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At least 163 records · Page 9Linked to original sources

[The pyramidal tract is involved in the control of an autonomic response (skin potential response), in the cat (author's transl)].

On Cats paralyzed by gallamine, electrical stimulation of corticospinal fibers still evoked skin potential responses, after a transection of the medulla only sparing the pyramidal tract. These responses persisted even after aspiration of the medullary tissue posterior to the section and overlying the pyramids. These results indicate that the pyramidal tract can participate in the control of electrodermal activities, besides reticular influences that also act upon the spinal level.

Animals↗

Is glutamic acid the pyramidal tract neurotransmitter?

Applied by microiontophoresis, 1-hydroxy-3-amino-pyrrolidone-2 (HA-966) antagonized excitation by glutamic acid but not by acetylcholine of neurones in the rat cuneate nucleus. HA-966 blocked the short latency excitation of cuneate neurones following stimulation of the pyramidal tract on 28 of 40 cells (70%). Thus, glutamate or a related amino-acid may be the neurotransmitter released by pyramidal tract neurones.

Acetylcholine↗

The dynamic sensitivity of pyramidal tract neurones is influenced by previous activity.

The dynamic sensitivity of Pyramidal Tract (PT) neurones has been examined in silent cells and after pre-activation with an action potential evoked at different intervals before the discharge onset. In the resting conditions the dynamic sensitivity increases after the first interspike interval of the repetitive discharge. When a conditioning spike precedes the discharge onset by 50 ms (i.e. of a time sufficient for its afterhyperpolarization, AHP, to fade out) the dynamic sensitivity becomes uniform throughout the ramp. This linearizing effect progressively declines when the conditioning interval is increased to 100 and 150 ms and is attributed to the "depression" induced by the conditioning spike on the AHP of the first spike of the ramp discharge. In natural conditions, the effect would be entirely developed when the neurones fire at their minimal discharge rate (1/AHP duration).

Animals↗

Axons of the pyramidal tract do not increase their transport of growth-associated proteins after axotomy.

We compared the effects of axotomy on the composition of fast axonally transported proteins in rat sciatic sensory axons and pyramidal tract axons, 7 days after axotomy. L-[35S]methionine was administered to dorsal root ganglia or sensorimotor cortex and after 6 or 4 h, respectively, labelled proteins were obtained from sciatic nerve or pyramidal tract. Transported proteins were characterized by one- and two-dimensional electrophoresis, followed by fluorography. As previously reported, sciatic axotomy produced changes in the labelling of fast-transported proteins, notably, increased labelling of a spot designated GAP43. In contrast axotomy of pyramidal axons produced no increased labelling of GAP43, although it could be identified in both normal and axotomized samples. Autoradiography of spinal cord distal to the lesion confirmed that our procedures did indeed label axons and that the axotomy did interrupt these axons. Our finding that axotomy does not stimulate changes in composition of fast-transported proteins in the corticospinal tract agrees with previous studies on mammalian retinal ganglion cell axons and leads us to conclude that this failure to respond to axotomy is a general feature of non-regenerating CNS axons.

Animals↗

[18p-syndrome with bilateral pyramidal tract signs, dystonia of the lower extremities and concentric visual field defect].

A case, diagnosed as 18p-syndrome by typical clinical appearance and by chromosomal analysis, presented with multiple nervous system defects consisting of bilateral pyramidal tract signs, weakness and focal dystonia of the lower extremities, and concentric visual field defect. Chromosomal analysis revealed karyotype 46, X, dic (Y;18) (p11;p11), inv(9) (p11q13), and the points of chromosomal breakages were thought to be in the short arm of chromosome 18 and in the short arm of Y chromosome. 18p-syndrome is caused by a chromosomal deletion, and presents with a wide variety of clinical appearances. Many cases have been reported since the original descriptions by de Grouchy in 1963, though with few mentions of neurological deficits other than mental retardation. Furthermore, there have been no reports of pyramidal tract signs, weakness and focal dystonia of the lower extremities, or visual field defect, without recognizable anatomical abnormalities. Our case of 18p-syndrome is quite rare because of multiple nervous system abnormalities mentioned above, not accompanied by malformations of the central nervous system.

Adult↗

Pontine tegmentum hematoma: a case report with the "one-and-a-half" syndrome without pyramidal tract deficit.

