, unpublished material. see ref. 592.)

Comparison of patterns of monosynaptic excitation from muscle spindle Ia‐afferents and recurrent inhibition via motor axon collaterals in motor nuclei supplying various hindlimb muscles in cat. Experimental arrangement and neuronal circuits as illustrated in the scheme. Motor nuclei recorded from are listed to left of diagram and nerves whose orthodromic and antidromic effects were compared are indicated above. Homonymous connections, always with both Ia excitation and recurrent inhibition, are indicated by dotted areas. Heteronymous Ia excitation and recurrent inhibition are indicated by hatched and shaded areas, respectively. Diagram is constructed from data obtained in the cat. It indicates a complete overlap of Ia excitation and recurrent inhibition, but with recurrent inhibition more widely distributed than Ia excitation. Sart, sartorius; Q, quadriceps; Sm, semimembranosus; AB, anterior biceps; St, semitendinosus; PB, posterior biceps; Per, peroneus; G‐S, gastrocnemius‐soleus; FDL, flexor digitorum longus; Pl, plantaris; Add, adductor femoris and longus; Grac, gracilis.

Convergence of recurrent inhibition in a primate (baboon) gracilis (Grac) motoneuron with correlation to location of motor nuclei whose efferent axons have been stimulated. A: upper traces are intracellular averaged records (calibration pulse 1 mV, 4 ms) from the gracilis motoneuron. Lower traces are simultaneous records from the cord dorsum. Dorsal roots have been cut and nerves indicated have been stimulated at supramaximal strength for α‐fibers (arrival of volleys at spinal cord indicated by arrows). B: segmental location of motor nuclei tested in A (at the end of each experiment the rostrocaudal distribution of motor nuclei were tested by stimulation of individual ventral roots with simultaneous recording from peripheral muscle nerves). Position of recorded gracilis motoneuron is indicated by arrow. Results suggest that recurrent inhibition is not organized according to proximity principle. Note large recurrent IPSPs from semitendinosus and posterior biceps whose motor nuclei are among the most caudal ones, but no effect at all from quadriceps despite a similar rostrocaudal location of quadriceps and gracilis motor nuclei. Q, quadriceps; Sm, semimembranosus; Pl, plantaris; AB, anterior biceps; Sart, sartorius; TA, tibialis anterior; EDL, extensor digitorum longus; St, semitendinosus; PB, posterior biceps. (From H. Hultborn, E. Jankowska, and S. Lindström, unpublished material. Cited in ref. 292.)

Diagrams illustrating the hypothesis that Renshaw system serves as a variable gain regulator at motoneuronal level. A: input and output connections of α‐motoneurons and Renshaw cells. B: simplified diagram of input‐output relations of a motoneuronal pool during inhibition and facilitation of transmission in recurrent pathway. C: concept of motor output stage. Neurons constituting output are framed by thick lines. Hatched lines indicate parallel connections to α‐ and γ‐motoneurons and corresponding Ia inhibitory interneurons. α, α‐Motoneurons; γ, γ‐motoneurons; RC, Renshaw cells; Ia IN, Ia inhibitory interneurons.

Distribution of heteronymous monosynaptic excitation evoked by impulses in muscle spindle Ia‐afferents from proximal hindlimb muscles in cat. Ia‐afferents of an individual muscle (indicated by coils) evoke excitatory effects via monosynaptic pathways in α‐motoneurons of muscles (marked by open triangles). TFL, musculus tensor fasciae latae.

Long‐lasting excitability increase of α‐motoneurons induced via polysynaptic Ia pathways. B, C: simultaneous intracellular records at different gains from a triceps surae motoneuron in a decerebrate, decerebellate cat (experimental arrangement in A). Ventral roots were intact, but γ‐loop was opened by relaxation with gallamine triethiodide (Flaxedil). Short stimulus trains to medial gastrocnemius nerve (on: MG) caused a depolarizing shift of membrane potential and a firing of motoneuron. This effect was reversed by a short stimulus train to superficial peroneal nerve (off: SP). D, E: monosynaptic reflexes (MSR) evoked by stimulation of nerve from medial gastrocnemius and recorded from central end of cut S₁–L₇ ventral roots (γ‐loop open) in a spinal unanesthetized cat after injection of 5‐hydroxytryptophan (50 mg/kg; experimental arrangement in D). E: integrated amplitude of MSR (arbitrary units, horizontal lines give mean ± SEM) is plotted against time. Stimulation of lateral gastrocnemius‐soleus nerve (on: LG‐S) increased amplitude of MSR while a short stimulus train to the SP nerve (off: SP) brought it back to control value. Values obtained during LG‐S or SP stimulation are not included in the calculation.

Distribution of disynaptic inhibition evoked by impulses in muscle spindle Ia‐afferents from proximal hindlimb muscles in cat. Ia‐afferents of an individual muscle (indicated by coils) evoke inhibitory actions via disynaptic pathways in α‐motoneurons of muscles (marked by closed triangles). TFL, musculus tensor fasciae latae.

Convergence of Ia‐afferents on α‐motoneurons and interneurons that mediate disynaptic Ia inhibition to motoneurons of antagonists (Ia inhibitory interneurons). Scheme in G illustrates experimental arrangement and neuronal circuits. A–C: upper traces are intracellular records from a semitendinosus (St) motoneuron (identified by antidromic invasion in A). Lower traces are records from L₇ dorsal root entry zone. Voltage calibrations apply to intracellular records. Activation of Ia‐afferents from St, posterior biceps (PB), and gracilis (Grac) muscles evokes monosynaptic EPSPs. D–F: intracellular (averaged) records from a vastocrureus (V–Cr) motoneuron (direct antagonist to St). Calibration pulse: 2 ms, 0.5 mV. Stimulation strength (in times threshold of lowest threshold afferent fibers): D) PB, 1.2; St, 1.1; E) Grac, 1.3; St, 1.05; F) Grac, 1.3; PB, 1.2. Appearance of disynaptic IPSPs in motoneuron (bottom traces in D–F) upon conjoint stimulation of PB and St (D), Grac and St (E), and Grac and PB (F) demonstrates convergence of monosynaptic excitation from respective Ia‐afferents on common inhibitory interneurons that thus receive same excitatory convergence as the St motoneurons.

