猫丘脑中央外侧核内脊丘系终末的超微结构和突触联系

用顺行溃变的方法首次在电镜水平对猫丘脑中央外侧核内脊丘系终末的超微结构和突触联系进行了研究。在横断脊髓第四颈节一侧的外侧索和部分前索４－５天后，电镜下发现，在损毁同侧的丘脑中央外侧核的中段和尾段均有少量的溃变终末。     

Unilateral retrogasserian rhizotomy causes contralateral degeneration in spinal trigeminal nuclei of cats: an ultrastructural study

We are studying the response to injury within the brainstem trigeminal nucleus following trigeminal nerve lesions. We have previously shown with light microscopy and reduced silver stains that unilateral retrogasserian rhizotomy results not only in massive degeneration throughout the ipsilateral spinal trigeminal nucleus; in addition, degeneration is seen in a ventral position at the periobex region (involving caudal pars interpolaris and rostral pars caudalis) in the contralateral spinal trigeminal nucleus. In the present study, we have used electron microscopy to identify the source of the degenerating elements seen bilaterally after unilateral retrogasserian rhizotomy in eight adult felines with survival times ranging from 3 to 20 days. At short survival times (3–7 days) degenerating terminals with round synaptic vesicles (R terminals) and type 1, asymmetric contacts predominate bilaterally, while fewer degenerating terminals with flattened synaptic vesicles (F terminals) and type 2, symmetric contacts are seen. At longer survival times more F terminal degeneration is seen, especially on the contralateral side. Postsynaptic sites and dendrites show minimal alterations. These findings suggest that the degenerating R terminals seen on the contralateral side originate from primary afferents while the degenerating F terminals seen on the contralateral side originate from intrinsic sources involving a crossed internuclear pathway. In addition, the finding of degenerating F terminals may represent a novel form of selective transynaptic change of intrinsic neurons, associated with minimal dendritic or somatic alterations.     

The relationship of dorsal root afferents to motoneuron somata and dendrites in the adult bullfrog: a light and electron microscopic study using horseradish peroxidase

The relationship of lumbar dorsal root afferents to lateral motor column motoneurons was studied using anterograde injury filling of dorsal roots and retrograde injury filling of ventral roots with horseradish peroxidase. At the light microscopic level, horseradish peroxidase labelled dorsal root axons were observed to separate into a medial division of large diameter axons which enter the dorsal funiculus and a lateral division of small diameter axons which form a compact bundle in the dorsolateral funiculus which may be homologous to the mammalian tract of Lissauer. Within the spinal gray, primary afferents terminate in two distinct regions. The more ventral of these terminal fields, which receives collaterals of primary afferent axons in the dorsal funiculus, overlaps the dendritic arborizations of the lateral motor column motoneurons. Some axons leave the ventral terminal field to enter the dorsal lateral motor column. Here they terminate on the primary dendrites and somata of lateral motor column motoneurons. At the electron microscopic level, labelled primary afferent terminals were seen to synapse upon lateral motor column motoneuron dendrites as well as upon the somata of dorsally positioned lateral motor column motoneurons. These terminals contain small spherical vesicles and occasional dense-cored vesicles. The synaptic specializations are characterized by a small amount of postsynaptic material. The lateral motor column may be divided into dorsal and ventral portions on the basis of the primary afferent distribution and this is in accord with functional, physiological and developmental data.     

Synaptic organization of the cat entopeduncular nucleus with special reference to the relationship between the afferents to entopedunculothalamic projection neurons: An electron microscope study by a combined degeneration and horseradish peroxidase tracing technique

The synaptic organization of the feline entopeduncular nucleus was studied electron microscopically. After horseradish peroxidase injections into the ventral anterior and ventral lateral nuclear complex of the thalamus, normal axon terminals synapsing with entopedunculothalamic projection neurons were classified into four types on the basis of the size and shape of synaptic vesicles in them, and types of the postsynaptic membrane differentiation. Type I and type II axon terminals were characterized by symmetrical synaptic contacts, and large ovoid or small ovoid synaptic vesicles, respectively. Type II axon terminals were further classified into two subtypes as to their sizes: one was small (IIa), the other large (IIb). Type III and type IV axon terminals were characterized by asymmetrical synaptic contacts, and large ovoid or small ovoid synaptic vesicles, respectively.