The author reports the case of a 54-year-old male patient with a pontine hematoma and with the one-and-a-half syndrome, cerebellar ataxia and no signs of pyramidal tract involvement. The absence of involvement of the pyramidal tract in the case reported herein is likely due to variation in the vascular anatomy of the pons. The pathophysiologic mechanisms of the one-and-a-half syndrome and of the clinical findings recorded are discussed.

Cerebral Hemorrhage↗

GABAB receptor antagonist CGP 35348 shortens transcallosal response latency of pyramidal tract neurons.

The effects of a specific GABAB receptor antagonist, p-(3-aminopropyl)-p-diethoxymethyl-phosphonic acid (CGP 35348), on pyramidal tract neuron responses to transcallosal stimulation were investigated in the cat motor cortex in vivo. Iontophoretic application of CGP 35348 significantly increased the number of spikes from 10.3 +/- 4.4 (control; n = 27; mean +/- S.D.) to 16.7 +/- 7.2 (CGP 35348) for 20 transcallosal stimulation trials, while the latency of neuronal activity was significantly shortened from 4.4 +/- 2.1 ms (control; n = 27; mean +/- S.D.) to 3.8 +/- 1.7 ms (CGP 35348). In conclusion, CGP 35348 facilitated transcallosal synaptic transmission between pyramidal tract neurons by removal of GABAB inhibition.

Action Potentials↗

Preoperative assessment of motor cortex and pyramidal tracts in central cavernoma employing functional and diffusion-weighted magnetic resonance imaging.

BACKGROUND: Functional MRI (fMRI) combines anatomic with functional information and has therefore been widely used for preoperative planning of patients with mass lesions affecting functionally important brain regions. However, the courses of functionally important fiber tracts are not visualized. We therefore propose to combine fMRI with diffusion-weighted MRI (DWI) that allows visualization of large fiber tracts and to implement this data in a neuronavigation system. METHODS: DWI was successfully performed at a field strength of 1.5 Tesla, employing a spin-echo sequence with gradient sensitivity in six noncollinear directions to visualize the course of the pyramidal tracts, and was combined with echo-planar T2* fMRI during a hand motor task in a patient with central cavernoma. RESULTS: Fusion of both data sets allowed visualization of the displacement of both the primary sensorimotor area (M1) and its large descending fiber tracts. Intraoperatively, these data were used to aid in neuronavigation. Confirmation was obtained by intraoperative electrical stimulation. Postoperative MRI revealed an undisrupted pyramidal tract in the neurologically intact patient. CONCLUSION: The combination of fMRI with DWI allows for assessment of functionally important cortical areas and additional visualization of large fiber tracts. Information about the orientation of fiber tracts in normal appearing white matter in patients with tumors within the cortical motor system cannot be obtained by other functional or conventional imaging methods and is vital for reducing operative morbidity as the information about functional cortex. This technique might, therefore, have the prospect of guiding neurosurgical interventions, especially when linked to a neuronavigation system.

Adult↗

Differential connections by intracortical axon collaterals among pyramidal tract cells in the cat motor cortex.

1. Recurrent EPSPs were produced in fast pyramidal tract (PT) cells in the cat motor cortex by stimulation of the medullary pyramid and/or by the glutamate-induced activity of neighbouring PT cells using the spike-triggered averaging (spike-TA) method. 2. In fast PT cells located lateral to the end of the cruciate sulcus, predominantly the motor cortical representation area of the distal forelimb, two components (fast and slow) of recurrent EPSPs were produced by pyramid stimulation. 3. In response to pyramid stimulation, the appearance of the fast and slow components of recurrent EPSPs correlated with the appearance of N1 and N2 field potentials, respectively. 4. The monosynaptic nature of both the fast and slow components of recurrent EPSPs was demonstrated by a double shock test (interstimulus interval less than 5 ms) and high frequency repetitive stimulation (50-100 Hz). 5. The generation of the fast and slow components of recurrent EPSPs was attributed to the synaptic action of recurrent collaterals of fast and slow PT cells, respectively. 6. The amplitude of the slow component of recurrent EPSPs markedly increased with an increase in the stimulus frequency whereas that of the fast component did not, despite the change in stimulus frequency. 7. Selected spike-triggered averaging also revealed frequency facilitation of recurrent individual EPSPs produced in fast PT cells by the activity of single slow PT cells. 8. In fast PT cells located in the anterior and posterior lips of the cruciate sulcus, the motor cortical representation area of the proximal limb or trunk, only the slow component of recurrent EPSPs was produced by pyramid stimulation. 9. It is concluded that the pattern of recurrent connections between neighbouring PT cells differs depending on the motor cortical representation area, and that frequency facilitation of recurrent EPSPs is caused mainly by the input from axon collaterals of slow PT cells.