Identification of interneurons mediating disynaptic Ia inhibition (Ia inhibitory interneurons) from quadriceps (Q) afferents to posterior biceps and semitendinosus (PBSt) motoneurons. Experimental arrangement and neuronal circuits are illustrated in D (for records A–G) and J (for records I, K). Upper traces in A–G are intracellular records from a PBSt motoneuron (A–C) and a lamina VII interneuron (E–G). Lower traces are records from L₅ dorsal root entry zone. Upper trace in I is an extracellular record from a lamina VII interneuron that is excited by electrophoretic ejection of glutamate from the recording electrode. Lower trace is a simultaneous intracellular record from a PBSt motoneuron. K shows averaged intracellular response from I (lower trace) triggered by extracellular interneuronal spike (upper trace). Voltage calibrations refer to intracellular records. Stimulation strength of Q nerve is given in times threshold of lowest threshold afferent fibers; stimulation of ventral roots (VRs) was supramaximal for α‐fibers. A–C: disynaptic Ia IPSPs from Q afferents in a PBSt motoneuron (A, B) and its depression by conditioning stimulation of L₅ + L₆ VRs (C). E–G: lamina VII interneuron with convergence required for mediation of effects recorded in PBSt motoneuron of A–C, i.e., monosynaptic activation from Q Ia‐afferents (E, F) and recurrent inhibition from L₆ VR (G). H: summarizing diagram giving location in L₆ of a number of interneurons with convergence illustrated in E–G. I–K: synaptic action in a PBSt motoneuron by an interneuron with convergence shown in E–G and location shown in H. Monosynaptic unitary IPSP evoked by interneuronal activity proves that interneuron with monosynaptic Ia excitation and disynaptic inhibition from motor axons mediates reciprocal Ia inhibition.

Connections to interneuron in reciprocal Ia inhibitory pathway. A: circuit diagram of some connections to interneuron in reciprocal Ia inhibitory pathway, i, Ipsilateral; co, contralateral; Vs, vestibulospinal tract; Cs, corticospinal tract; Rs, rubrospinal tract; Ps, propriospinal tract; cut, cutaneous afferents; FRA, flexor reflex afferents; Mn, motoneurons; R, Renshaw cells. B–K: parallel projection from nucleus vestibularis lateralis (ND) onto α‐motoneurons and corresponding Ia inhibitory interneurons. Experimental arrangement and neuronal circuits as illustrated in K. Upper traces are intracellular records from a posterior biceps‐semitendinosus motoneuron (PBSt; B–E), a quadriceps (Q) motoneuron (I, J), and a Ia inhibitory interneuron (F–H) presumably intercalated in the Ia inhibitory pathway from Q to PBSt. Lower traces are records from dorsal root entry zone in L₇ (B–E) or L₆, (F–J). Voltage calibrations refer to intracellular records. Ipsilateral ND stimulated with 80 μA in C–E and 200 μA in G. Q nerve (B–E, F) stimulated with 1.1 times threshold of the lowest threshold afferent fibers. Ventral roots (VR) were stimulated with single stimuli, supramaximal for α‐fibers. B–E: facilitation of the Q Ia IPSP in a PBSt motoneuron from vestibulospinal tract (B–D) and depression of facilitated IPSP from L₅ + L₆ VRs (E). Results indicate convergence of vestibulospinal excitation and inhibition from motor axon collaterals on common Ia inhibitory interneurons projecting to PBSt motoneurons. F‐H: monosynaptic excitation from the ND (G) of a Q‐activated Ia inhibitory interneuron (F) and its disynaptic inhibition from L₅ + L₆ VRs (H). Note that these direct recordings from interneuron (F–H) correspond to convergent actions from the ND and the VR on the Ia IPSP recorded in the PBSt motoneuron (B–E). I, J: monosynaptic activation of a Q motoneuron (I, homonymous EPSP) from lateral vestibulospinal tract (J). L: schematic drawing of parallel projections (broken lines) onto α‐ and γ‐motoneurons innervating a muscle and the Ia inhibitory interneuron inhibiting the motoneurons of its antagonist. Notice also the mutual inhibition between opposite Ia inhibitory interneurons. Further description in the text.

Convergence on interneurons in Ib inhibitory pathway to motoneurons. Upper traces, intracellular recordings from motoneurons to gastrocnemius‐soleus (A–C) and to flexor digitorum longus (E–H). Lower traces, incoming volleys recorded from L₇ dorsal root entry zone. Voltage calibrations refer to intracellular records. Stimulus strengths of peripheral nerves are given in multiples of thresholds for lowest threshold afferents. A–C: facilitatory interaction in inhibitory transmission to motoneurons from Ib muscle afferents from plantaris (Pl) and cutaneous afferents in superficial peroneal nerve (SP). E–H: facilitatory interaction between a single descending volley in rubrospinal tract (stimulation of red nucleus, NR) and a Ib volley in quadriceps nerve (Q); G, H compare the lack of facilitation with weaker nerve stimulation that mainly activates Ia‐afferents in E, F. Arrow below records in H indicates time of arrival of the fastest descending volleys in rubrospinal tract to the L₆ level. Corresponding graphs in D and I show time course of facilitation obtained by varying conditioning‐testing interval. Zero on abscissa indicates simultaneous arrival at segmental level of both conditioning and testing volleys. Delay of facilitation by a cutaneous volley (D) suggests a disynaptic linkage to Ib inhibitory interneurons. Facilitatory action at simultaneous arrival (and even with the conditioning volley arriving slightly after the test) in the case of rubrospinal volley (I) strongly indicates a monosynaptic linkage from rubrospinal tract. Circuit diagram summarizes most of the neuronal connections to Ib inhibitory interneurons.

Convergence onto a lamina V and VI interneuron possibly interposed in Ib reflex pathways to motoneurons. Upper traces (A‐F), intracellular records from a lamina V and VI interneuron; lower traces (A‐C) and middle traces (D‐F), records of afferent volleys from L₇ dorsal root entry zone; lower traces (D‐F), records of changes in muscle length (increase in length downward). A‐C: convergence of monosynaptic excitation from group I afferents in nerve from plantaris (Pl), of disynaptic excitation from cutaneous afferents in superficial peroneal nerve (SP) and of monosynaptic excitation from ipsilateral descending fibers (i. desc.). Stimulus strength is given in times threshold for lowest threshold fibers. D‐F: analysis by graded brief stretches of plantaris muscle of contribution from muscle spindle Ia‐afferents and Golgi tendon organ Ib‐afferents to the group I excitation illustrated in A. Small stretch in D (cf. calibration to right of F) selectively activates muscle spindle Ia‐afferents, the larger muscle stretches in E and F are near maximal for Ia‐afferents and above threshold for Ib‐afferents, respectively. This series of records thus strongly indicates that both Ia‐ and Ib‐afferents contribute monosynaptic excitation. G: reconstruction of soma and part of the axonal projections of interneuron whose excitatory input is illustrated in A‐F. Interneuron was stained by ejecting horseradish peroxidase from the microelectrode after the recording. Notice the axonal projection into region of motoneurons (large neurons, probably motoneurons, are indicated by hatched areas). (From E. Jankowska, T. Johannisson, and J. Lipski, unpublished observations.)