To determine the origin of each type of terminal, electrolytic lesions of the caudate nucleus or the subthalamic nuclear region were combined with horseradish peroxidase injections into the thalamus or the subthalamic nuclear region. After electrolytic lesions of the caudate nucleus, degeneration was seen in type I axon terminals contacting entopedunculothalamic projection neurons. Following electrolysis or horseradish peroxidase injection into the subthalamic nuclear region, type IIa and type IV axon terminals showed degenerations or horseradish peroxidase labelling. Such terminals also synapsed with entopedunculothalamic projection neurons. It was demonstrated that these projection neurons relay the striatal or subthalamic inputs directly to the thalamus. After horseradish peroxidase injection into the thalamus, many labelled type II axon terminals were observed to synapse with entopedunculothalamic projection neurons. Type III axon terminals were left unchanged throughout these experiments. In addition, the entopeduncular neuron was observed to receive convergent inputs from both the caudate nucleus and probably the subthalamic nucleus. Axoaxonal synapses were also found to be involved in the synaptic triad.

These results indicate that type I axon terminals originate from the caudate nucleus, part of type IIa and type IV axon terminals originate from the subthalamic nucleus or caudal to the subthalamic nuclear region, and part of type IIa and type IIb terminals come from intrinsic axon collaterals.     

Some properties of sympathetic neuron inhibition by depressor area and intraspinal stimulation

In Nembutal anesthesized cats single shock stimulation of the depressor area of the medulla oblongata evoked inhibition of spontaneous and glutamate-evoked activity of sympathetic preganglionic units. Single shocks to the lateral funiculus of the cervical or upper thoracic spinal cord in acute spinal cats evoked inhibition of the spontaneous and glutamate-evoked activity of single units and of the segmental reflex mass discharge evoked by spinal afferent stimulation. Cats studied 4 to 6 weeks after a complete transection of the spinal cord also showed, on stimulation of the lateral funiculus below the transection, an inhibition of the segmental reflex with time course similar to that seen in the acute spinal state, but of lower threshold and greater intensity. These results suggest that the inhibitory coupling between supraspinal levels and sympathetic preganglionic units is mediated, at least in part, by propriospinal neuronal system which survive after chronic spinal section. On the assumption that the observed changes in the properties of inhibition are due to plastic changes consequent to partial denervation the results also suggest that continuous descending tracts exist, and that both the continuous and the propriospinal descending tracts may be converging onto some common neural element.     

Reimplantation of avulsed lumbosacral ventral roots in the rat ameliorates injury-induced degeneration of primary afferent axon collaterals in the spinal dorsal columns

Injuries to the cauda equina/conus medullaris portion of the spinal cord can result in motor, sensory, and autonomic dysfunction, and neuropathic pain. In rats, unilateral avulsion of the motor efferents from the lumbosacral spinal cord results in at-level allodynia, along with a corresponding glial and inflammatory response in the dorsal horn of the spinal cord segments immediately rostral to the lesion. Here, we investigated the fate of intramedullary primary sensory projections following a motor efferent lesion. The lumbosacral (L6 and S1) ventral roots were unilaterally avulsed from the rat spinal cord (VRA; n=9). A second experimental group had the avulsed roots acutely reimplanted into the lateral funiculus (Imp; n=5), as this neural repair strategy is neuroprotective, and promotes the functional reinnervation of peripheral targets. A laminectomy-only group served as controls (Lam; n=7). At 8 weeks post-lesion, immunohistochemical examination showed a 42% reduction (P<0.001) in the number of RT97-positive axons in the ascending tracts of the dorsal funiculus of the L4-5 spinal segment in VRA rats. Evidence for degenerating myelin was also present. Reimplantation of the avulsed roots ameliorated axon and myelin degeneration. Axons in the descending dorsal corticospinal tract were unaffected in all groups, suggesting a specificity of this lesion for spinal primary sensory afferents. These results show for the first time that a lesion restricted to motor roots can induce the degeneration of intramedullary sensory afferents. Importantly, reimplantation of the lesioned motor roots ameliorated sensory axon degeneration. These data further support the therapeutic potential for reimplantation of avulsed ventral roots following trauma to the cauda equina/conus medullaris.     

