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Notes: Summary Spinocerebellar tract (SCT) neurones in and around the central cervical nucleus (CCN) were physiologically identified by antidromic activation of these cells on stimulation of the cerebellum. Among the Spinocerebellar tract cells thus identified, those ascending the contralateral spinal funiculi were found in the CCN and ventralwards, whereas those ascending the ipsilateral funiculi existed mostly dorsal to the CCN partly overlapping with crossed cells in the nucleus. Mapping sites from which CCN cells were antidromically activated showed that axons of the CCN-SCT cross at the same segment, ascend the ventral funiculus initially, the lateral funiculus at rostral C1 and the lateral border of the medulla to reach the cerebellar peduncle, enter the cerebellum mainly via the restiform body but possibly also via the superior peduncle. Systematic mapping of stimulation within the cerebellum indicated that the CCNSCT projects to the medial part of the anterior lobe and the posterior lobe bilaterally. Projection to lobules I–II was found in almost all CCN-SCT cells examined. Three fourths of CCN-SCT cells projected to the posterior lobe, as revealed by less extensive mapping. Mapping of axonal regions of the same single CCN-SCT cells showed that they project multifocally in the cerebellum, where projection to lobules I–II was common and that to other areas varied with individual cells. Conduction velocites decreased within the cerebellum probably as the result of repeated branching. Mossy fibre responses evoked on stimulation of the C2 dorsal root in cats with the transected dorsal funiculi were shown to be mediated mostly via the CCN-SCT. Mapping the field potential showed that the response was by far the largest in lobules I–II. This suggested that the terminals provided by the CCN-SCT are the densest in these lobules.

Notes: Summary Extracellular and intracellular recordings were made from spinocerebellar tract neurones of the central cervical nucleus (CCN) in C1–C3 segments of the anaesthetized cat. These neurones were identified by antidromic activation from the cerebellar peduncle. Stimulation of the ipsilateral dorsal root elicited extracellular spikes or EPSPs with a monosynaptic latency in almost all CCN neurones in the same segment (segmental input). Late excitatory effects were also observed in about one third of CCN neurones. The monosynaptic EPSP was occasionally followed by an IPSP. The excitatory input from the dorsal root to CCN neurones was extended over several segments for some CCN neurons (extrasegmental input). Monosynaptic excitation was evoked in CCN neurones after stimulation of dorsal neck muscle nerves as well; i.e. splenius (SPL), biventer cervicis and complexus (BCC), rectus capitus dorsalis, and obliquus capitus caudalis. Thresholds for this excitation were near the threshold of the nerve, suggesting that it originated from group I fibres. The component of excitation added after strong stimulation of neck muscle nerves would be attributed to group II fibres. When a CCN neurone received excitatory input from the nerve of one muscle, it was generally not affected by stimulation of other nerves in the same segment. Such muscle specificity of segmental input was the principal pattern of connexion of neck muscle afferents with CCN neurones. In some cases, however, excitatory convergence from SPL and BCC nerves onto single CCN neurones or excitation from the SPL nerve and inhibition from the BCC nerve were also observed. Nearly half of the CCN neurones received input from one muscle nerve of the same segment and not from the afferent of the same muscle of different segments, indicating a segment specificity of input. In the remaining CCN neurones, weaker excitatory effects were induced from afferents of different segments as well. In such extrasegmental effects, inputs to CCN neurones from caudal segments predominated in frequency over those from rostral segments. The origin of extrasegmental input was generally confined to the same muscle. Low threshold muscle afferents from the SPL and BCC were intraaxonally stained with HRP. The collaterals of the stained fibre distributed branchlets and terminals to the CCN, laminae VII, VIII, and motor nuclei. Two fibres responding to local muscle prodding or stretch showed a similar morphology. The findings indicated that muscle spindle afferents from primary endings projected to the CCN.

Notes: Summary 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.

Notes: Summary Intracellular recording was made in the C3-C4 segments from cell bodies of a previously described system of propriospinal neurones (PNs), which receive convergent monosynaptic excitation from different higher motor centres and mediate disynaptic excitation and inhibition from them to forelimb motoneurones. Inhibitory effects in these PNs have now been investigated with electrical stimulation of higher motor centres and forelimb nerves. Short-latency IPSPs were evoked by volleys in the cortico-, rubro- and tectospinal tracts and from the reticular formation. Latency measurements showed that those IPSPs which required temporal summation were disynaptically mediated. After transection of the corticospinal tract in C2, only small and infrequent disynaptic IPSPs were evoked from the pyramid. It is postulated that disynaptic pyramidal IPSPs only to a small extent are evoked by monosynaptic excitation of reticulospinal inhibitory neurones known to project directly to the PNs, and that they are mainly mediated by inhibitory interneurones in the C3-C4 segments. Tests with spatial facilitation revealed monosynaptic excitatory convergence from tecto-, rubro- and probably also from reticulospinal fibres on inhibitory interneurones monosynaptically excited from corticospinal fibres (interneuronal system I). Disynaptic IPSPs were also evoked in the great majority of the PNs by volleys in forelimb muscle and skin nerves. A short train of volleys was usually required to evoke these IPSPs from group I muscle afferents. In the case of cutaneous nerves and mixed nerves single volleys were often effective, and the lack of temporal facilitation of IPSPs produced by a train of volleys showed strong linkage from these nerves. The results obtained after transection of the dorsal column at different levels show that the relay is almost entirely rostral to the forelimb segments. Test with spatial facilitation revealed that interneurones monosynaptically activated from forelimb afferents receive convergent excitation from corticospinal but not or only weakly so from tecto- or rubrospinal fibres. There was also convergence from group I muscle afferents and low threshold cutaneous afferents on common interneurones. It is postulated that the disynaptic IPSPs from forelimb afferents are mediated by inhibitory interneurones (interneuronal system II) other than those receiving convergent descending excitation. Volleys in corticospinal fibres, in addition to the disynaptic IPSPs, evoke late IPSPs in the PNs. Similar late IPSPs were evoked from the ipsilateral forelimb by stimulation of the FRA. Monosynaptic IPSPs were evoked in the majority of the PNs on weak stimulation of the lateral reticular nucleus (LRN) and from regions dorsal to it. Results from threshold mapping suggest that these IPSPs are due to antidromic stimulation of ascending inhibitory neurones which also project to the C3-C4 PNs, and that the ascending collaterals terminate in the LRN or/and the base of the cuneate nuclei. Activity in the ascending collaterals may give higher centres information regarding inhibitory control of the PNs. It is postulated that interneuronal system I subserves descending feed-forward inhibition and interneuronal system II feed-back inhibition from the forelimb of transmission through the C3-C4 PNs to motoneurones.