Facilitation from corticospinal tract of a cutaneous reflex originating from plantar cushion. Scheme in A illustrates experimental arrangement and the involved neuronal circuits. Stippled area symbolizes a pool of interneurons and emphasizes that the actions from both systems are relayed in polysynaptic pathways. Actual site of interaction is not known. Upper traces in B‐E are records from ventral root; lower traces are simultaneous recordings from dorsal root entry zone. Monosynaptic test reflex of plantar muscles (B) is moderately facilitated by a weak (conditioning) electrical stimulus to the pad (C). Stimulation of cortex (D) had no detectable effect on test reflex, but combined action from the 2 conditioning systems resulted in a large spatial facilitation (E).

Interaction of cortico‐ and rubrospinal tracts with lumbar cutaneous reflex pathways. Upper traces in A‐K are intracellular records from different α‐motoneurons and interneurons. A‐C: posterior biceps‐semitendinosus motoneuron. D‐F: gastrocnemius‐soleus motoneuron. I‐K: pretibial flexor motoneuron supplied by deep peroneal nerve. G, H: L₇ dorsal horn interneuron. Lower traces are records from dorsal root entry zone at the respective segmental levels. Voltage calibrations refer to intracellular records. A‐F: facilitation of cutaneous actions from cortex. Liminal synaptic actions evoked from sural nerve (Sur; stimulated alone in A and D) were conditioned by preceding stimulation of cortex (C and F). Cortex was stimulated alone in B and E. The ensuing increase of the polysynaptic potentials indicates excitatory convergence by corticospinal volleys and cutaneous afferent volleys on interneurons in excitatory and inhibitory cutaneous reflex pathways. G, H: monosynaptic activation of a lumbar dorsal horn interneuron from cutaneous (Sur) afferents (G) and short‐latency (probably monosynaptic) activation from the cortex (H). This pattern suggests that, in the action illustrated in A‐F, the corticospinal tract may project monosynaptically onto first‐order interneurons in lumbar cutaneous pathways. I‐K: monosynaptic excitation from rubrospinal tract of last order interneurons in a cutaneous reflex pathway. I shows a liminal IPSP evoked from red nucleus (NR) with a single shock of 200 μA (arrows below surface records in I and K mark arrival at segmental level of descending volley in rubrospinal tract). Conditioning stimulation of superficial peroneal nerve (SP) at 1.4 times threshold of the lowest threshold afferents increased the disynaptic rubrospinal IPSP (K; SP alone in J). L: comparison of location in cat lumbar cord of focal potentials evoked from rubrospinal and corticospinal tracts. Transverse section shows areas in which field potentials were evoked from indicated sites with an amplitude above 80% (black and hatched area) and 50% (continuous and interrupted lines) of their maximal amplitudes. Dorsal location of field from cortex and ventral location of NR field would be compatible with hypothesis that corticospinal fibers interact with first–order interneurons (cf. A‐F, G, H) and rubrospinal fibers interact with last‐order interneurons (cf. I‐K) in trisynaptic cutaneous reflex pathways in the lumbar spinal cord.

EPSPs from group II muscle afferents, joint afferents, and cutaneous afferents in a motoneuron to flexor digitorum longus. Upper traces, intracellular records; lower traces, incoming volleys recorded from dorsal root entry zone in L₇. Stimulus strengths are given in multiples of threshold for each nerve. Voltage calibration applies to intracellular records. A‐D: graded stimulation of nerve from flexor digitorum longus (FDL; maximal homonymous Ia EPSP at 2 times threshold in A). E‐H: graded stimulation of nerves from posterior biceps and semitendinosus (PBSt). I‐K: graded stimulation of posterior knee joint nerve. L: stimulation of cutaneous afferents in sural nerve (Sur). To estimate the central latency of group II effects, it is necessary to relate them to arrival of the group II volley to the spinal cord. The group II incoming volley was therefore recorded at end of experiment from transected dorsal root. Minimum linkage for group II EPSP in extensor motoneurons seems to be disynaptic. Notice similarity of group II actions from FDL and PBSt as well as from joint and skin afferents. (From A. Lundberg, K. Malmgren, and E. Schomburg, unpublished observations; see ref. 416.)

EPSPs from group II muscle afferents, cutaneous afferents, and joint afferents in a lamina VII interneuron. Upper traces, intracellular records; lower traces, incoming volleys recorded from dorsal root entry zone in L₇. Stimulus strengths are given in multiples of threshold for each nerve. Voltage calibration applies to intracellular records. A‐D: graded stimulation of nerve from gastrocnemius‐soleus (G‐S). E, F: graded stimulation of nerve from flexor digitorum longus (FDL). G, H: stimulation of quadriceps (Q) and sartorius (Sart) nerves. I, J: stimulation of sural nerve (Sur). K: stimulation of posterior knee joint nerve (joint). Central latency from arrival of group II incoming volley to spinal cord (as judged from recording from transected dorsal roots at end of experiment) of the group II effects from G‐S (C, D) and from FDL (G) indicates a monosynaptic linkage from group II afferents. Note additional convergence of polysynaptic EPSPs from group II afferents (C, D, H) and from cutaneous and joint afferents. This type of interneuron has a pattern of convergence that makes it a likely candidate for transmitting the type of reflex actions illustrated in Fig. 16. (From A. Lundberg, K. Malmgren, and E. Schomburg, unpublished observations.)