Terminations of reticulospinal fibers originating from the gigantocellular reticular formation in the mouse spinal cord

The present study investigated the projections of the gigantocellular reticular nucleus (Gi) and its neighbors—the dorsal paragigantocellular reticular nucleus (DPGi), the alpha/ventral part of the gigantocellular reticular nucleus (GiA/V), and the lateral paragigantocellular reticular nucleus (LPGi)—to the mouse spinal cord by injecting the anterograde tracer biotinylated dextran amine (BDA) into the Gi, DPGi, GiA/GiV, and LPGi. The Gi projected to the entire spinal cord bilaterally with an ipsilateral predominance. Its fibers traveled in both the ventral and lateral funiculi with a greater presence in the ventral funiculus. As the fibers descended in the spinal cord, their density in the lateral funiculus increased. The terminals were present mainly in laminae 7–10 with a dorsolateral expansion caudally. In the lumbar and sacral cord, a considerable number of terminals were also present in laminae 5 and 6. Contralateral fibers shared a similar pattern to their ipsilateral counterparts and some fibers were seen to cross the midline. Fibers arising from the DPGi were similarly distributed in the spinal cord except that there was no dorsolateral expansion in the lumbar and sacral segments and there were fewer fiber terminals. Fibers arising from GiA/V predominantly traveled in the ventral and lateral funiculi ipsilaterally. Ipsilaterally, the density of fibers in the ventral funiculus decreased along the rostrocaudal axis, whereas the density of fibers in the lateral funiculus increased. They terminate mainly in the medial ventral horn and lamina 10 with a smaller number of fibers in the dorsal horn. Fibers arising from the LPGi traveled in both the ventral and lateral funiculi and the density of these fibers in the ventral and lateral funiculi decreased dramatically in the lumbar and sacral segments. Their terminals were present in the ventral horn with a large portion of them terminating in the motor neuron columns. The present study is the first demonstration of the termination pattern of fibers arising from the Gi, DPGi, GiA/GiV, and LPGi in the mouse spinal cord. It provides an anatomical foundation for those who are conducting spinal cord injury and locomotion related research.     

The projection of the lateral geniculate nucleus to area 17 of the rat cerebral cortex. I. General description.

Lesions were made in the lateral geniculate nucleus of the rat and the consequent degeneration in area 17 of the cerebral cortex was studied by light and electron microscopy. These lesions produced prominent degeneration of axon terminals in layer IV extending into layer III and a much lesser amount in layers I and VI. The darkened degenerating axon terminals forming asymmetric synaptic junctions and were frequently surrounded by hypertrophied astrocytic processes. These terminals appeared to be disposed randomly, forming no discernible patterns. In layer IV 83% of the synapsing, degenerating terminals formed junctions with dendritic spines, 15% with dendritic shafts, and 2% with neuronal perikarya. The dendritic shafts and neuronal perikarya appeared to belong to spine-free stellate cells. The dendrites giving rise to the spines receiving degenerating axon terminals could not be identified, for most of the spines appeared as isolated profiles that could not be traced back to their dendritic shafts. One example of a degenerating axon terminal synapsing with an axon initial segment was encountered. Small, degenerating myelinated axons were prevalent in layers VI, V and IV, but were only infrequent in the supragranular layers. These results are compared with those obtained in other studies of thalamocortical projections.     