Animals↗

Relation of size and activity of motor cortex pyramidal tract neurons during skilled movements in the monkey.

Activity of motor cortex pyramidal tract neurons (PTNs) was recorded in monkeys making large (20 degrees), high velocity and small (1 to 2 degrees), low velocity pronation-supination arm movements in a visual pursuit-tracking paradigm. Antidromic response latencies (ADLs) or PTNs were examined in relation to PTN modulation with the large and small movements to test the hypothesis that PTNs would exhibit a "size principle" analogous to that of spinal cord motoneurons. It was found that smaller PTNs (i.e., those having longer ADLs) discharged just as strongly with small, slow movements as with large, fast movements, while about one-third of the larger PTNs (even those selected for a significant relation to small movement) discharged more intensely with the large movement. Another analysis dealing with PTNs in a selected set of penetrations in an area focal for pronation-supination showed that PTNs with longer ADLs (greater than 1 msec) were more likely to reach maximum frequency with small, slow movement. There was, however, much overlap in the behavior of small and large PTNs, and while there was a statistically significant relation between size and movement-related activity of PTNs, there did not seem to be a "size principle" in the strict sense that this term has been used with reference to spinal cord motoneurons.

Animals↗

Morphometry of the pyramidal tract in the spinal cord of normal rats.

A morphometric study of the pyramidal tract at the spinal cord level in the normal albino rat is reported. The area, perimeter, axonal and glial cell count, and axonal concentration were determined at the seventh cervical, second thoracic, and third lumbar spinal cord levels. The results show consistent diminishing values of the area, axonal and glial cell count, and axonal concentration with the tract descent in the spinal cord.

Animals↗

Morphological characterization of slow and fast pyramidal tract cells in the cat.

In adult cats the morphology of slow and fast pyramidal tract (Pt) neurons was studied following intracellular HRP injections and Golgi impregnation. Both types of neurons are pyramidal cells and their soma are all located in the fifth layer of the motor area. As a rule, fast Pt neurons have large somata and their basal and apical dendrites occupy a larger territory in the tangential plane. In layer I, terminal apical dendrites of fast Pt neurons are smooth and divide poorly while those of slow Pt neurons bear a moderate amount of spines and branch profusely. Midway between the pia and layer V, in the third layer, the apical shafts of both types of Pt cells run upward with little branching. These shafts are more numerous in fast Pt cells (7 to 16) and they are almost devoid of spines. Those of slow Pt cells in layer III number between 5 and 9 and are densely covered with spines. Oblique and horizontal branches of slow and fast Pt neurons extend in layer V and some of them invade the lower part of layer III. It is suggested that this zone corresponds to a true fourth layer in the motor area. In both types of cells oblique and lateral branches bear numerous spines. Within the basal dendritic territory of Pt cells, one has to distinguish two dendritic systems: a short and a long one. The former spreads downward obliquely and appears to remain within layer V. The latter is made up of long descending vertical (antiapical) and oblique dendrites (tap root). While both types of cells may have long antiapical dendrites that run down radially to the lower part of layer VI, tap root dendrites which expand laterally below the cell body for considerable distances are a distinctive feature of fast Pt neurons. Though basal dendrites of all Pt cells bear spines, their number, distribution and shape are very variable in fast Pt cells.

Animals↗

Location of human pyramidal tract in the internal capsule: anatomic evidence.

A patient with a small infarct located posteriorly in the internal capsule had 9 years of weakness of the contralateral face, arm, and leg. At necropsy, it was found that degeneration of the corticospinal tract was almost complete in the midbrain and medullary pyramid. This case supports the increasing evidence that the human pyramidal tract is located in the third quarter of the posterior limb of the internal capsule.

Brain Mapping↗

Immunocytochemical distribution of the protein kinase C substrate B-50 (GAP43) in developing rat pyramidal tract.