Interaction of descending tracts with flexor reflex afferent (FRA) pathways. Upper traces show intracellular records from a posterior biceps‐semitendinosus motoneuron (A‐C), 2 gastrocnemius‐soleus motoneurons (D‐F and G‐I), and a tibial motoneuron (J‐L). Lower traces are records from dorsal root entry zone. Voltage calibrations apply to intracellular records. Stimulation strengths of gastrocnemius‐soleus (G‐S) in A‐C and J‐L and plantaris (Pl) in D‐F are indicated in times threshold (xT) of lowest threshold afferents. Stimulation of posterior knee joint nerve (joint) in G‐I activated high‐threshold joint afferents. Stimulation strength of ipsilateral Deiters' nucleus (ND) is given in μA. A‐I: facilitation of excitatory (A‐C) and inhibitory (D‐I) FRA actions from cortex (postsigmoid gyrus). A, D, G show responses to nerve stimulation alone. B, E, H show responses to stimulation of cortex alone. C, F, I show effects of combined stimulation. Initial negative potential in A and C is a Ia field potential (same shape at an extracellular position), the short‐latency EPSP in D and F is a heteronymous Ia EPSP. The EPSP facilitated in C is due to activation of group II fibers. The IPSP in F is due to activation of relatively high‐threshold group II afferents and group III afferents (stimulation of Pl with 11 xT was without effect). J‐L: facilitation of a disynaptic vestibulospinal EPSP from contralateral (co) FRA. J illustrates disynaptic vestibulospinal EPSP that is markedly increased by preceding stimulation of the coG‐S (L; G‐S alone in K). M: diagram summarizing neuronal connections revealed by records in A‐I. Stippled area symbolizes a pool of interneurons and emphasizes that the actions from both cortex and peripheral afferents are relayed by polysynaptic pathways. Actual site of convergence is not known. Records in A‐C, D‐F, G‐I do not show whether all the afferent systems are relayed via common interneurons or through separate channels. The first alternative is the most likely, however, since spatial facilitation among all these afferent systems (including cutaneous afferents) have been described in other investigations, and since many interneurons in the intermediate region display the required convergence, including corticospinal excitation 420. As indicated, the same convergence applies for interneurons in excitatory (A‐C) and inhibitory (D‐F, G‐I) pathways to motoneurons. N: diagram summarizing neuronal connections revealed by records in J‐L. Interneurons mediating disynaptic vestibulospinal excitation are also last‐order interneurons in the cross‐extensor reflex.

Actions of flexor‐reflex afferents (FRA) in α‐motoneurons before and after activation of reticulospinal noradrenergic pathways by intravenous injection of L‐hydroxyphenylalanine (dopa). Upper traces are intracellular records from 4 different posterior biceps‐semitendinosus motoneurons (A‐E; F‐J; K‐O; P‐S). Lower traces are records from L₇ dorsal root entry zone. Voltage calibrations refer to intracellular records. Stimulation strength of afferent nerves is indicated in times threshold of the lowest threshold afferent fibers. Stimulation of L₆ ventral roots (VR; Q‐S) was supramaximal for α‐fibers. In A‐O the left 3 columns show effect of single stimuli at fast sweep speed (calibration below M), the right 2 columns show effect of short trains of stimuli at slow time base (calibration below N). All records were obtained in spinal unanesthetized cats. PBSt, posterior biceps‐semitendinosus; G‐S, gastrocnemius and soleus; Sur, suralis; ABSm, anterior biceps and semimembranosus; joint, posterior knee joint nerve; coH, contralateral hamstring. A‐E: polysynaptic short‐latency EPSPs from FRA without dopa. F‐J: depression of short‐latency effects after injection of dopa and appearance of long‐latency excitation (compare I, J and D, E). Depolarization remaining in F is homonymous monosynaptic Ia EPSP in the motoneuron. K‐O: reappearance of short‐latency FRA actions about 2 h after dopa and parallel disappearance of long‐latency excitation. P‐S: reciprocal inhibition of long latency obtained in a flexor motoneuron by stimulation of contralateral (co) FRA after injection of dopa. Depression of IPSP by stimulation of L₆ VR (Q, expanded in R) indicates its mediation by Ia inhibitory interneurons (L₆ VR alone in S).

Organization of a spinal network giving reciprocal activation of flexor and extensor muscles. Upper traces in A‐C and G‐I are intracellular records from 2 α‐motoneurons to posterior biceps‐semitendinosus muscles (PBSt) and gastrocnemius‐soleus muscles (G‐S) in D‐F and J‐L upper traces are extracellular records from interneurons. Lower traces are from dorsal root entry zone. Voltage calibrations refer to intracellular records. Stimulation strength of afferent nerves is given in times threshold of lowest threshold afferent fibers. N‐O are simultaneous records from efferent nerves to a flexor and an extensor muscle. All records were obtained in spinal unanesthetized cats after injection of dopa (100 mg/kg). A‐L: half‐center organization of interneuronal network released after dopa. In flexor motoneuron (A‐C) a train of volleys in high‐threshold muscle afferents evoked the characteristic long‐latency EPSP (B), which was effectively inhibited (C) by a preceding (cond) train of volleys in contralateral high‐threshold muscle afferents (contralateral hamstring nerve, co.H). In the extensor motoneuron (G‐I) long‐latency EPSP was evoked from contralateral high‐threshold muscle afferents (H) and inhibited from the ipsilateral posterior nerve to the knee joint (joint, I). D‐F and J‐L are corresponding records from interneurons that were located in a region dorsal to motor nuclei. Neuron in D‐F was excited from high‐threshold afferents in G‐S (E) and inhibited from contralateral high‐threshold cutaneous afferents (co. sural nerve, co. Sur; F). Neuron of J‐L was excited from co.H (K) and completely inhibited from high‐threshold afferents in the i.G‐S (L). M: tentative diagram showing principle organization of an interneuronal network that could account for results illustrated in A‐L, N,O. Inhibition could be exerted by pre‐ or postsynaptic actions. A single interneuron in the diagram represents a chain of neurons. N,O: alternating discharges in flexor and extensor efferents triggered by short trains of impulses in ipsilateral and contralateral FRA. Acute spinal cat pretreated with nialamide (10 mg/kg) before administration of 100 mg/kg dopa. Records from nerves to a flexor (medial sartorius, Sart) and to an extensor (medial vastus of quadriceps, Vast). N: stimulation of high‐threshold afferents in contralateral quadriceps nerve (co.Q; timing of stimulus train marked by arrow and the vertical interrupted line) during a spontaneous discharge in flexor efferents is followed by a pause in flexor nerve and a discharge in extensor nerve. Activity in flexor nerve is resumed after cessation of extensor discharge, and a 2nd extensor discharge then occurs after this flexor burst. O: stimulation of ipsilateral saphenous nerve (i.saph) evokes a long‐latency discharge in the flexor nerve that, after additional stimulation of co.Q, is followed by a series of alternating bursts in the efferent nerves. P: original hypothesis of organization of spinal “primary half‐centers” projecting to flexor and extensor muscles with reciprocal inhibition acting between them As described in text, Graham Brown 214 later proposed the existence of “interposed half‐centers” to describe interneurons (intercalated between primary afferents and motoneurons) with mutual inhibition as in the diagram in M.