The lateral cervical nucleus in the cat III. An electron microscopical study after transection of spinal afferents

Summary The ultrastructure of terminal degeneration within the lateral cervical nucleus (LCN) after transection of its spinal afferent fibers 2 days–2 years earlier is described. The degeneration after 2 days was of both the neurofilamentous and dense type. The highest number of degenerating terminals, about 15%, was found after 4–5 days. Then most of the degenerating boutons were of the dense type. The degenerating terminals had synaptic contact with cell bodies and dendrites of LCN-neurons. Removal of the degenerating boutons seemed to be effected by a phagocytic cell present in increased number compared to the normal LCN. In cases with long survival times an increase in the number of astroglial filaments was observed. In an animal where the spinal afferents to the LCN had been cut 2 years earlier a decrease in medium size of the neurons was observed. The amount of dendritic spines was also considerably smaller than normally.     

Synaptic architecture in the medial geniculate body (ventral division)

Summary An electron and light microscope study of the ventral division of the medial geniculate body using Golgi techniques, neurofibrillar stains and experimentally induced secondary degeneration. Geniculo-cortical relay cells and Golgi type II interneurons are easily recognized in the Golgi picture; under the electron microscope the two cell types and their dendrites can be identified on the basis of their different plasma structure. Synaptic arrangement of this region is analysed by a detailed comparison between the EM structure and the Golgi picture of the dendrites and axonal arborizations, the neurofibrillar picture of synapses, as well as degeneration pictures after lesions of the inferior colliculus and of the auditory cortical fields. Criteria derived from the light microscope study concerning size and distribution of various nerve endings, as well as secondary degeneration, have been used to identify various axon endings under the EM. The synapses of specific auditory afferents are confined to synaptic clusters arranged around the interdigitating dendritic tufts of relay cells. Although these synaptic clusters resemble in many respects the synaptic glomeruli of the lateral geniculate body, they cannot be termed as such due to lack of a glial capsule and also to less regularity in topographic arrangement of their various axonal and dendritic elements. It became nevertheless possible to identify in the synaptic clusters (1) the terminals of the specific auditory afferents of inferior collicular origin, (2) the axon terminals of Golgi II type neurons and, with less certainty (3) another axonal ending that might belong to descending cortical fibers originating from the auditory region. All types of axons have contacts with the dendrites of relay cells. It is not quite clear, whether the dendrites of Golgi type II cells are involved in these synaptic clusters, but this is very probable. Axo-axonic synapses between type (1) and (2) are frequent, type (1) (the auditory afferent) being always presynaptic. Very numerous synaptic contacts on the distal dendrites of both main cell types are found outside the synaptic clusters. They do not belong to either type (1) or type (2), many look like type (3) and may undergo degeneration after lesions of auditory cortical regions.     

An electron microscopic analysis of pyramidal tract terminations in the spinal cord of the cat

Summary The ultrastructure of the external basilar region (EBR) of the spinal cord has been investigated in normal cats and after ablation of the contralateral sensorimotor cortex. This region (lateral part of lamina V of Rexed) is the main site of termination of descending pyramidal fibres.The EBR contains neurons with light and dark cytoplasm and correspondingly light and dark dendrites. Axon terminals in the EBR can be divided into four types on the basis of the following structural criteria: (1) spheroid synapt vesicles, (2) flattened synaptic vesicles, (3) spheroid clear vesicles and large dense-core vesicles, (4) electron-dense plasma matrix and numerous spheroid vesicles. Types (1) and (2) prevail, forming mainly axondendritic contacts, generally with thin protrusions and spine-like appendages of the dendrites. A few larger synaptic arrangements of glomerular structure were observed.Signs of terminal degeneration can be recognized in the EBR as early as 30 hours after cortical ablation. The structural elements of these terminals are fused into a compact electron-dense material corresponding to the known dark type of degeneration. Three to five days after the lesions a second set of degenerating terminals become recognizable, in which the lysis of cytoplasmic elements is prevalent. This slower modus of degeneration might be distinguished as the light type. Degenerating terminals are located mainly on dendrites of the EBR neurons and are of small size. The shape of the synaptic vesicles can be recognized in some terminals undergoing degeneration according to the light type; they are, as a rule, of flattened type. Synaptic terminals do not degenerate in the glomerular complexes.     