Notes: Summary Extracellular spikes were recorded from secondary vestibular neurons in the cat medial vestibular nucleus (MVN) and were identified as type I or II neurons by horizontal rotation. Type I neurons were further classified as excitatory or inhibitory premotor neurons on the basis of their axonal termination in the contralateral or ipsilateral abducens nucleus, demonstrated by spike-triggered averaging of abducens nerve discharges, or by antidromic activation using systematic microstimulation within the abducens nucleus. Both excitatory and inhibitory premotor type I MVN neurons exhibited a rhythmic modulation of their firing rate in association with nystagmus elicited by rotation or electrical stimulation of the vestibular nerve. Their tonic activity during the slow phase was suppressed at the quick phase directed to the ipsilateral side. Excitatory type I MVN neurons terminating in the contralateral abducens nucleus sent collateral axons to the contralateral MVN. These commissural neurons also showed a nystagmus-related discharge pattern. Type II MVN neurons activated at short latency by stimulation of the contralateral vestibular nerve exhibited burst discharges when the activity of ipsilateral type I neurons was suppressed at the quick phase. These type II neurons made monosynaptic inhibitory connections with type I neurons as shown by the post-spike average of the membrane potential of secondary MVN neurons triggered from spikes of single type II neurons. Thus, the inhibitory action originating from burst activity of type II MVN neurons contributes to suppression of type I premotor MVN neurons during fast eye movements.

Notes: Summary A class of interneurons in the cat abducens nucleus was identified by its antidromic activation from the contralateral ascending MLF, disynaptic activation from the contralateral vestibular nerve and type II response to rotation of the turntable. They were also activated antidromically from the contralateral oculomotor nucleus, the region of medial rectus motoneurons. Extracellular spikes of single interneurons, spontaneous or glutamate-driven, were used as triggers for perior post-spike averaging of three kinds of potentials. (1) The average of the extracellular field potentials within the contralateral oculomotor nucleus consisted of an early positive or positive-negative spike and a late, slow negative wave. The early spike was an action current caused by impulses along the axon of the interneuron. The late potential was the extracellular counterpart of unitary EPSPs. (2) The averaged membrane potential of contralateral medial rectus motoneurons revealed unitary EPSPs with monosynaptic latencies, evidence that interneurons were excitatory in nature. (3) The average of compound potentials of the contralateral medial rectus nerve showed a monosynaptic excitatory effect relevant to unitary EPSPs. This effect was observed with nearly all interneurons. All interneurons thus identified exhibited discharge patterns closely correlated with the activity of medial rectus motoneurons in both slow and quick phases of vestibular nystagmus. It was concluded that these interneurons controlled activities of contralateral medial rectus motoneurons associated with conjugate horizontal eye movements by their monosynaptic excitatory connections.

Notes: Summary 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 monosynapic 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.

Notes: Based on accurate X-ray diffraction intensity data collected from spherically shaped single crystals, net atomic charges and electron density distributions have been studied for MnO, Mn2SiO4, Mg2Si2O6, LiAlSi2O6 and CaMgSi2O6. Examination of various procedures for determining atomic charges in a given structure has led to the conclusion that the following approach appears to be most reliable. (1) For cations: the number of electrons in the sphere of radius ER, effective distribution radius, which is defined according to the characteristics of radial distribution functions or difference-Fourier maps, is calculated. (2) For oxygen atoms: with the cation charges fixed at the values obtained from the above procedure and the total charge of the crystal constrained to be neutral, oxygen charges are estimated from least-squares refinements using atomic scattering factors. The final charges of atoms examined are less ionic than the corresponding formal ones: those of Li, O, Mg, Al, Si, Ca and Mn are respectively + 0.7 (1), -1.1 to -1.5, + 1.4 (1) to + 1.8, + 2.4(1), + 2.2 (1) to + 2.6, + 1.4 (2) and + 1.2 (1) to + 1.6 e. Residual electron densities between Si and O have been clearly observed in difference-Fourier maps after charge refinements for crystals of LiAlSi2O6, CaMgSi2O6 and Mg2Si2O6.

Notes: Abstract Deciduous teeth affected by dentinogenesis imperfecta were obtained from two patients with osteogenesis imperfecta. Electronmicroscopy of the dentin revealed some structural alterations. The striation of the collagen fibrils was not clear, and the crystals were less dense than in normal dentin. The amino acid analysis of dentin collagen was slightly different from normal dentin. There were slight increases in the amounts of hydroxylysine. serine and acidic acids. On the other hand, lysine and arginine were reduced. The elevation of hexosyllysine content and an increase of carbohydrate were also observed.These results indicate that either dentin collagen is altered, or noncollagenous matrices associated with collagen are increased in dentinogenesis imperfecta dentin.