Inhibitory action from short‐latency flexor‐reflex afferent (FRA) pathways on transmission in long‐latency FRA pathways. Upper traces in A‐D are intracellular records from a motoneuron innervating posterior biceps‐semitendinosus muscles (PBSt); in E‐H they are extracellular records from a lumbar interneuron located dorsal to the motor nuclei. Lower traces are records from dorsal root entry zone. Voltage calibration applies to intracellular records. Both neurons were recorded in unanesthetized acute spinal cats after injection of dopa (100 mg/kg). A‐D: recording from PBSt motoneuron shows EPSPs of long latency and duration following stimulation of ipsilateral FRA (ipsilateral nerve to anterior biceps‐semimembranosus muscle, iABSm; stimulation strength is 37 times threshold of lowest threshold afferent fibers). Bars below A‐D indicate duration of repetitive stimulation. Notice that prolongation of repetitive stimulation of FRA delays onset of EPSP. E‐H: stimulation of ipsilateral sural nerve (iSur) elicits long‐latency and long‐lasting activation of interneuron that is typical after dopa. Notice that response is delayed with prolongation of repetitive stimulation (thickening of base lines is due to stimulation artifacts). I: tentative diagram of neuronal connections that could explain illustrated effects. A single interneuron in the diagram represents a chain of interneurons. Inhibition of short‐latency pathway A (A' and A”) from descending noradrenergic systems (NA) releases transmission in long‐latency pathway B (records A‐H were obtained in this condition). The prolongation in onset of late discharge found in motoneurons and interneurons of B (the interneuron in E‐H should belong to this population) illustrates inhibitory interaction from short‐latency on long‐latency FRA pathways. The short‐latency pathway A is subdivided into A' and A” to accomodate the finding that the noradrenergic system may block the short‐latency reflex action onto motoneurons when there is still an inhibitory action on transmission through the long‐latency pathway B. Mn, motoneuron.

Diagram showing alternative reflex pathways from flexor reflex afferents (FRA) with descending (desc) excitatory connections to interneurons of these pathways and its inhibitory interactive connections with the other reflex pathways from the FRA. Mn, motoneuron.

Definition of propriospinal relay neurons in C₃‐C₄ segments. Experimental arrangement and neuronal circuits as illustrated in G (for records A‐F) and in N (for records H‐M). Upper traces, intracellular records from 2 biceps (Bi) motoneurons (A‐F; H‐M); lower traces, records from C₆ dorsal root entry zone. Voltage calibration refers to intracellular records. Stimulation strength of contralateral pyramid (Pyr) is given in μA. Dots below surface records in B, C, I, J indicate arrival of 3rd pyramidal volley. Dashed lines below records B, E, I mark sections that are shown at an expanded time scale in C, F, J. A‐F: disynaptic (1.5 ms) Pyr EPSP before (A‐C) and after (D‐F) transection of corticospinal tract (CST) in C₅. Comparison of antidromic spike potentials in A and D suggests that recording conditions before and after lesion were similar. Results indicate presence of propriospinal neurons (P) above the C₅ lesion that transmit disynaptic corticospinal excitation to forelimb motoneurons (FMn). H‐M: near disappearance of disynaptic Pyr EPSP after CST transection at rostral (r) C₃. Grading of the Pyr stimulation strength in L and M suggests that the very small disynaptic EPSP that remained after lesion was a unitary response. These results indicate that the most rostral location of the propriospinal neurons intercalated in disynaptic corticomotoneuronal pathway is in caudal C₂ or rostral C₃.

Convergence on C₃‐C₄ propriospinal neurons (P) from corticospinal (CST) and rubrospinal (RST) tracts and from forelimb cutaneous afferents (superficial radial nerve, SR). Experimental arrangement and neuronal circuits as illustrated in J. Convergence was judged indirectly from intracellular recording from a forelimb motoneuron (FMn; upper traces in A‐H) with CST transected completely in C₅ (compare in I records from lateral funiculus in C₆ before, upper trace, and after, lower trace, the C₅ lesion). The same lesion transected the RST only partially. Lower traces in A‐H are records from C₆ dorsal root entry zone. Voltage calibration applies to intracellular records. Stimulation strengths: SR, 1.5 times threshold of lowest threshold fibers; red nucleus (NR), 65 μA; pyramid (Pyr), 200 μA. Note that disynaptic EPSP appears only in A, B when 2 rubral stimuli and 1 pyramidal stimulus are given together with the cutaneous SR volley that indicates excitation of common propriospinal neurons (P). All other possible combinations were ineffective (C‐H). Dashed line below A indicates the part of the traces that is expanded in B.

Convergence on C₃‐C₄ propriospinal neurons (P). Scheme in H summarizes monosynaptic excitatory convergence onto them as well as their direct projection to forelimb motoneurons (FMn). Intracellular records in A‐G (upper traces) illustrate a propriospinal neuron (identified from the lateral funiculus in C₅ in A) with monosynaptic excitation from forelimb group I muscle afferents (D‐G: deep radial nerve, DR; stimulation strength in times threshold of the lowest threshold fibers), from corticospinal tract (B: stimulation of contralateral pyramid, Pyr, with 100 μA), and from rubrospinal tract (C: stimulation of contralateral red nucleus, NR, with 100 μA). Lower traces are records from dorsal root entry zone in C₇ (in G also from C₃). Voltage calibration refers to intracellular records.

Collateral projection of C₃‐C₄ propriospinal neurons (P) to forelimb segments and to lateral reticular nucleus (LRN). Scheme in G illustrates experimental arrangement and neuronal circuits. A‐F: upper traces, intracellular records from a propriospinal neuron in C₃ (antidromic activation from the C₇ segment in E); lower traces, records from C₃ dorsal root entry zone. Voltage calibration applies to intracellular records. A, B show antidromic activation of propriospinal neuron from LRN (stimulation strength in μA); note monosynaptic IPSP from LRN in A (see Fig. 39). C illustrates monosynaptic EPSP from contralateral pyramid (Pyr, 100 μA). D‐F: collision of antidromic spike (F) evoked in propriospinal neuron from C₇ (E) by preceding LRN stimulation (D).