The action of capsaicin on primary afferent central terminals in the superficial dorsal horn of newborn mice

Capsaicin was injected subcutaneously (50 mg/kg) into 10 mice on days 2 or 3 after birth, and 12 h, 3 and 5 days later the distribution and structure of degenerated primary afferent central axons or terminals (C-terminals) in the lumbar spinal dorsal horn were examined by electron microscopy. Degenerated terminal axons with dense or lamellar bodies or higher electron density were conspicuous 12 h after treatment with capsaicin. Severely degenerated unmyelinated axons, including dense or lamellar bodies engulfed by microglial cells, were numerous in the most superficial (marginal) layer, but rarely seen in the substantia gelatinosa. Two types of primary afferent central terminals in the substantia gelatinosa showed various extents of degeneration: small dark C-terminals (CI-terminals) with densely packed agranular synaptic vesicles, and large light ones (CII-terminals) with less dense agranular synaptic vesicles and a few granular synaptic vesicles. Thus, many central axon terminals of dorsal root ganglion (DRG) neurons that are sensitive to capsaicin enter the marginal layer and substantia gelatinosa. Degenerated primary afferent central axons or terminals markedly decreased in the superficial dorsal horn 3 and 5 days after capsaicin treatment, still, there were many degenerating DRG neurons at this time as shown by our previous study. Previously we also reported that fewer slightly degenerating unmyelinated dorsal root axons and small DRG neurons appear at 12 h and larger DRG neurons degenerate later than smaller ones after treatment with capsaicin. As a result, the discovery of many severely degenerated terminal axons in the superficial dorsal horn soon after treatment supports the idea that capsaicin first acts on the central terminals and that this is followed by damage to larger DRG neurons.     

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

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

A GABA immunocytochemical study of rat motor thalamus: light and electron microscopic observations.

A light and electron microscopic study of GABA-immunoreactive neurons and profiles in the ventroanterior-ventrolateral and ventromedial nuclei of rat dorsal thalamus was conducted using antiserum raised against GABA. Less than 1% of the neurons in these motor-related nuclei exhibited GABA immunoreactivity, confirming previous reports that these nuclei are largely devoid of interneurons. Immunoreactive neurons in the ventral anterior-ventral lateral complex and ventromedial nucleus were bipolar or multipolar in shape, and tended to be smaller than non-immunoreactive neurons. GABA immunoreactivity in the neuropil consisted of labeled axon terminals and myelinated and unmyelinated axons, and was lower in the ventral anterior-ventral lateral complex and ventromedial nucleus than in neighboring thalamic nuclei. The density of neuropil immunolabeling was slightly higher in ventral anterior-ventral lateral complex than in ventromedial nucleus. GABA-immunoreactive axon terminals, collectively termed MP boutons for their medium size and pleomorphic vesicles (and corresponding to "F" profiles of some previous studies of thalamic ultrastructure), formed symmetric synapses and puncta adhaerentia contacts predominantly with large and medium-diameter (i.e. proximal) non-immunoreactive dendrites. Approximately 12 and 18% of boutons in the ventral anterior-ventral lateral complex and ventromedial nucleus, respectively, were GABA-immunopositive. Many of these immunoreactive profiles probably arose from GABAergic neurons in the thalamic reticular nucleus, substantia nigra pars reticulata and entopeduncular nucleus. Two types of non-immunoreactive axon terminals were distinguished based on differences in morphology and synaptic termination sites. Boutons with small ovoid profiles and round vesicles that formed prominent asymmetric synapses onto small-diameter dendrites were observed. Mitochondria were rarely observed within these boutons, which arose from thin unmyelinated axons. These boutons composed approximately 82 and 74% of boutons in the ventral anterior-ventral lateral complex and ventromedial nucleus, respectively, and were considered to arise predominantly from neurons in the cerebral cortex. In contrast, boutons with large terminals that contained round or plemorphic vesicles and formed multiple asymmetric synapses predominantly with large-diameter dendrites were also observed. Puncta adhaerentia contacts were also common. Mitochondria were numerous within large boutons with round vesicles, which arose from myelinated axons. Many of the large boutons were likely to have originated from neurons in the cerebellar nuclei. Approximately 6% of the boutons in the ventral anterior-ventral lateral complex and 8% in ventromedial nucleus were of the large type.(ABSTRACT TRUNCATED AT 400 WORDS)     