The neuron-specific phosphoprotein B-50 is a major substrate of kinase C in fetal nerve growth cones, neonatal neural and synaptosomal plasma membranes. B-50 is identical to a growth-associated protein GAP43. Similarly, increases in B-50 occur during rat brain development, neuronal differentiation and axon regeneration. To document the relation between the expression of B-50 and the outgrowth of central axons, we studied B-50 in the developing pyramidal tract in rats at postnatal days 2, 7 and 90 (P2, P7 and P90), at the third cervical spinal segment C3, using affinity-purified antibodies to B-50. At P2 and P7, when outgrowth of pyramidal tract fibers is occurring, B-50 immunoreactivity (BIR) is intense in these fibers. BIR is reduced from P2 to P7 in the ascending fiber tracts of the cuneatus and the gracilis, which develop earlier. At P90 when most of the dorsal funiculus fibers have reached their targets and many are myelinated, BIR is dramatically reduced. In agreement, a 10-fold decrease in B-50 content was measured at P90, as compared to P7. Therefore, our results indicate that B-50 is only expressed relatively abundant in axons of the funiculus posterior during outgrowth. By inference, B-50 may be a differentiating marker to detect elongating fibers.

Animals↗

Autosomal dominant juvenile amyotrophic lateral sclerosis and distal hereditary motor neuronopathy with pyramidal tract signs: synonyms for the same disorder?

Autosomal dominant juvenile amyotrophic lateral sclerosis (ALS) is a rare disorder and so far only one family has been reported. Genetic linkage studies mapped the disease locus to chromosome 9q34 (ALS4). The diagnosis of ALS in this family is based on the clinical signs with almost exclusively lower motor neurone pathology in combination with less prominent pyramidal tract signs. Atypical features include normal life expectancy, the absence of bulbar involvement and the symmetrical distal distribution of atrophy and weakness. We performed a molecular genetic study in three families that we had diagnosed as having distal hereditary motor neuronopathy, i.e. distal spinal muscular atrophy or spinal Charcot-Marie-Tooth syndrome, and found linkage to the ALS4 locus. The clinical phenotype in these three families, of different geographic origin (Austria, Belgium and England), is strikingly similar to the autosomal dominant juvenile ALS family except for a younger onset age in two of the distal hereditary motor neuronopathy families. These data suggest that ALS4 and distal hereditary motor neuronopathy with pyramidal tract signs may be one and the same disorder.

Adolescent↗

Tests for presynaptic modulation of corticospinal terminals from peripheral afferents and pyramidal tract in the macaque.

The efficacy of sensory input to the spinal cord can be modulated presynaptically during voluntary movement by mechanisms that depolarize afferent terminals and reduce transmitter release. It remains unclear whether similar influences are exerted on the terminals of descending fibres in the corticospinal pathway of Old World primates and man. We investigated two signatures of presynaptic inhibition of the macaque corticospinal pathway following stimulation of the peripheral nerves of the arm (median, radial and ulnar) and the pyramidal tract: (1) increased excitability of corticospinal axon terminals as revealed by changes in antidromically evoked cortical potentials, and (2) changes in the size of the corticospinal monosynaptic field potential in the spinal cord. Conditioning stimulation of the pyramidal tract increased both the terminal excitability and monosynaptic fields with similar time courses. Excitability was maximal between 7.5 and 10 ms following stimulation and returned to baseline within 40 ms. Conditioning stimulation of peripheral nerves produced no statistically significant effect in either measure. We conclude that peripheral afferents do not exert a presynaptic influence on the corticospinal pathway, and that descending volleys may produce autogenic terminal depolarization that is correlated with enhanced transmitter release. Presynaptic inhibition of afferent terminals by descending pathways and the absence of a reciprocal influence of peripheral input on corticospinal efficacy would help to preserve the fidelity of motor commands during centrally initiated movement.

Animals↗

Somatosensory input onto pyramidal tract neurons in rodent motor cortex.

This study was performed to determine whether pyramidal tract neurons (PTNs), the output cells of the motor cortex, are targets of direct input from the somatosensory cortex (SI). PTNs were identified by light microscope (LM) and electron microscope (EM) retrograde tract tracing techniques. For LM analysis, they were intracellularly filled to exhibit their full dendritic arbor. Axons originating from the electrophysiologically identified forelimb representation of SI were labeled by LM and EM anterograde tract tracing techniques. LM analysis of dual-labeled tissue showed that PTNs were situated to receive direct input from SI. The distribution and density of this input was predicted from the findings. EM analysis confirmed that PTNs receive direct input from SI. The input is sparse and not all PTNs appear to receive input. SI terminals do not appear to target specific segments of PTN dendrites. This corticocortical pathway may provide MI with the short latency sensory feedback which is needed to produce coordinated voluntary movements.

Amidines↗