Segmental afferent input depolarizing terminals of muscle spindle Ia‐afferents (A), Golgi tendon organ Ib‐afferents (B), and cutaneous afferents (C). Approximate relative amount of depolarization contributed by each input has been estimated from results quoted in text and is indicated by width of arrows. Mn, motoneurons; Ia, Ib, II, and III are the respective muscle afferents; Cut, myelinated cutaneous fibers. A: ipsilateral inputs depolarizing Ia‐fibers of flexor (left) and extensor (right) muscles. B: ipsi‐ and contralateral inputs depolarizing Ib‐fibers. C: ipsi‐ and contralateral inputs depolarizing cutaneous afferent fibers. Note that this pattern of effects is partly changed after administration of dopa to acute spinal cat (described in the text).

Inhibitory action from flexor reflex afferents (FRA) on transmission to Ia‐afferents illustrated by recording Ia EPSPs in motoneurons (A‐D), by the antidromic discharge of Ia‐afferents following stimulation of their terminals in the spinal cord (E‐H), and by recording dorsal root potentials (I‐L). A‐D: upper traces, intracellular records from a gastrocnemius‐soleus motoneuron (G‐S); lower traces, from L₇ dorsal root entry zone. Voltage calibration refers to intracellular records. Stimulus strengths are given in multiples of threshold for lowest threshold fibers. Homonymous test Ia EPSP is shown in A. In B there is no effect by a conditioning volley in the sural (Sur) nerve. Depression in C is evoked by a short train of maximal Ia volleys in nerve from posterior biceps‐semitendinosus (PBSt). With combined conditioning with sural and PBSt nerves there is a removal of the depression (D). E‐H: intraspinal excitability measurements of Ia‐afferent terminals in gastrocnemius‐soleus (G‐S) motor nucleus. Test response (E) was recorded in G‐S nerve. Conditioning stimulation of superficial peroneal nerve (SP; cutaneous afferents only) does not change excitability (F). The facilitation (G, reflecting an excitability increase) is evoked by a train of PBSt Ia volleys. Record in H shows that a volley in SP can remove facilitatory action from PBSt Ia volleys. I‐L: upper traces are dorsal root potentials (DRPs) recorded from the most caudal dorsal rootlet in L₆. Lower traces are recorded from L₇ dorsal root entry zone. I shows test DRP evoked from a train of maximal Ia volleys from PBSt. J shows response to stimulation of the sural nerve. In K and L there is combined stimulation of sural and PBSt nerves (cond. + test). Note pronounced depression of DRP from PBSt Ia‐afferents (K) as well as the long duration of this effect (L). M: tentative diagram showing connections through which volleys in FRA depress transmission from Ia to Ia‐terminals. Terminals with 2 branches are excitatory. Circles indicate presynaptic terminals making synaptic contacts with presynaptic terminals. In the diagram a single interneuron may represent a chain of interneurons.

Long‐latency depolarization evoked from flexor reflex afferents (FRA) in Ia‐terminals after dopa administration. Unanesthetized decorticate acute spinal cat. Graphs in A–C give excitability measurements of Ia‐afferent terminals from gastrocnemius‐soleus nerve (G‐S) before (A) and after (B, C) injection of dopa. Intraspinal stimulation of G‐S afferent terminals with a microelectrode (test) was conditioned (cond) with a short train of stimuli to anterior biceps–semimembranosus (ABSm) nerve (stimulation strength is indicated in times threshold, XT, of lowest threshold afferent fibers). Abscissa gives interval between 1st conditioning volley and test stimulus to G‐S terminals. Ordinate gives amplitude of conditioned response in percent of unconditioned test response. Comparison of A and C shows that after dopa FRA stimulation causes an increased excitability of Ia‐fibers of long latency (conditioning group I stimulation is without effect, B). D–G illustrate simultaneous recordings of dorsal root potentials (DRPs) evoked from ABSm nerve. Comparison of E and G shows that parallel to excitability increase in Ia‐terminals following stimulation of FRA there is also a long‐latency DRP. H: tentative diagram of connections from FRA to Ia‐afferents. Filled circles, connections exerting either pre‐ or postsynaptic inhibition; open circles, termination on presynaptic terminals. Excitatory synaptic terminals are indicated by two branches. Each symbol represents a chain of interneurons. It is assumed that activity in short‐latency FRA pathway (left) inhibits long‐latency pathway to Ia‐afferent terminals. Inhibition from a descending noradrenergic (NA) pathway of short‐latency FRA system releases transmission in long‐latency path from FRA to Ia‐terminals.

Rubrospinal facilitation of segmental transmission to primary afferents. A–G: upper traces, dorsal root potentials (DRPs) recorded from the most caudal filament of the L₆ dorsal root; lower traces, records from cord dorsum at L₇. Voltage calibration beside F applies to DRPs of A–F. A–F: facilitation from red nucleus (NR) of DRPs evoked from cutaneous (B, C: sural nerve, Sur, stimulation at 3 times threshold of lowest threshold afferent fibers) and joint afferents (E, F: high‐threshold afferents in posterior knee joint nerve). Increased amplitude of DRP in C is due to facilitation of 2nd component of cutaneous DRP that is mediated by an FRA pathway. G, H: origin of DRPs evoked by tegmental stimulation. The DRPs of G were evoked with 100‐μA stimulation at sites marked in H in a drawing of a correspnding transverse section of brain stem. The DRPs are evoked from a rather restricted area within the NR. CA, central aqueduct; NIII, oculomotor nucleus; L, lateral and H, horizontal Horsley‐Clarke coordinates.