The electron microscopic localization of methionine-enkephalin within the superficial layers (I and II) of the spinal cord

The synaptic relationships of methionine-enkephalin containing axon terminals within layers I and II of the rat spinal cord have been investigated using immunocytochemical techniques. Labelled terminals contained large numbers of spherical synaptic vesicles and formed synaptic contacts with dendritic shafts and spines and to a lesser extent with cell bodies within the superficial layers of the dorsal horn. A large number of labelled terminals were seen in apposition to profiles containing pleomorphic vesicles, particularly within layer I and outer layer II. Following rhizotomy, degenerating primary afferent axon terminals were found throughout layers I and II but only in one case was a synaptic relationship with a labelled terminal observed.Thus we were unable to find a morphological correlate of the reported effects of opiates on sensory axons and terminals.     

Axonal projection of descending pathways responsible for eliciting forelimb stepping into the cat cervical spinal cord

Summary The descending pathways responsible for eliciting forelimb stepping are located in the lateral funiculus (Yamaguchi 1986). In order to determine into which spinal segments the descending pathways project and to know the projections and functions of the other descending system, the ventral funicular pathways, we placed various lesions in the cervical spinal cord of decerebrate cats with the lower thoracic cord transected and studied their effects on forelimb stepping evoked by stimulation of the midbrain locomotor region. (1) The lateral funiculus was transected on one side. The operation removes descending input to all the segments caudal to the lesion. Experiments with serial transections from the caudal to rostral segment revealed that stepping activity of the limb on the lesioned side is reduced when the lesion is placed at the level between the C6 and C7 segment and then between C5 and C6. A slight reduction of activity was also observed after a lesion placed between C7 and C8. (2) Consistently, bilateral transection of the lateral funiculus at the level between C5 and C6 abolished stepping movements of both forelimbs. (3) The cervical cord was split in the parasagittal plane through the dorsal root entry. The operation removes the descending input to the segment in which the lesion is placed. The parasagittal lesions from the C1 to C6 did not abolish stepping activity, although a lesion placed between C5 and C6 could slightly affect stepping. The results, (1)–(3) suggest that the lateral funicular pathways project into the spinal segments mainly at the C6–C7 level with some rostrocaudal extension into C5 and C8. (4) Complete transections of the medial part of the spinal cord cut extensor bursts short and raised stepping frequency. Nevertheless, if the lesion at C1–C5 spared the ventromedial part of the ventral funiculus, it did not result in such high-frequency stepping or in weakened extensor activity. In the case of segments caudal to C6, medial transections which spared the corresponding region could result in such stepping. It is suggested that the pathways descending through the ventromedial part of the ventral funiculus in the rostral segments provide extensor activity during stepping. They may change their course in the more dorsal part of the ventral funiculus below the C6 and presumably project into the grey matter of more caudal segments.     

Nigral and cerebellar synaptic terminals in the intermediate and deep layers of the cat superior colliculus revealed by lesioning studies

The presence of degenerating nigral and cerebellar synaptic terminals in the intermediate and deep layers of the cat superior colliculus was demonstrated by electron microscopy following lesions of the substantia nigra or brachium conjunctivum. The superior colliculus was taken for analysis 4–5 days after operation. Nigral terminals underwent a dark type of degeneration following kainic acid lesion of the pars reticulata of the substantia nigra. The majority of nigral degenerating terminals and axons were found in the stratum griseum intermediate with a few in the stratum griseum profundum. Two kinds of cerebellar terminals were distinguished by general appearances such as size, type of synaptic contact and type of synaptic vesicle and by the pattern of degenerative changes following electrical lesion of the brachium conjunctivum. Large elongated synaptic terminals 4–7 μm in diameter, were found mainly in the stratum griseum profundum. They often had double termination with conventional dendrites and with vesicles containing dendrites. This kind of terminal had a filamentous type of degeneration. A second type of degenerating cerebellar terminal, characterized by an electron-lucent type of degeneration, was predominantly located in the stratum griseum intermediale. These terminals were circular, about 4 μm in diameter, and did not have synaptic contact with vesicle-containing profiles. The finding of the two types of degenerating terminal after lesion of the brachium conjunctivum can be considered as evidence of the coexistence of at least two kinds of cerebellar terminals in the superior colliculus. The presence of nigral and cerebellar terminals in the intermediate and deep layers of the superior colliculus implicates the involvement of the substantia nigra and cerebellum in control of collicular visuomotor function.     