Depression by dorsal reticulospinal system of flexor reflex afferent (FRA) inhibition in gastrocnemius‐soleus (G‐S) motor nucleus. A: schematic drawing of experimental arrangements. Right, 3 transverse sections: from brain stem (about 6 mm rostral of obex) showing the stimulation; from lower thoracic cord, hatched area indicating transection of whole cord except the right dorsolateral fascicle; from lumbar cord with microelectrode recording in left ventral horn. Left ventral quadrant and dorsolateral fascicle are mounted on electrodes for recording ascending discharges. Ventral root (VR) discharges are recorded from S₁ and L₇ segments, and dorsal root potentials are recorded in a caudal filament of the L₆ dorsal root (DR fil.), both on left. B–E: upper traces, monosynaptic reflexes recorded from ventral root; lower traces, incoming volleys at the dorsal root entry zone. Recording was done with 2 sweep speeds simultaneously and records therefore consist of double sets (left traces at slow and right traces at fast sweep speeds; see calibrations below E). B: monosynaptic reflex from group Ia‐afferents in G‐S nerve. C: same reflex inhibited by a preceding volley in high‐threshold afferents (20 times threshold for lowest threshold fibers) from anterior biceps and semimembranosus (ABSm). D, E: same as B and C respectively but conditioned by a train of 5 stimuli in brain stem that removes most of FRA inhibition (compare C and E), without any effect on monosynaptic test reflex itself (compare B and D). F: diagram of a transverse brain stem section about 6 mm above obex. Filled circles of different size indicate points of stimulation and magnitude of effect on FRA inhibitory actions; X indicates points stimulated without effect on transmission from FRA. G, H: dorsal root records (upper traces) showing that no dorsal root potential (DRP) is evoked by the same brain stem (BS) stimulation that was used in D, E, whereas there is a large DRP with the same amplification from a single volley in the sural nerve (Sur) at 20 times threshold for the lowest threshold fibers. I: time course of brain stem action illustrated in C and E. Inhibition of monosynaptic reflex by the ABSm volley (100% refers to inhibition seen without preceding brain stem stimulation) is plotted against time interval between onset of brain stem stimulation and arrival of ABSm volley at the cord.

Action of dorsal reticulospinal system in lumbar interneurons. Upper traces in A–J are records from 3 different interneurons (A–C; D–F; G–J) located at 1.8 mm–2.0 mm depth from cord dorsum. Lower traces are records from dorsal root entry zone (not present in C, F, I). Voltage calibrations refer to intracellular records. Stimulation strength for nerves is indicated in times threshold of lowest threshold afferent fibers. Experimental arrangement is shown in Fig. 31 A. A–F: excitation from high‐threshold fibers of posterior knee joint nerve (A: joint) and inhibition from high‐threshold muscle afferents of gastrocnemius‐soleus nerve (D; G‐S) were both depressed by conditioning stimulation of brain stem (B, E; BS). BS stimulation alone evoked neither postsynaptic potentials in interneurons (C, F) nor dorsal root potentials (not illustrated), which indicates inhibition from BS in FRA pathways to interneurons from which recording was done. G–J: interneuron with synaptic inhibition from BS. G: monosynaptic activation from superficial peroneal nerve (SP; stimulation at 6 times threshold for lowest threshold fibers). H: inhibitory postsynaptic potential (IPSP) evoked by 3 stimuli in BS. I: onset of IPSP evoked by a single shock (beginning of 1st deflection is marked by arrow). J: IPSP evoked by a single stimulus of contralateral dorsolateral funiculus (DLF) just rostral to spinal cord lesion. A comparison of the latencies to onset of inhibition in I and J suggests that responsible descending fibers have a conduction velocity of 25 m/s.

Effect of dopa on transmission from high‐threshold muscle afferents in motoneurons and reversal of effects by the α‐receptor blocker phenoxybenzamine. Graphs show effect of single conditioning volleys on monosynaptic test reflex (MSR) from flexor posterior biceps‐semitendinosus nerve (PBSt). Ordinate gives amplitude of MSR in percent of unconditioned MSR. Abscissa gives interval between arrival at spinal cord of conditioning and testing group I volleys. Strength of conditioning stimulation of plantaris nerve (PI) is indicated in times threshold (xT) of lowest threshold afferent fibers. A was evoked before injection of dopa; B evoked 10 min after injection of dopa; and C evoked 25 min after dopa and 15 min after injection of phenoxybenzamine. The FRA facilitation of the flexor MSR (A) is abolished after dopa (B), which indicates inhibition of transmission in short‐latency flexor reflex afferent (FRA) pathways. Reversal of inhibition by phenoxybenzamine indicates that effect of injected dopa is mediated by α‐receptors.

Release of Ib‐ and flexor reflex afferent (FRA) actions after bilateral lesions of dorsolateral funiculi. Graphs show effect of single conditioning volleys in nerve to flexor digitorum longus (FDL) on monosynaptic test reflexes evoked from gastrocnemius‐soleus (G‐S). Ordinate gives amplitude of reflexes in percent of unconditioned test reflex. Abscissa gives interval between arrival at spinal cord of conditioning and testing group I volleys. Strength of conditioning stimulation (cond) is indicated in times threshold (xT) of lowest threshold afferent fibers. It was chosen to activate group I fibers in A and D, groups I and II fibers in B, and groups I, II, and III fibers in C and E. At each conditioning strength the curves were obtained after the ipsilateral (i) and contralateral (co) lesions indicated schematically in A (for A–C) and in D (for D, E). Transverse spinal cord drawings in A show symbols used in A–C to illustrate effects of sequential lesions; the initial lesion of the dorsal column and dorsolateral on the contralateral side, and ventral funiculi (O), the additional transection of ipsilateral ventral funiculus (x, cf. histological reconstruction to left), and the complete spinal transection (•). Drawings in D similarly show initial lesion of dorsal column and dorsolateral on the ipsilateral side, and ventral quadrants (O), the additional lesion of the contralateral dorsal funiculus (x, cf. histological reconstruction to left), and complete spinal transection (•).

Differential release of transmission in excitatory and inhibitory flexor reflex afferent pathways by brain stem lesions. Graphs show effect of single conditioning volleys in nerve to flexor digitorum longus (FDL) on monosynaptic test reflexes evoked from gastrocnemius‐soleus (G‐S, A–C) or from posterior biceps‐semitendinosus (PBSt, D, E). Ordinate gives amplitude of reflexes in percent of unconditioned test reflexes. Abscissa gives interval between arrival at spinal cord of conditioning and testing group I volleys. Strength of conditioning stimulation (cond) is indicated in times threshold (xT) of lowest threshold afferent fibers. It was chosen to activate group I fibers in A and D, groups I and II fibers in B, and groups I, II, and III fibers in C and E. At each conditoning strength the curves were obtained after brain stem lesions indicated in F.

Monosynaptic connections to α‐motoneurons from corticospinal and rubrospinal tracts in primate (rhesus monkey). Lower traces in A–F are intracellular records from 2 motoneurons. Upper traces are cord dorsum potentials monitoring afferent incoming volleys and corticospinal volleys. All traces in G, H are intracellular records. A–F: frequency potentiation of monosynaptic excitatory postsynaptic potential (EPSP) evoked from motor cortex (MC) in a motoneuron to flexor digitorum longus (FDL, in A–C) and to gastrocnemius‐soleus (G‐S, in D–F). Antidromic invasion from FDL and G‐S nerves in A and D, respectively. Monosynaptic EPSPs following a single shock stimulation of motor cortex are shown in B, E. Growth of monosynaptic EPSPs with repetitive stimuli shown in C, F; same stimulus strengths as in B, E, respectively. Notice the greater potentiation in F than in C. Calibration pulse 1 ms, 5 m V in A, D; 1 ms, 2 m V in B, C, E, F. G, H: convergence of monosynaptic EPSPs from motor cortex (MC) and red nucleus (NR) in an FDL motoneuron. Superimposed traces of monosynaptic EPSPs evoked by stimulation of MC (G) and NR (H) of different intensities given to right of each trace. Note differences in amplitude and time course from MC and NR.

Diagram illustrating 2 different ways in which ascending neurons may monitor interneuronal activity. A: by ascending collaterals from interneurons interposed in segmental reflex pathways. B: by separate ascending neurons that receive collateral projections from interneurons interposed in segmental reflex pathways. Mn, motoneuron; asc., ascending neuron; prim. aff., primary afferent.

Decerebrate control of transmission to ascending ventral pathways activated from flexor reflex afferents (FRA). Diagram in J illustrates experimental arrangement with a bilateral section of ventral quadrants (VQ) and recording from right VQ of ascending discharge evoked from highthreshold afferents in left hamstring nerve (1. Ham; A, D, G) and left sural nerve (1. Sur; B, E, H). C, F, I show background activity in VQ without stimulation. Comparison of records obtained before (A‐C), during (D–F), and after (G–I) cooling of dorsal part of spinal cord (the dorsal column removed) with a thermode illustrates effective blockade of transmission from FRA to ascending tracts in decerebrate state with conducting dorsolateral funiculi (A–C; G–I), and release in the spinal state, i.e., during blockade of impulse transmission in dorsal part of the spinal cord (D–F).

Wiring diagrams illustrating 2 examples of ascending information from collaterals of neurons interposed in spinal neuronal circuits. A: ascending collaterals from propriospinal neurons in C₃–C₄ (P) to lateral reticular nucleus (LRN). Mn, motoneuron. This connection is illustrated in Fig. 26. B: ascending collaterals to LRN from inhibitory interneurons (with monosynaptic excitation from forelimb afferents) projecting to propriospinal neurons in C₃‐C₄.

Wiring diagrams illustrating hypothesis that information transferred by ventral spinocerebellar tract (VSCT) neurons reflects relation between input to and output from inhibitory segmental interneurons. A: diagram illustrating convergence on a VSCT neuron of monosynaptic excitation from primary afferents (prim. aff.) and disynaptic inhibition evoked from the same primary afferents. Disynaptic inhibition of VSCT neuron is due to a collateral projection from interneurons transmitting disynaptic inhibitory postsynaptic potentials to motoneurons (Mn). In this case the VSCT neuron would compare excitatory input to interneurons from primary afferents and the resulting activity of the inhibitory interneuron. B: in addition to connections in A there is also a descending motor pathway (desc) giving monosynaptic excitation and disynaptic inhibition of VSCT neuron. The descending monosynaptic excitation is collateral to excitation of interneurons, and the disynaptic inhibition is again due to collateral projection from interneuron. Such a VSCT neuron thus compares excitatory input to interneurons from primary afferents and the descending pathway with the resulting activation of the interneuron.

Recurrent depression of a Ia inhibitory postsynaptic potential (IPSP) in a ventral spinocerebellar tract (VSCT) neuron. Experimental arrangement and relevant neuronal circuits are illustrated in A. Mn, motoneuron; RC, Renshaw cell; Q, quadriceps. Upper traces in B–E are intracellular records from a VSCT neuron (identification from ipsilateral anterior lobe of cerebellum in E). Lower traces are records from L₅ dorsal root entry zone. Voltage calibrations refer to intracellular records. B–D: disynaptic Ia IPSPs from Q nerve. Stimulation strength is indicated in times threshold of lowest threshold afferent fibers. F: averaged records of submaximal Ia IPSPs from Q (upper trace) combined with conditioning stimulation of L₅–S₁ ventral roots (VRs; lower trace). Arrow below lower trace indicates arrival of the VR volley to the spinal cord (calibration pulse 1 mV, 2 ms).

Facilitation of Ia inhibitory postsynaptic potentials (IPSPs) in ventral spinocerebellar tract (VSCT) neurons from vestibulospinal and rubrospinal tracts. A shows experimental arrangement and relevant neuronal circuits. Mn, motoneurons; ND, Deiters' nucleus; NR, red nucleus. Upper traces in B–D and F–H are intracellular records from 2 different VSCT neurons. Lower traces are from dorsal root entry zone. Voltage calibrations refer to intracellular records. Strength of stimulation in ND and NR is indicated in μA, stimulation of nerves in times threshold of lowest threshold afferent fibers. B–E: facilitation of a quadriceps‐evoked (Q) Ia IPSP from the ND. Graph in E gives amplitude of IPSP in percent of unconditioned test (ordinate) in relation to time interval between arrival of descending volley from ND (zero ms on abscissa) and incoming Q volley (interrupted line indicates synchronous arrival). Facilitation started with Q volley arriving slightly before ND volley, which indicates monosynaptic coupling of descending fibers with interneuron mediating the Ia IPSP. F–I: facilitation from NR of IPSPs evoked from posterior biceps‐semitendinosus nerve (PBSt). Records in F–H show a facilitation of a Ia IPSP from PBSt. Graph in I shows time course of facilitation of a Ia IPSP from Q in another VSCT neuron. Amplitude of IPSP is given in percent of unconditioned test (ordinate) in relation to time interval in arrival of 1st rubrospinal volley (zero ms on abscissa) and the incoming Q volley (interrupted line indicates synchronous arrival).