Male-female differences in the intra-amygdaloid input to the medial amygdala

Following lesion of the posterior cortical nucleus of the amygdala (PCAN), the number of degenerating axon terminals and alterations of synaptic pattern were studied in the molecular layer (ML) of the medial nucleus of the amygdala (MAN) of male and female rats. Semiquantitative analyses by electron microscopy indicated that, 1 and 2 days after the lesion, the number of degenerating terminals in the ventral ML of male rats was statistically greater than that of female rats. Ten days after the operation, intact synapses remaining on dendritic shafts of the medial ML and those on dendritic spines of the ventral ML of male rats significantly decreased in number, compared with unoperated controls. On the other hand, no significant reduction was noted in synapses of the lesioned female rats killed 10 days after the operation. Thus, the number of axon terminals in the male ML originating from the lesioned area was greater than that of the female ML. The number of synapses in the ML of unoperated male rats was statistically greater than that of unoperated females. However, these sex differences in synaptic number became undetectable 10 days after the operation. These findings provide morphological evidence indicating that the fibers from and/or through the PCAN participate in emergence of synaptic sexual dimorphism in the ML of the MAN.     

Skilled digit movements in feline and primate--recovery after selective spinal cord lesions

Recovery of voluntary movements after partial spinal cord injury depends, in part, on a take-over of function via unlesioned pathways. Using precise forelimb movements in the cat as model, spinal pathways contributing to motor restitution have been investigated in more detail. The food-taking movement by which the cat graSPS a morsel of food with the digits and brings it to the mouth is governed by interneurones in the forelimb segments (C6-Th1) and is normally controlled via the cortico- and rubrospinal tracts. Food-taking disappears after transection of these pathways in the dorsal part of the lateral funiculus (DLF) in C5/C6, but then recovers during a period of 2-3 weeks. Experiments with double lesions showed that the recovery depends on a take-over via ipsilateral ventral systems; a ventrally descending pathway, most probably cortico-reticulospinal, and a pathway via propriospinal neurones in the C3-C4 segments. It is postulated that the recovery involves a plastic reorganization of these systems. Dexterous finger movements in the macaque monkey are generally considered to depend on the monosynaptic cortico-motoneuronal (CM) connexion, which is lacking in the cat. Such movements are abolished after pyramidotomy at the level of the trapezoid body. However, experiments with transection of the corticospinal tract in the DLF and partly ventral part of the lateral funiculus in C5, showed a fast (1-28 days) recovery of precision grip and, to some extent, independent finger movements. Deficits in preshaping during the final approach to the morsel as well as lack of force were observed. A C5 DLF lesion spares corticofugal pathways to the brainstem and upper cervical segments. It is suggested that indirect corticomotoneuronal pathways may provide for recovery of dexterous finger movements and that the role of CM pathways for such movements should be broadened to include not only the monosynaptic connexion.     

The differential effects of baclofen on segmental and descending excitation of spinal interneurones in the cat

Summary Intravenous baclofen (1–6.25 mg kg^-1) substantially reduced the monosynaptic excitation of neurones in the intermediate nucleus of the cat spinal cord by impulses in group I extensor muscle primary afferent fibres, but had little or no effect on excitation by stimulating fibres of the ipsilateral dorsolateral funiculus or the contralateral red nucleus. Relatively low concentrations of baclofen thus appear not to influence the release of excitatory transmitter from the terminals of rubrospinal, corticospinal and long descending propriospinal fibres, in contrast to the reduction of the release of primary afferent transmitters.